Tresch and Aronow's cardiovascular

disease in the elderly Sixth Edition

Aronow
Visit to download the full and correct content document:
https://textbookfull.com/product/tresch-and-aronows-cardiovascular-disease-in-the-el
derly-sixth-edition-aronow/
More products digital (pdf, epub, mobi) instant
download maybe you interests ...

Frailty and Cardiovascular Diseases Research into an

Elderly Population Nicola Veronese

https://textbookfull.com/product/frailty-and-cardiovascular-
diseases-research-into-an-elderly-population-nicola-veronese/

3-Dimensional Modeling in Cardiovascular Disease 1st

Edition M.D. Zahn

https://textbookfull.com/product/3-dimensional-modeling-in-
cardiovascular-disease-1st-edition-m-d-zahn/

Epidemic of Cardiovascular Disease and Diabetes:

Explaining the Phenomenon in South Asians Worldwide Raj
S Bhopal

https://textbookfull.com/product/epidemic-of-cardiovascular-
disease-and-diabetes-explaining-the-phenomenon-in-south-asians-
worldwide-raj-s-bhopal/

Handbook of Cardiovascular Disease Management in

Rheumatoid Arthritis 1st Edition Anne Grete Semb (Eds.)

https://textbookfull.com/product/handbook-of-cardiovascular-
disease-management-in-rheumatoid-arthritis-1st-edition-anne-
grete-semb-eds/
Braunwald’s Heart Disease : A Textbook of
Cardiovascular Medicine, Eleventh Edition Douglas P.
Zipes

https://textbookfull.com/product/braunwalds-heart-disease-a-
textbook-of-cardiovascular-medicine-eleventh-edition-douglas-p-
zipes/

Braunwald’s Heart disease: A Textbook of Cardiovascular

Medicine 11th Edition Douglas P. Zipes

https://textbookfull.com/product/braunwalds-heart-disease-a-
textbook-of-cardiovascular-medicine-11th-edition-douglas-p-zipes/

Dietary Fiber for the Prevention of Cardiovascular

Disease: Fiber’s Interaction between Gut Micoflora,
Sugar Metabolism, Weight Control and Cardiovascular
Health 1st Edition Rodney A. Samaan Md Mph Bs
https://textbookfull.com/product/dietary-fiber-for-the-
prevention-of-cardiovascular-disease-fibers-interaction-between-
gut-micoflora-sugar-metabolism-weight-control-and-cardiovascular-
health-1st-edition-rodney-a-samaan-m/

Medical Ethics and the Elderly 3rd Edition Rai

https://textbookfull.com/product/medical-ethics-and-the-
elderly-3rd-edition-rai/

Rational Suicide in the Elderly Clinical Ethical and

Sociocultural Aspects 1st Edition Robert E. Mccue

https://textbookfull.com/product/rational-suicide-in-the-elderly-
clinical-ethical-and-sociocultural-aspects-1st-edition-robert-e-
mccue/
Tresch and Aronow’s Cardiovascular
Disease in the Elderly
Tresch and Aronow’s Cardiovascular
Disease in the Elderly
Sixth Edition

Edited by
Wilbert S. Aronow, MD
Professor of Medicine and Director of Cardiology Research
Westchester Medical Center/New York Medical College
Jerome L. Fleg, MD
Division of Cardiovascular Sciences, National Heart, Lung, and Blood
Institute, National Institutes of Health
Michael W. Rich, MD
Professor of Medicine
Washington University School of Medicine
CRC Press
Taylor & Francis Group
6000 Broken Sound Parkway NW, Suite 300
Boca Raton, FL 33487-2742

© 2019 by Taylor & Francis Group, LLC

CRC Press is an imprint of Taylor & Francis Group, an Informa business

No claim to original U.S. Government works

Printed on acid-free paper

International Standard Book Number-13: 978-1-138-55829-8 (Hardback)

This book contains information obtained from authentic and highly regarded sources. Reasonable efforts have been made to publish reliable data and
information, but the author and publisher cannot assume responsibility for the validity of all materials or the consequences of their use. The authors and
publishers have attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to
publish in this form has not been obtained. If any copyright material has not been acknowledged please write and let us know so we may rectify in any future
reprint.

Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic,
mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval
system, without written permission from the publishers.

For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright.com/) or contact the
Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses
and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been
arranged.

Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without
intent to infringe.

Library of Congress Cataloging‑in‑Publication Data

Names: Aronow, Wilbert S., editor. | Fleg, Jerome L., editor. | Rich, Michael W., editor.
Title: Tresch and Aronow’s cardiovascular disease in the elderly / edited by Wilbert S. Aronow, Jerome L. Fleg, and Michael W. Rich.
Other titles: Cardiovascular disease in the elderly
Description: Sixth edition. | Boca Raton, FL : CRC Press/Taylor & Francis Group, [2019] | Includes bibliographical references and index.
Identifiers: LCCN 2018035161 | ISBN 9781138558298 (hardback : alk. paper)
Subjects: | MESH: Cardiovascular Diseases--physiopathology | Cardiovascular Diseases--therapy | Aged
Classification: LCC RC669 | NLM WG 120 | DDC 618.97/61--dc23
LC record available at https://lccn.loc.gov/2018035161

Visit the Taylor & Francis Web site at

http://www.taylorandfrancis.com

and the CRC Press Web site at

http://www.crcpress.com
Contents

Foreword vii
Preface ix
Editors xi
Contributors xiii

1 Cardiovascular changes with aging 1

Jerome L. Fleg
2 Morphologic features and pathology of the elderly heart 28
Atsuko Seki, Gregory A. Fishbein, and Michael C. Fishbein
3 General principles on caring for older adults 49
Dae Hyun Kim and Sandra M. Shi
4 Cardiovascular drug therapy in the elderly 64
William H. Frishman, Wilbert S. Aronow, and Angela Cheng-Lai
5 Systemic hypertension in the elderly 95
Wilbert S. Aronow and William H. Frishman
6 Disorders of lipid metabolism 111
Mays T. Ali and Seth S. Martin
7 Diabetes mellitus and cardiovascular disease in the elderly 128
Samuel C. Durso
8 Epidemiology and prevention of coronary heart disease in older adults 149
Nathan D. Wong, David Tehrani, and Stanley S. Franklin
9 Diagnosis of coronary heart disease in the elderly 166
Wilbert S. Aronow and Jerome L. Fleg
10 Angina pectoris in the elderly 187
Wilbert S. Aronow and William H. Frishman
11 Therapy of acute myocardial infarction 206
Joshua M. Stolker and Michael W. Rich
12 Management of the older patient after myocardial infarction 239
Howard A. Cooper, Julio A. Panza, and Wilbert S. Aronow
13 Surgical management of coronary artery disease 255
Melissa M. Anastacio, Alejandro Suarez Pierre, and Jennifer S. Lawton
14 Percutaneous coronary intervention in the elderly 266
Kashish Goel and David R. Holmes
15 Exercise training and comprehensive cardiac rehabilitation in older cardiac patients 282
Daniel E. Forman
16 Aortic valve disease in the elderly 293
Madhur A. Roberts, Ryan K. Kaple, and Wilbert S. Aronow
17 Mitral regurgitation, mitral stenosis, and mitral annular calcification in the elderly 323
Hasan Ahmad and Wilbert S. Aronow
18 Infective endocarditis in older adults 353
Sairia Dass and Lona Mody
19 Cardiomyopathies in the elderly 366
John Arthur McClung, Srihari S. Naidu, and Wilbert S. Aronow

v
vi Contents

20 Thyroid heart disease in the elderly 383

Myron Miller and Steven R. Gambert
21 Heart failure with reduced ejection fraction in older adults 406
Ali Ahmed and Jerome L. Fleg
22 Heart failure with preserved ejection fraction in older adults 422
Bharathi Upadhya and Dalane W. Kitzman
23 Supraventricular tachyarrhythmias in the elderly 442
Jason T. Jacobson, Sei Iwai, Ali Ahmed, and Wilbert S. Aronow
24 Ventricular arrhythmias in the elderly 468
Jason T. Jacobson, Sei Iwai, and Wilbert S. Aronow
25 Bradyarrhythmias and cardiac pacemakers in the elderly 490
Naktal Hamoud, Fernando Tondato, and Win-Kuang Shen
26 Cerebrovascular disease in the elderly patient 512
Laura Stein and Jesse Weinberger
27 Evaluation and management of syncope and related disorders in the elderly 530
Andrea Ungar, Martina Rafanelli, and Michele Brignole
28 Pericardial disease in the elderly 544
Massimo Imazio
29 Venous thromboembolic disease in older adults 563
Laurie G. Jacobs, Justin B. Kaplan, and Ruchi Jain
30 Management of peripheral arterial disease in the elderly 584
Wilbert S. Aronow
31 Perioperative cardiovascular evaluation and treatment of elderly patients undergoing noncardiac surgery 602
Dipika Gopal, Monika Sanghavi, and Lee A. Fleisher
32 Ethical decisions and end-of-life care in older patients with cardiovascular disease 626
Esther S. Pak, James N. Kirkpatrick, Craig Tanner, and Sarah J. Goodlin

Index 639
Foreword
It is indeed a pleasure to write this foreword for the new
sixth edition of Tresch and Aronow’s Cardiovascular Disease
in the Elderly. This work has now become a classic in the
field of geriatric cardiology, and the new edition contains a
great deal of up-to-date information concerning the diag-
nosis and therapy of cardiovascular disease in this ever-
expanding segment of our population.
All of the chapters have been revised to reflect the latest
research in this large and complex field. Excellent summa-
ries are found at the outset of each chapter in order to facili-
tate easy reading, and there is a comprehensive bibliography
for readers interested in delving more deeply into a particu-
lar topic. Contemporary evidence-based recommendations
are suggested when available, and there is continued strong
emphasis on new research findings. For example, readers
will find an extensive discussion of the direct-acting anti-
thrombotic agents that are rapidly replacing warfarin.
This is truly a lovely book that should be studied by med-
ical practitioners throughout the world, given the remark-
able increase in the number of elderly patients with cardiac
and vascular disorders in recent years. The editors and
authors are to be congratulated for this outstanding contri-
bution to the scientific understanding and clinical care of
older patients with cardiovascular disease.
Joseph S. Alpert, MD
University of Arizona College of Medicine
Editor-in-Chief, The American Journal of Medicine
vii
Preface
In 2010, the first of the baby boomers turned 65 years old,
and we are now in the midst of an explosive growth in the
older adult population in the United States, from 49 mil-
lion in 2016 to approximately 73 million by 2030, with
a further increase to 86 million by 2050.1 Moreover, the
most rapid growth will occur in the subgroup 85 years of
age or older—from 6.4 million in 2016 to 9.0 million in
2030 and 18.6 million by 2050, an almost threefold rise.
Similar demographic shifts are occurring in many coun-
tries around the world. Accompanying this graying of
the population is a dramatic rise in the number of older
persons with cardiovascular disorders, including hyper-
tension, coronary artery disease, valvular heart disease,
heart failure, and cardiac rhythm disturbances. Since per-
sons over age 65 already account for more than 80% of all
deaths attributable to cardiovascular disease, it is essential
for all clinicians involved in the care of older adults—not
just primary care physicians, geriatricians, and cardiolo-
gists, but also surgeons, anesthesiologists, other medical
subspecialists, and nurse practitioners—to have a basic
understanding of the effects of aging on cardiovascular
structure and function, as well as the impact of aging and
prevalent comorbid conditions on the clinical presenta-
tion, diagnosis, and response to therapy in older adults
with cardiovascular disease.
As with prior editions, the primary objective of the pres-
ent volume is to provide an up-to-date and in-depth, yet
clinically relevant and readable overview of the epidemiol-
ogy, pathophysiology, evaluation, and treatment of cardio-
vascular disorders in older adults. To the extent possible,
clinical recommendations are evidence based, but it is also
acknowledged that existing data are often quite limited or
nonexistent in the very elderly (persons 85 years of age or
older), and especially in older adults with multiple coexist-
ing conditions and/or frailty. Thus, careful consideration
of each patient’s unique clinical and psychosocial circum-
stances, medical and nonmedical needs, and personal pref-
erences is required in designing an individualized care plan.
1 US Census Bureau. 2017 National Population Projections Tables.
Available at: https://www.census.gov/data/tables/2017/demo/
popproj/2017-summary-tables.html (accessed July 23, 2018).
Indeed, it is perhaps in the compassionate management of
these challenging patients where the “art” of medicine most
clearly flourishes.
This edition appears 4 years after the fifth edition,
which was published in 2014. During the intervening
period, an extensive body of new research relevant to the
­diagnosis and treatment of cardiovascular disorders in
older adults has been reported. In addition to an expand-
ing literature derived from population-based observa-
tional studies, an increasing number of clinical trials
focusing on older adults have been undertaken, practice
guidelines are increasingly providing explicit commen-
tary on the diagnosis and management of older adults,
and both the American College of Cardiology and the
American Heart Association have established sections
focusing on issues relevant to older adults with cardiovas-
cular disease.
With the sixth edition of this work, we have added a new
chapter entitled “General Principles on Caring for Older
Adults,” which subsumes and expands the chapter on dis-
ability and frailty from the fifth edition. We also expanded
the chapter on heart failure to two chapters addressing
“Heart Failure with Reduced Ejection Fraction in Older
Adults” and “Heart Failure with Preserved Ejection Fraction
in Older Adults” in recognition of the importance of the lat-
ter form of heart failure in older patients. In addition, all
chapters have been thoroughly revised and updated by rec-
ognized experts to incorporate the most recent knowledge
in the field.
We would like to thank all of the contributors for their
outstanding work. We also wish to express our gratitude
to Ben O’Hara, Shivangi Pramanik, and Mouli Sharma at
Taylor & Francis Group for their dedication and support in
bringing this sixth edition to fruition. Finally, we want to
thank you, the reader, for your commitment to providing
the best possible care for your older patients with cardio-
vascular disease. We hope you will find this volume to be
a valuable resource as you strive to help your older patients
enjoy both longer and fuller lives. We welcome any com-
ments you may have.
Michael W. Rich, MD, FACC, AGSF
Wilbert S. Aronow, MD, FACC, FAHA
Jerome L. Fleg, MD, FACC, FAHA
ix
Editors
Wilbert S. Aronow, MD is currently Professor of Medicine
and Director of Cardiology Research at Westchester Medical
Center and New York Medical College. He received his MD
from Harvard Medical School. He has edited 16 books; has
authored or coauthored 1,657 papers or book chapters,
518 commentaries, 47 Letters to the Editor, and 1,102
abstracts; and has presented or copresented 1,473 talks at
meetings. Dr. Aronow is a Fellow of the ACC, the AHA, the
ACP, ACCP, the ASPC, the AGS (Founding Fellow of Western
Section), and the GSA. He also received a Distinguished
Fellowship Award from the International Academy of
Cardiology. He has been a member of 172 editorial boards
of medical journals. He has received numerous teaching and
research awards. He has been a member of four national
guidelines committees, including being a coauthor of the
2010 American Medical Director Association guidelines
for heart failure, a co-chair of the 2011 ACC/AHA expert
consensus document on hypertension in the elderly, a
coauthor of the 2015 AHA/ACC/ASH scientific statement on
treatment of hypertension in patients with coronary artery
disease, and a coauthor of the 2017 ACC/AHA/AAPA/ABC/
ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for
the prevention, detection, evaluation, and management of
high blood pressure in adults.
Jerome L. Fleg, MD, FACC, FAHA is a Medical Officer,
Division of Cardiovascular Sciences, National Heart,
Lung, and Blood Institute, Bethesda, Maryland and
Guest Researcher, Laboratory of Cardiovascular Science,
Gerontology Research Center, National Institute on Aging,
Baltimore, Maryland. Dr. Fleg received his MD from the
University of Cincinnati College of Medicine and has
authored over 350 peer-reviewed articles, book chapters,
reviews, and editorials related to cardiovascular aging and
disease. He serves on multiple journal editorial boards and
is an associate editor for the Journal of Cardiopulmonary
Rehabilitation and Prevention and Aging: Clinical and
Experimental Research.
Michael W. Rich, MD, FACC, FAHA, AGSF is Professor of
Medicine, Washington University School of Medicine, and
Director, Cardiac Rapid Evaluation Unit, Barnes–Jewish
Hospital, St. Louis, Missouri. Dr. Rich received his MD from
the University of Illinois College of Medicine, Chicago. He
has published over 300 journal articles and more than 70
books and book chapters. Dr. Rich is Senior Associate Editor
for the Journal of Cardiac Failure, Associate Editor for The
American Journal of Medicine, and Consulting Editor for
the Journal of the American Geriatrics Society.
xi
Contributors

Hasan Ahmad Howard A. Cooper

Division of Cardiology Division of Cardiology
Westchester Medical Center Westchester Medical Center and New York Medical
and College
Assistant Professor of Medicine Valhalla, New York
New York Medical College
Valhalla, New York Sairia Dass
Division of Geriatric Medicine and Gerontology
Ali Ahmed Johns Hopkins University School of Medicine
Veterans Affairs Medical Center Baltimore, Maryland
and
Department of Medicine Samuel C. Durso
George Washington University Division of Geriatric Medicine and Gerontology
Washington, District of Columbia Johns Hopkins University School of Medicine
Baltimore, Maryland
Mays T. Ali
Department of Medicine Gregory A. Fishbein
Division of Cardiology Department of Pathology and Laboratory Medicine
The Johns Hopkins University School of Medicine David Geffen School of Medicine at UCLA
Baltimore, Maryland Los Angeles, California

Michael C. Fishbein
Melissa M. Anastacio
Department of Pathology and Laboratory Medicine
MedStar Washington Hospital Center
David Geffen School of Medicine at UCLA
Washington, District of Columbia
Los Angeles, California

Wilbert S. Aronow Jerome L. Fleg

Divisions of Cardiology, Geriatrics and Pulmonary/Critical Division of Cardiovascular Diseases
Care National Heart, Lung, and Blood Institute
Department of Medicine National Institutes of Health
Westchester Medical Center and New York Medical Bethesda, Maryland
College
Valhalla, New York Lee A. Fleisher
Department of Anesthesiology and Critical Care
Michele Brignole University of Pennsylvania School of Medicine
Department of Cardiology Philadelphia, Pennsylvania
Arrhythmologic Centre
Lavagna, Italy Daniel E. Forman
Section of Geriatric Cardiology
Angela Cheng-Lai University of Pittsburgh Medical Center (UPMC)
Department of Pharmacy Pittsburgh, Pennsylvania
Montefiore Medical Center
Bronx, New York

xiii
xiv Contributors

Stanley S. Franklin Sei Iwai

Heart Disease Prevention Program Director, Cardiac Electrophysiology Program
Division of Cardiology Westchester Medical Center
University of California Valhalla, New York
Irvine, California
Laurie G. Jacobs
William H. Frishman Professor and Chair, Department of Internal Medicine
Division of Cardiology Hackensack Meridian School of Medicine at Seton Hall
Department of Medicine Nutley, New Jersey
Westchester Medical Center and New York Medical College and
Valhalla, New York
Chair, Department of Internal Medicine
Hackensack University Medical Center
Steven R. Gambert Hackensack, New Jersey
Department of Medicine
University of Maryland School of Medicine
and Jason T. Jacobson
Department of Medicine Associate Professor, New York Medical College
The Johns Hopkins University School of Medicine and
Baltimore, Maryland Director, Complex Arrhythmia Ablation Program
Westchester Medical Center
Valhalla, New York
Kashish Goel
Division of Cardiovascular Diseases
Vanderbilt University Ruchi Jain
Nashville, Tennessee Critical Care Pharmacy Specialist
Hackensack University Medical Center
Sarah J. Goodlin Hackensack, New Jersey
Professor, Oregon Health and Science University
and Justin B. Kaplan
Chief, Geriatrics and Palliative Medicine Clinical Pharmacy Specialist – Critical Care
VA Portland Healthcare System Overlook Medical Center/Atlantic Health System
Portland, Oregon Summit, New Jersey

Dipika Gopal
Ryan K. Kaple
Department of Medicine
Yale School of Medicine
Division of Cardiology
Yale New Haven Hospital
University of Pennsylvania
New Haven, Connecticut
Philadelphia, Pennsylvania

Naktal Hamoud Dae Hyun Kim

Department of Medicine Department of Medicine
University of Arizona College of Medicine Harvard Medical School
Tucson, Arizona Boston, Massachusetts

David R. Holmes James N. Kirkpatrick

Department of Cardiovascular Diseases University of Washington
Mayo Clinic Division of Cardiology
Rochester, Minnesota Department of Bioethics and Humanities
Seattle, Washington
Massimo Imazio
Azienda Ospedaliera Città della Salute e della Dalane W. Kitzman
Scienza di Torino Cardiovascular Medicine Section
University Cardiology Department of Internal Medicine
Turin, Italy Wake Forest School of Medicine
Winston-Salem, North Carolina
 Contributors xv

Jennifer S. Lawton Julio A. Panza

Division of Cardiac Surgery Division of Cardiology
The Johns Hopkins University School of Medicine Westchester Medical Center and New York Medical
Baltimore, Maryland College
Valhalla, New York
Seth S. Martin
Department of Medicine Martina Rafanelli
Division of Cardiology Syncope Unit
The Johns Hopkins University School of Medicine Department of Geriatrics
Baltimore, Maryland Careggi University Hospital
Florence, Italy
John Arthur McClung
Michael W. Rich
Professor of Clinical Medicine
Mercy Clinic Heart and Vascular
and
Washington, Missouri
Professor of Clinical Public Health
New York Medical College and
Valhalla, New York
Washington University School of Medicine
St. Louis, Missouri
Myron Miller
Department of Medicine
Madhur A. Roberts
Sinai Hospital of Baltimore
Internal Medicine
and
Piedmont Atlanta Hospital
Department of Medicine
Atlanta, Georgia
The Johns Hopkins University School of Medicine
Baltimore, Maryland
Monika Sanghavi
Department of Medicine
Lona Mody Division of Cardiology
Amanda Sanford Hickey Professor of Internal Medicine University of Pennsylvania
and Philadelphia, Pennsylvania
Associate Division Chief, Geriatric and Palliative Care
Medicine Atsuko Seki
and Department of Pathology and Laboratory Medicine
Director, UM Pepper Center Pilot and Exploratory Studies Cleveland Clinic
Core Cleveland, Ohio
and
Associate Director, Clinical and Translational Research, Win-Kuang Shen
Geriatrics Center Department of Cardiovascular Diseases
University of Michigan Geriatrics Mayo Clinic
Ann Arbor, Michigan Phoenix, Arizona

and
Srihari S. Naidu
Professor of Medicine Mayo Clinic College of Medicine
New York Medical College Rochester, Minnesota
and
Director of Cardiac Cath Labs and Director of Sandra M. Shi
Hypertrophic Cardiomyopathy Center Geriatric Medicine
Westchester Medical Center Harvard Medical School
Valhalla, New York Boston, Massachusetts

Esther S. Pak Laura Stein

University of Pennsylvania Department of Neurology
Division of Cardiovascular Medicine Icahn School of Medicine at Mount Sinai
Philadelphia, Pennsylvania New York City, New York
xvi Contributors

Joshua M. Stolker Andrea Ungar

Mercy Clinic Heart and Vascular Syncope Unit
Washington, Missouri Department of Geriatrics
Careggi University Hospital
Alejandro Suarez Pierre Florence, Italy
Division of Cardiac Surgery
The Johns Hopkins University School of Medicine
Bharathi Upadhya
Baltimore, Maryland
Cardiovascular Medicine Section
Department of Internal Medicine
Craig Tanner
Wake Forest School of Medicine
Medical Director, Legacy Hospice
Winston-Salem, North Carolina
Legacy Health System
Portland, Oregon
Jesse Weinberger
David Tehrani Department of Neurology
Heart Disease Prevention Program Icahn School of Medicine at Mount Sinai
Division of Cardiology New York City, New York
University of California
Irvine, California
Nathan D. Wong
Heart Disease Prevention Program
Fernando Tondato
Division of Cardiology
Cardiac Electrophysiology
University of California
Kaiser Permanente
Irvine, California
Portland, Oregon
 1
Cardiovascular changes with aging

JEROME L. FLEG

Introduction 1 LV afterload 13
Methodological issues 2 Arterial/ventricular load matching 13
Arterial changes: The root cause of unsuccessful aging 2 Sympathetic modulation 14
Intimal medial thickening 2 Sympathetic neurotransmitters 14
Endothelial dysfunction 3 Deficits in cardiac β-adrenergic receptor signaling 14
Arterial stiffness and compliance 4 Relevant aging changes in other organ systems 14
Pulse wave velocity 4 Electrocardiography and arrhythmias 14
Reflected pulse waves 4 Anatomical conduction system changes 14
Systolic, diastolic, and pulse pressure 6 Electrocardiography 15
Interventions to retard or prevent accelerated arterial Sinus node function 15
aging 6 P waves 15
Cardiac structure and resting function 7 P–R interval 16
CV physical findings in older adults 9 QRS complex 16
CV response to stress 9 Repolarization 17
Orthostatic stress 10 Arrhythmias 17
Pressor stress 10 Atrial arrhythmias 17
Aerobic exercise capacity 10 Atrial fibrillation 17
Mechanisms of impaired LV ejection during maximal Paroxysmal supraventricular tachycardia 18
aerobic exercise in healthy older adults 13 Ventricular arrhythmias 18
Myocardial contractility 13 References 20

INTRODUCTION Nevertheless, it is important to define normal CV struc-

As longevity increases throughout the world, disorders and
diseases associated with aging assume increasing impor-
tance. In the United States, approximately 13% of the pop-
ulation is 65 years and older; this proportion is expected
to reach nearly 20% by the year 2030, comprising over
70 ­million people (1). The fastest-growing age group, com-
prising those 85 years or older, has more than quadrupled
since 1960 and will exceed 20 million by 2060 (Figure 1.1).
Because both the prevalence and incidence of cardiovascu-
lar (CV) disease increase dramatically with age, this “gray-
ing” of the population has created a huge number of older
adults requiring treatment. However, aging per se is not
necessarily accompanied by CV disease. This chapter will
set the stage for those that follow by delineating the changes
in the CV system that occur during the aging process in
the absence of detectable CV disease. This is a challeng-
ing task, given the many factors that blur their separation.
ture and function in older adults to facilitate the accurate
diagnosis of CV disease in this rapidly growing segment of
society.
Another important goal of this chapter will be to dem-
onstrate how aging changes in the CV system may them-
selves predispose individuals to the development of CV
disease. The enhanced CV risk associated with age indicates
important interactions between mechanisms that underlie
aging and those that underlie diseases. The nature of these
interactions is complex and involves not only mechanisms
of aging but also multiple defined and undefined risk fac-
tors. Yet quantitative information on age-associated altera-
tions in CV structure and function is essential to define and
target the specific characteristics of CV aging that render it
such a major risk factor. Such information is also required
to differentiate between the limitations of an elderly person
that relate to disease and those that are within expected
normal limits.
1
2 Cardiovascular changes with aging
From Pyramid to Pillar: A Century of Change
1960 2060
Ages Male Female Male Female
85+
80–84
75–79
70–74
65–69
60–64
55–59
50–54
45–49
40–44
35–39
30–34
25–29
20–24
15–19
10–14
5–9
0–4
15 10 5 0 5 10 15 15 10 5 0 5 10
Millions of people Millions of people
Figure 1.1 Projected growth of the U.S. population between
1960 and 2060, stratified by age group. (From United States
Bureau of the Census, www.census.gov/population/www/
estimates/popest.html. March 13, 2018.)
METHODOLOGICAL ISSUES
There are multiple methodological issues that must be
addressed in defining “normal” aging. Because the popu-
lation sample from which norms are derived will strongly
influence the results obtained, it should be representative
of the general population. Thus, neither a seniors cycling
club nor nursing home residents would provide appropriate
normal values for maximal exercise capacity that could be
applied to the majority of elders. In addition, the degree of
screening used to define “normal” can profoundly influence
the results. In clinically healthy older adults, a resting elec-
trocardiogram (ECG), echocardiogram, or exercise perfusion
imaging study will often identify silent CV disease, especially
coronary artery disease (CAD). If multiple screening tests are
used, only a small proportion of the older population may
qualify as normal, limiting the applicability of findings to the
majority of older adults. Furthermore, the inclusion limits
chosen for body fatness, blood pressure, smoking status, and
other constitutional or lifestyle variables will significantly
influence the normal range for CV variables. For example, if
a systolic pressure of ≥130 mmHg is considered hypertension
as per recent guidelines, and if hypertension is considered
a disease, then individuals with a systolic pressure between
130 and 140 mmHg, who were previously considered normo-
tensive, are now identified as having CV disease. Numerous
studies have shown that individuals who manifest even mod-
est elevations in systolic and pulse pressures are more likely
to develop overt CV disease or die from it.
Further methodological issues can affect the definitions
of normal aging. Cross-sectional studies, which study indi-
viduals across a wide age range at a single time point, may
underestimate the magnitude of age-associated changes
because older normal persons included in such studies
represent “survival of the fittest.” True age-induced changes
are better estimated by longitudinal studies, in which indi-
viduals are examined serially over time. A reality of aging
research, however, is that most data are derived from cross-
sectional studies because they are easier to perform. Even
longitudinal studies have their limitations—changes in
methodology or measurement drift over time and develop-
ment of disease in previously healthy persons. Finally, secu-
lar trends such as the downward drift in serum cholesterol
or increasing obesity of Americans can alter age-related lon-
gitudinal changes.
In this chapter, emphasis will be given to data obtained
from community-dwelling persons screened for the absence
of clinical, and in some cases subclinical, CV disease as
15
well as major systemic disorders. A substantial portion of
the data presented derives from studies over the past three
decades in community-based volunteers from the Baltimore
Longitudinal Study of Aging (BLSA).
ARTERIAL CHANGES: THE ROOT CAUSE
OF UNSUCCESSFUL AGING
Intimal medial thickening
Age-associated changes in the arterial tree of apparently
healthy individuals may have relevance to the exponential
increase in CV disease with aging. Cross-sectional studies
in humans have found that wall thickening and dilatation
are prominent structural changes that occur within large
elastic arteries during aging (2). Postmortem studies indi-
cate that aortic wall thickening with aging consists mainly
of intimal thickening, even in populations with a low inci-
dence of atherosclerosis (3). Noninvasive measurements
made within the context of several epidemiological studies
indicate that the carotid wall intimal-medial (IM) thick-
ness increases nearly threefold between 20 and 90 years of
age, which is also the case in BLSA individuals rigorously
screened to exclude carotid or coronary arterial disease
(Figure 1.2a).
Some investigators believe that the age-associated
increase in IM thickness in humans represents an early
stage of atherosclerosis (4). Indeed, excessive IM thicken-
ing at a given age predicts silent CAD (4). Since silent CAD
often progresses to clinical CAD, it is not surprising that
increased IM thickness predicts future clinical CV dis-
ease. Multiple epidemiological studies of individuals not
initially screened to exclude occult CV disease have shown
that increased IM thickness is an independent predictor of
future CV events. Note in Figure 1.2b that the degree of risk
varies with the degree of vascular thickening and that the
risk gradation among quintiles of IM thickening is nonlin-
ear, with the greatest risk occurring in the upper quintile (5).
Thus, older adults in the upper quintile of IM thickness may
be considered to have aged “unsuccessfully” or to have “sub-
clinical” vascular disease. The potency of IM thickness as
a risk factor in older individuals equals or exceeds that of
most other, more traditional, risk factors.
 Arterial changes: The root cause of unsuccessful aging 3

0.12 It is currently believed that additional risk factors (e.g.,

hypertension, smoking, dyslipidemia, diabetes, diet, or
Male
0.10 as-yet-unidentified genetic factors) are required to inter-
Intimal medial thickness (cm)

Female act with vascular aging (as described above) to activate a

0.08 preexisting atherosclerotic plaque. According to this view,
atherosclerosis that increases with aging is not a specific
0.06 disease, but an interaction between atherosclerotic plaque
and intrinsic features related to vascular aging modu-
0.04 lated by atherosclerotic risk factors. Evidence support-
ing this view comes from studies in which an atherogenic
0.02 diet caused markedly more severe atherosclerotic lesions
in older versus younger rabbits and nonhuman primates
0.00 despite similar elevations of serum lipids (7,8). However,
20 30 40 50 60 70 80 90
studies in populations with clinically defined vascular dis-
(a) Age (years)
ease have demonstrated that pharmacological and lifestyle
100
(diet, physical activity) interventions can retard the pro-
Cumulative event-free rate (%)

95 1st quintile gression of IM thickening (9–14).

90
85
80
75
70
0 1 2 3
(b) Years
Figure 1.2 (a) The common carotid intimal-medial thick-
ness in healthy BLSA volunteers as a function of age.
(b) Common carotid intimal-medial thickness predicts
future cardiovascular events in the Cardiovascular Health
Study. Abbreviation: BLSA, Baltimore Longitudinal Study
of Aging. ([a] From Nagai, Y. et al., Circulation, 98, 1504–
1509, 1998. [b] From O’Leary, D.H. et al. N. Engl. J. Med.,
340, 14–22, 1999.)
The common finding of age-associated IM thickening in
the absence of atherosclerosis, both in laboratory animals
and in humans (3) suggests that such excessive IM thick-
ening is not necessarily “early” atherosclerosis. Rather,
“subclinical CV disease” is strongly correlated with arte-
rial aging. Interpreted in this way, the increase in IM thick-
ness with age is analogous to the intimal hyperplasia that
develops in aortocoronary saphenous vein grafts, which is
independent of atherosclerosis but predisposes to its later
development (6). Age-associated endothelial dysfunction,
arterial stiffening, and arterial pulse pressure widening can
also be interpreted similarly. Combinations of these pro-
cesses occurring to varying degrees determine the overall
vascular aging profile of a given individual (i.e., the degree
of “unsuccessful” vascular aging). Animal data suggest
that oxidative stress, inflammation, and defective cellu-
lar signaling underlie these adverse processes, initiating a
vicious cycle between vascular remodeling and increasing
arterial stiffness and blood pressure.
2nd quintile
3rd quintile Endothelial dysfunction
4th quintile
The endothelial monolayer that lines the luminal ­surface of
the vascular tree plays a pivotal role in regulating m ­ ultiple
arterial properties, including vessel tone, permeabil-
5th quintile
ity, response to inflammation, and angiogenesis. Several
of these functions undergo important age-­ associated
4 5 6 ­a lterations. Endothelium-derived mediators such as nitric
oxide (NO) and endothelin-1 are determinants of arterial
tone and compliance, suggesting that endothelial cells may
modulate arterial stiffness. Brachial arterial flow-mediated
dilation, mediated in large part by NO, declines with age in
both sexes, even in the absence of other CV risk factors (15).
A decline of ~75% in this flow-mediated vasodilation occurs
in men between the ages of 40 and 70 years. This decline
begins approximately a decade later in women, perhaps
because of the protective effect of estrogen, but is nearly
2.5 times as steep compared with men (15). The impair-
ment of ­endothelial-mediated vasodilatation with aging in
humans can be partially reversed by L-arginine adminis-
tration, suggesting that NO p ­ roduction becomes reduced
with aging (16). Plasma ­ levels of a­symmetric dimethyl
arginine, which reduces NO synthase (NOS) ­activity, also
increase with age in humans (16). A ­ ge-associated changes
in endothelial cell integrity, shape, and surface characteris-
tics affect the cell’s physical and chemical barrier, increasing
endothelial ­ permeability, leading to aberrant macromo-
lecular ­transport (17). In c­ontrast to endothelium-medi-
ated v­ asodilation, the vasodilator response to sublingual
­nitroglycerin is u­ nrelated to age (15).
Several CV risk factors and disorders are associated
with endothelial dysfunction, including hypertension,
hypercholesterolemia, insulin resistance, cigarette smok-
ing, CAD, and heart failure. Furthermore, impaired endo-
thelial vasoreactivity, in both the coronary and peripheral
arterial beds, is an independent predictor of future CV
events (18,19). Hypertensive individuals exhibit endothelial
dysfunction (20,21), and the mechanisms underlying their
endothelial dysfunction are similar to those that occur with
4 Cardiovascular changes with aging

normotensive aging, albeit they appear at an earlier age (21). 2500

Female

Pulse wave velocity (cm/sec)

The normotensive offspring of hypertensives also exhibit Male
endothelial dysfunction (22), suggesting that endothelial 2000
dysfunction may precede the development of clinical hyper-
1500
tension. Age-associated endothelial dysfunction, arterial
stiffening, and IM thickening are risk factors for arterial 1000
diseases, even after accounting for other risk factors, such
as arterial pressure, plasma lipids, smoking, and so on. The 500
interaction between arterial wall stiffening and CV diseases
may set in motion a vicious cycle. In this cycle, alterations 0
in the mechanical properties of the vessel wall contribute 20 40 60 80 100
(a) Age (years)
to endothelial cell dysfunction and, ultimately, to arterial
stiffening. Augmentation index (AI)
ΔP

Arterial stiffness and compliance PP

60 Female AI = ΔP
PP (%)
The increase in arterial wall thickening and reduction in Male
endothelial function with advancing age are accompanied

Augmentation index
40
by an increase in arterial stiffening and a reduction in com-
pliance. Age-associated structural changes in the arterial 20
media that increase vascular stiffness include increased col-
0
lagen content, covalent cross-linking of the collagen, reduced
elastin content, elastin fracture, and calcification (23,24). In –20
addition, there is a substantial increase in angiotensin II lev-
els and augmented angiotensin II signaling in aged arterial –40
walls, which may play a pivotal role in arterial aging, given 0 20 40 60 80 100
the potent pressor and mitogenic effects of angiotensin II. (b) Age (years)

Figure 1.3 Scatter plots of aortofemoral pulse wave

Pulse wave velocity
Each systolic contraction of the ventricle generates a pres-
sure wave that propagates centrifugally down the arterial
tree, slightly preceding the luminal flow wave generated
during systole. The propagation velocity of this wave is pro-
portional to the stiffness of the arterial wall. The velocity of
the pulse wave in vivo is determined not only by the intrin-
sic stress/strain relationship (stiffness) of the vascular wall
but also by the smooth muscle tone, which is reflected by the
mean arterial pressure.
Noninvasive measures of the velocity of this pulse wave
allow for large-scale epidemiological studies to examine its
determinants and prognostic importance. In both rigorously
screened normal subjects (25) and populations with varying
prevalence of CV disease (26,27), a significant age-associated
increase in pulse wave velocity (PWV) has been observed in
men and women (Figure 1.3a). In contrast to central arter-
ies, the stiffness of muscular arteries does not increase with
advancing age (28). Thus, the manifestations of arterial aging
may vary among the different vascular beds, reflecting dif-
ferences in the structural compositions of the arteries and,
possibly, differences in the age-­associated signaling cascades
that modulate the arterial properties, or differences in the
response to these signals across the arterial tree.
Increased PWV has traditionally been linked to struc-
tural alterations in the vascular media, such as those
observed with aging. Prominent age-associated increases
in PWV have been demonstrated in populations with
velocity (a), and carotid artery augmentation index
(b) as a function of age in healthy non-endurance-trained
BLSA volunteers. A similar age-associated increase in
both measures of arterial stiffness was seen in men and
women. Abbreviation: BLSA, Baltimore Longitudinal Study
of Aging. (From Vaitkevicius, P.V. et al., Circulation, 88,
1456–1462, 1993.)
little or no atherosclerosis, again indicating that these
vascular parameters are not necessarily indicative of
atherosclerosis (29). However, the data emerging from
­epidemiological studies indicate that increased large ves-
sel stiffening also occurs in the context of atherosclerosis
(30,31), ­metabolic syndrome (32), and diabetes (33,34).
Thus, altered mechanical properties of the vessel wall
facilitate the development of atherosclerosis, which in
turn increases arterial stiffness via endothelial cell dysfunc-
tion and other mechanisms.
Reflected pulse waves
In addition to the forward pulse wave, each cardiac cycle
generates a reflected wave, originating at areas of arterial
impedance mismatch, which travels back up the arterial
tree toward the central aorta, altering the arterial pres-
sure waveform. This reflected wave can be noninvasively
assessed from recordings of the carotid (25) or radial (35)
arterial pulse waveforms using applanation tonometry and
high-fidelity micromanometer probes. Dividing the late
 Arterial changes: The root cause of unsuccessful aging 5

systolic augmentation of the arterial pulse wave by the dis-
tance from the peak to the trough of the arterial waveform
(corresponding to the pulse pressure) yields the augmen-
tation index, representing the degree of late systolic pres-
sure increase (24). The augmentation index, like the PWV,
increases with age (Figure 1.3b) (24,25).
The velocity of the reflected flow wave is proportional
to the stiffness of the arterial wall. Thus, in young indi-
viduals whose vascular wall is compliant, the reflected wave
does not reach the large elastic arteries until diastole. With
advancing age and increasing arterial stiffening, the veloc-
ity of the reflected wave increases, and the wave reaches
the central circulation earlier in the cardiac cycle, during
systole. The pressure pulse augmentation provided by the
early return of the reflected wave is an added load against
which the aged ventricle must contract. Furthermore, the
diastolic pressure augmentation seen in compliant vessels,
caused by the late return of the reflected waves, is lost in the
elderly, decreasing diastolic blood pressure; this decrease in
diastolic pressure may reduce coronary blood flow because
most coronary flow occurs during diastole.
Numerous studies (27,36–39) indicate that increased
arterial stiffness, over and above blood pressure, is an
independent predictor of hypertension, atherosclerosis,
CV events, and mortality. Kaess et al. (38) and others have
demonstrated that increased arterial stiffness precedes the
development of hypertension.
Thus, a “primary” increase in large artery stiffness that
accompanies aging gives rise to an elevation of arterial pressure;
in turn, a “secondary” increase in large artery stiffness occurs
due to the increase in mean arterial pressure. Normotensive
individuals who fall within the upper quartile for measures
of arterial stiffness are more likely to subsequently develop
hypertension. Observations such as these reinforce the concept
that hypertension, at least in part, is a disease of the arterial
wall. The mechanisms of age-­associated changes in vascular
structure and function and the putative relationship of these
changes to development of CV disease are depicted in Table 1.1.

Table 1.1 Relationship of cardiovascular human aging in health to cardiovascular disease

Age-associated changes Plausible mechanisms Possible relation to human disease
CV structural remodeling Early stages of atherosclerosis production
⇑ Vascular intimal thickness ⇑ Migration of and ⇑ matrix by VSMC
Possible derivation of intimal cells from
other sources
⇑ Vascular stiffness Elastin fragmentation Systolic hypertension
⇑ Elastase activity
⇑ Collagen production by VSMC Stroke
and ⇑ cross-linking of collagen
Altered growth factor regulation/ tissue Atherosclerosis
repair mechanisms
⇑ LV wall thickness ⇑ LV myocyte size Retarded early diastolic cardiac filling
⇓ Myocyte number (necrotic and ⇑ Cardiac filling pressure
apoptotic death)
Altered growth factor regulation Lower threshold for dyspnea
Focal collagen deposition
⇑ Left atrial size ⇑ Left atrial pressure/volume ⇑ Prevalence of lone atrial fibrillation
CV functional changes
Altered regulation of vascular tone ⇓ NO production/effects Vascular stiffening; hypertension
⇓ β-AR responses
⇓ CV reserve ⇑ Vascular load Lower threshold for, and increased
severity of, heart failure
⇓ Intrinsic myocardial
Contractility
⇓ β-Adrenergic modulation of heart
rate, myocardial contractility, and
vascular tone
Reduced physical activity Learned lifestyle Exaggerated aging changes in some
aspects of CV structure and function;
negative impact on atherosclerotic
vascular disease, hypertension, and
heart failure
Abbreviations: β-AR, β-adrenergic receptor; CV, cardiovascular; LV, left ventricular; NO, nitric oxide; VSMC, vascular smooth muscle cell.
6 Cardiovascular changes with aging
Age-associated dilation of the proximal aorta has been
demonstrated in normal adults. Echocardiographic aor-
tic root diameter increased a modest 6% in BLSA men
between the fourth and eighth decades (40). Similarly, the
aortic knob diameter increased from 3.4 to 3.8 cm on serial
chest X-rays over 17 years (41). In addition, the aortic arch
lengthens with age due to arch widening (42). Both greater
aortic diameter and arch length were independently associ-
ated with higher aortic arch PWV and left ventricular (LV)
mass. Such aortic root dilation and lengthening provide an
additional stimulus for LV hypertrophy (LVH) because the
larger volume of blood in the proximal aorta represents a
greater inertial load that must be overcome before LV ejec-
tion can begin.
Systolic, diastolic, and pulse pressure
Arterial pressure is determined by the interplay of periph-
eral vascular resistance and arterial stiffness; the former
raises both systolic and diastolic pressure to a similar degree,
whereas the latter raises systolic but lowers diastolic pres-
sure. A rise in average systolic blood pressure across adult
age has been well documented (Figure 1.4) (43,44). In con-
trast, average diastolic pressure was found to rise until about
50 years of age, level off from age 50 to 60, and decline there-
after (43,44). Thus, pulse pressure (systolic minus diastolic),
a useful hemodynamic indicator of conduit artery vascular
stiffness, increases with age. These age-dependent changes in
systolic, diastolic, and pulse pressures are consistent with the
concept that blood pressure in younger people is determined
largely by peripheral vascular resistance, whereas in older
individuals it is determined more by central conduit vessel
stiffness.
Men
150
140 Systolic pressure
130
Blood pressure (mmHg)
120
110
100
90
Diastolic pressure
80
70
0 0
18–29 30–39 40–49 50–59 60–69 70–79
Age (years)
Figure 1.4 Change in blood pressure with age in healthy men and women of different ethnicities. (From Aronow, W.S.
et al., Circulation, 123, 2434–2506, 2011.)
Because systolic pressure is higher whereas diastolic
pressure is lower in older men and women, isolated systolic
hypertension emerges as the most common form of hyper-
tension in individuals older than 50 years (43). Isolated sys-
tolic hypertension, even when mild in severity, is associated
with an appreciable increase in CV disease risk (45,46). On
the basis of long-term follow-up of middle-aged and older
subjects, however, Framingham researchers have found
pulse pressure to be a better predictor of coronary disease
risk than systolic or diastolic blood pressures (47). A subse-
quent Framingham investigation found that pulse pressure
was especially informative of coronary risk in older subjects
(48) because of the J- or U-shaped association between dia-
stolic pressure and coronary risk. Thus, consideration of the
systolic and diastolic pressures jointly, as reflected in pulse
pressure, is preferable to consideration of either value alone.
INTERVENTIONS TO RETARD OR PREVENT
ACCELERATED ARTERIAL AGING
Despite the deleterious effects of aging on arterial structure
and function, it is noteworthy that the age increases in systolic
and pulse pressures are markedly blunted in ­hunter-gatherer
and forager-farmer societies (49). Furthermore, increasing
evidence has accrued that ­lifestyle modifications, includ-
ing aerobic exercise, and dietary modifications, including
reduction in sodium intake, caloric restriction, and weight
loss, can prevent or retard age-­associated IM thickening
(50,51) and arterial stiffening (52,53) and improve endo-
thelial function (54–57). Perhaps, the most promising of
these modifications is caloric ­restriction, which may pro-
long maximal life span in laboratory animals when begun
in youth or middle age. Limited studies in individuals have
Women
150
140
Systolic pressure
130
120
110 Non-Hispanic black
Non-Hispanic white
100 Hispanic
90
80
70
Diastolic pressure
>80 18–29 30–39 40–49 50–59 60–69 70–79 >80
Age (years)

demonstrated decreases in CV risk factors and inflamma-
tory markers with caloric ­restriction (51,58). In one study, 25
individuals aged 53 ± 12 years who had p ­ racticed v­ oluntary
caloric restriction of ~30% for an ­average of 6.5 years showed
markedly lower blood pressure and inflammatory markers
compared with controls matched for age and g­ ender (58).
In addition, the calorie restricted group demonstrated
higher transmittal early diastolic flow measures, similar to
those of younger adults (58). Whether such beneficial effects
can be derived by initiating caloric restriction at older ages
remains unknown.
Pharmacological intervention such as chronic a­ ngiotensin-
converting enzyme inhibition or angiotensin receptor
blockade, begun at an early age in animal models, markedly
delays the progression of age-associated arterial remodel-
ing. Beneficial effects include lesser IM thickening and
rupture of internal elastic lamina (59,60), attenuated mito-
chondrial dysfunction, reduced reactive oxygen species,
enhanced NO bioavailability, reduced fibrosis, and pro-
longed life (61–67). It is thus far unproven if such treatment
can prevent or retard unsuccessful aging of the vasculature
in younger to middle-aged animals or humans who exhibit
excessive subclinical evidence of accelerated arterial aging.
Although breaking nonenzymatic collagen cross-links with
a novel thiazolium agent reduces arterial stiffness in nonhu-
man primates (68) and humans (69), its clinical relevance is
unclear.
CARDIAC STRUCTURE AND RESTING
FUNCTION
Until the 1970s, autopsy was essentially the only method
for obtaining reliable measurements of cardiac structure
in normal persons. These studies were obviously flawed
by their inherent selection bias. A large autopsy series
by Linsbach et al. (70) in 7112 patients demonstrated an
increase in cardiac mass of 1–1.5 g/yr between 30 and
90 years of age. Because the study included individuals with
CV disease, the age-associated increase in heart weight may
have derived, at least in part, from the coexistence of car-
diac pathology. An autopsy study of 765 normal hearts from
persons 20 to 99 years old who were free from both hyper-
tension and CAD showed that heart weight indexed to body
surface area was not age related in men but increased with
age in women, primarily between the fourth and seventh
decades (71). In autopsies of hospitalized patients without
evident CV disease, Olivetti et al. (72) observed an age-
associated reduction of LV mass mediated by a decrease in
estimated myocyte number, although myocyte enlargement
occurred with age. These investigators subsequently found a
higher prevalence of apoptotic myocytes in older male than
in female hearts, which paralleled a decline of LV mass with
age in men but not in women (73).
Widespread application of echocardiography finally
allowed accurate noninvasive assessment of age-associated
changes in cardiac structure and function. In healthy nor-
motensive BLSA men, Gerstenblith et al. (40) found a 25%
Cardiac structure and resting function 7
increase in echocardiographic LV posterior wall thickness
between the third and eighth decades, a finding replicated
by others (74,75). Because LV diastolic cavity size was not
significantly age-related in the BLSA (40), calculated LV
mass also increased substantially with age. However, more
recent studies using magnetic resonance imaging (MRI) to
estimate LV mass in three dimensions has helped to resolve
the divergent finding between autopsy and echocardio-
graphic studies. In 136 men and 200 women without CV
disease, MRI-derived LV wall thickness increased with age
and short-axis diastolic dimension was not age related, sim-
ilar to earlier echocardiographic findings. In contrast, LV
length declined with age in both sexes (i.e., the LV became
more spherical) (76). Thus, MRI-derived LV mass was unre-
lated to age in women and demonstrated an age-associated
decline in men (because of their lesser age-related increase
in wall thickness), similar to autopsy findings (73). Three-
dimensional echocardiography has confirmed this preser-
vation of LV mass across age in women and a reduction of
LV mass in older men (77). In 5004 healthy volunteers from
the MESA study, cardiac MRI revealed age-related declines
in both LV diastolic and systolic volumes and an increase in
the LV mass/volume ratio in both sexes (78); stroke volume
decreased modestly with age. Longitudinal MRI follow-up
over 10 years confirmed a modest decline in LV diastolic
volume and increase in LV mass/volume ratio (79). Thus,
the normal LV becomes smaller, thicker, and more spherical
with advancing age.
Although the mechanisms for the age-associated remod-
eling of the LV and increase in myocyte size are not clear,
they may be adaptive responses to the arterial changes that
accompany aging. Putative stimuli for cardiac cell enlarge-
ment with age are an increase in vascular load due to arte-
rial stiffening and a stretching of cells due to dropout of
neighboring apoptotic myocytes (80). Phenotypically, the
age-associated increase in LV thickness resembles the LVH
that develops from hypertension. This finding, coupled
with the increase in systolic blood pressure that occurs over
time even in healthy individuals, has led to consideration
of aging as a muted form of hypertension. In older rodent
hearts, which demonstrate a similar increase in LV mass
and myocyte size as observed in humans, a stretching of
cardiac myocytes and fibroblasts releases growth factors
such as angiotension II, a known stimulus for apoptosis.
As a result, the heart becomes stiffer, that is, less compliant,
with age. Enhanced secretion of atrial natriuretic (81) and
opioid (82) peptides is also observed.
Echocardiographic LV shortening fraction (74) and
radionuclide LV ejection fraction (83,84), the two most
common measures of global LV systolic performance, are
unaffected by age at rest in healthy normotensive persons.
Because LV stroke volume (SV) is the difference of LV end-
diastolic volume (EDV) and end-systolic volume (ESV), the
radionuclide-determined supine resting LV stroke volume
is also unrelated to age (84). Prolonged contractile activa-
tion of the thickened LV wall (85) maintains a normal ejec-
tion time in the presence of the late systolic augmentation
8 Cardiovascular changes with aging
of aortic impedance, preserving systolic cardiac pump
function at rest. However, a downside of prolonged con-
tractile ­activation is that at the time of the mitral valve
opening, myocardial relaxation is less complete in older
than in younger individuals, contributing to a reduced
early LV filling rate. Over the last decade, two-dimensional
speckle tracking echocardiography has allowed quantita-
tive measurement of LV myocardial deformation, that is,
strain. The most widely used such measurement is global
longitudinal strain (GLS). Among 1266 healthy adults from
the third through ninth decades, GLS declined modestly
with age, especially after 60 years (86), a finding confirmed
by others (87).
In contrast to the general preservation of resting LV
systolic performance across the adult age span, LV dia-
stolic performance is profoundly altered by aging. Reduced
mitral valve E–F closure slope on M-mode echocardiogra-
phy first documented these age changes in diastolic perfor-
mance (40,74). Pulsed Doppler (88) and radionuclide (89)
techniques confirmed that the transmitral early diastolic
peak filling rate declined by ~50% between the ages of 20
and 80 years (Figure 1.5). Conversely, peak A-wave velocity,
which represents late LV filling facilitated by atrial contrac-
tion, increases with age (88). This greater atrial contribution
to LV filling is accomplished via a modest age-associated
increase in left atrial size demonstrable on echocardiogra-
phy. Tissue Doppler and color M-mode techniques, both less
influenced by preload and afterload than pulsed Doppler,
have confirmed the age-associated reduction in early dia-
stolic filling rate and increased late filling (90). Because the
resting LV EDV is preserved across adult age in BLSA vol-
unteers, the augmented atrial contribution to LV filling in
older adults can be considered a successful adaptation to the
reduced early diastolic filling rate in the thicker, and presum-
ably stiffer, senescent LV. Thus, the relative importance of
early and late diastolic LV filling is reversed with aging.
Reduction of early LV filling with age may derive in
part from decreased LV diastolic compliance due to the
increase in LV wall thickness. An age-associated reduc-
tion in ventricular compliance has been shown in animals.
Studies in man have confirmed an age-associated reduction
in LV compliance, which was minimally changed in older
adults after a full year of endurance training (91). In both
intact animal hearts and isolated cardiac muscle, studies
have demonstrated prolonged isovolumic relaxation and
increased myocardial diastolic stiffness. Studies in both
mice and healthy volunteers have shown age-associated
increases in MRI-derived extracellular volume, thought to
represent myocardial fibrosis, representing another poten-
tial mechanism for reduced LV compliance with aging (92).
This slower isovolumic relaxation observed in cardiac mus-
cle from older animals (93) may be secondary to diminished
rate of Ca2+ accumulation by the sarcoplasmic reticulum
(94). A conceptual framework for the cardiac adaptations
to age-associated arterial stiffening is shown in Figure 1.6.
Although the diminished early LV diastolic filling rate
with age may not compromise resting EDV or stroke volume,
Young
15
LV filling
Advanced age
Peak filling rate (EDV/sec)
12
9
6
Max.
3
Rest
0
20 30 40 50 60 70 80 90
Age (years)
Figure 1.5 Changes with age in peak early diastolic filling
rates derived from radionuclide ventriculography at rest
and during maximal upright cycle ergometry. The inset
shows the transmittal flow velocity profile derived from
Doppler echocardiography in a young adult and older
adult. Note the shift from a dominant early (E) filling wave
in the young to a dominant late (A) filling wave in the
elderly. (From Schulman, S.P. et al., Am. J. Physiol., 263,
H1932–H1938, 1992.)
an underlying reduction of LV compliance might cause a
greater rise in LV diastolic pressure in older persons, espe-
cially during stress-induced tachycardia, thereby causing
a lower threshold for dyspnea than in the young. It might
also be anticipated that the loss of atrial contribution to LV
filling that occurs during atrial fibrillation would elicit a
greater deterioration of diastolic performance in older than
in younger individuals. Indeed, it is attractive to speculate
that the frequent occurrence of heart failure in the elderly
despite preserved LV systolic function derives, at least in
part, from the age-associated impairment of early diastolic
filling (Table 1.1).
The difficulty in imaging the right ventricle by echocar-
diography has limited obtaining information regarding
aging changes in right ventricular (RV) structure and func-
tion. However, cardiac MRI can provide such information.
In 4204 MESA participants aged 45–84 years who were free
of clinical CV disease, cardiac MRI showed declines in both
RV mass and volumes but a modest increase in RV ejection
fraction with age (95). RVEDV, mass, and ejection frac-
tion were positively related to systolic blood pressure and
inversely related to diastolic blood pressure. The pulmonary
arteries also appear to undergo age-associated remodeling,
resulting in increased pulmonary artery (PA) stiffness and
PA systolic pressure. In 1413 Olmsted County, Minnesota,
residents ≥45 years old, PA systolic pressure estimated
by Doppler echocardiography increased modestly from
26 ± 4 mmHg in persons 45–54 years old to 30 ± 6 mmHg
in those 72–96 years old (96). Higher PA systolic pressure
was an independent mortality predictor (hazard ratio [HR]
1.46 per 10 mmHg) (96). Healthy adults demonstrate an
exaggerated rise in PA systolic and mean pressures with age
during cycle ergometry (Figure 1.7) (97).
 CV response to stress 9

Arterial stiffening

Pulse wave velocity

Arterial systolic and Aortic root size
early reflected waves
pulse pressure Aortic wall thickness
late peak in systolic pressure

Aortic impedance
and LV loading

LV wall tension

LV wall thickness Prolonged myocardial

contraction

Normalization of Myocardial Prolonged force Early diastolic

L atrial size
LV wall tension contraction bearing capacity filling rate
Atrial filling velocity
Maintenance of
Slightly increased Preserved end- Energetic ejection time
end-diastolic volume systolic volume efficiency
and ejection fraction

Figure 1.6 Conceptual framework for the cardiovascular adaptations to arterial stiffening that occur with aging.
Abbreviation: LV, left ventricular.

s­ econd heart sound is audible in only ~30%–40% of indi-

mPAP
50 viduals older than 60 years, presumably because of reduced
compliance of the pulmonary v­ asculature. In contrast, an
40 S4 gallop is commonly heard in older but not younger
persons because of the age-­associated increase in late
30 60–80 yrs ­d iastolic filling mediated by vigorous atrial ­contraction
mmHG

40–59 yrs
20
20–39 yrs
p < 0.0001
10
0
Rest Leg raise 25% 50% 75%
Figure 1.7 Age-associated changes in mean pulmonary
artery pressure (mPAP) during leg raising and graded
aerobic exercise (25%, 50%, and 75% of maximal oxygen
consumption). (From Wolsk, E. et al., J. Am. Coll. Cardiol.
HF., 5, 337–346, 2017.)
CV physical findings in older adults
Several age-associated alterations in CV structure and
function may manifest themselves during the CV exami-
nation. Because of the stiffening of the large arteries,
­systolic blood pressure is often elevated with a normal or
low diastolic blood pressure. Therefore, the carotid artery
upstroke is usually brisk in the elderly and may mask
­significant aortic valve stenosis. The apical cardiac impulse
may be difficult to palpate secondary to senile ­emphysema
and chest wall deformities. Respiratory s­plitting of the
into a thicker-walled, less compliant LV. A soft basal ejec-
tion murmur occurs in 30%–60% of elders. This murmur
is thought to arise from a dilated, tortuous aorta or from
sclerosis of the aortic valve.
CV RESPONSE TO STRESS
The CV response of older adults to stress (e.g., to increases
in arterial pressure, to postural maneuvers, or to physi-
cal exercise) is of considerable clinical importance for sev-
eral reasons. First, physicians are often asked to provide
advice and information concerning the CV potential of
the elderly (e.g., the effect or importance of conditioning
status on the maintenance of function). Second, the CV
response to stress is important in assessing the ability of
older individuals to respond to disease states. Third, the
CV stress response is valuable in the diagnosis and man-
agement of older patients with CV disease. Despite the
high prevalence of CV disease among older Americans,
it is important to understand their exercise capabilities.
Exercise testing is a diagnostic tool that is frequently uti-
lized to detect and quantify the severity of CV disease. The
utility of such diagnostic testing clearly depends on pre-
cise information regarding the normal limits of such stress
testing procedures relative to age.
10 Cardiovascular changes with aging
Orthostatic stress
In healthy, community-dwelling elders, arterial pres-
sure changes little with the assumption of upright posture,
and postural hypotension or acute orthostatic intolerance
(i.e., dizziness or fainting when assuming an upright from
a supine position or during a passive tilt) is uncommon.
Orthostatic hypotension (OH), defined by a decline of sys-
tolic blood pressure by ≥20 mmHg or diastolic blood pres-
sure by ≥10 mmHg, occurred in 16% of volunteers aged
65 and older from the Cardiovascular Health Study (CHS)
(98) and in 7% of men aged 71–93 years from the Honolulu
Heart Program (99); in both of these older cohorts, the prev-
alence of OH increased with age. In the former study, OH
was associated with higher supine blood pressure, greater
LV wall thickness, and smaller LV cavity size (100). In the
latter study, OH was an independent predictor for mortality
(relative risk [RR] = 1.64), and there was a linear relation-
ship between the magnitude of orthostatic decline in systolic
blood pressure and 4-year mortality rate (99). In contrast
to healthy, community-dwelling older volunteers, OH and
orthostatic intolerance are common in debilitated institu-
tionalized elders with chronic illnesses. Within such popula-
tions, the likelihood for OH is increased among individuals
who exhibit very low LV filling rates and small EDV and
SV in the supine position (101). In such individuals, how-
ever, the effects of advanced age cannot be dissociated from
those of profound deconditioning and multiple diseases and
medications.
With advancing age, the acute heart rate increase to
orthostatic stress decreases in magnitude and takes longer
to achieve. The baroreceptor sensitivity (i.e., the slope of the
relationship of the change in heart rate versus the change in
arterial pressure) is negatively correlated with age and rest-
ing arterial pressure (102). The low-pressure baroreceptor,
or cardiopulmonary reflex, also decreases with age in nor-
motensives, but not in hypertensives.
Despite the lesser heart rate increase during orthostatic
stress in older than in younger BLSA volunteers, the SV
reduction tends to be less in the older group; thus, the pos-
tural change in cardiac output does not vary significantly
with age, because a lesser reduction in SV balances the lesser
increase in heart rate in older individuals (103). Similarly,
some studies have found cardiac output to be reduced with
age in the supine position because of a reduced SV in older
versus younger men; this age effect was abolished in the sit-
ting position because of lesser reduction in SV in the older
men on sitting.
Pressor stress
Acute increases in blood pressure represent another com-
mon CV stress. Sustained, isometric handgrip increases
both arterial pressure and heart rate. The response varies in
magnitude in proportion to the relative level and duration
of effort. After sustained submaximal or maximal hand-
grip, heart rate was observed to increase more in younger
than in older healthy individuals, whereas blood pressure
increased more in older persons (104,105). In BLSA volun-
teers, 3 minutes of submaximal sustained handgrip elicited
mild increases in echocardiographic LV diastolic and sys-
tolic dimensions and atrial filling fraction; these increases
correlated positively with age (105). Thus, pressor stress
accentuated the age-associated dependence on late dia-
stolic filling.
Application of a pressor stress has also been used to
assess the intrinsic myocardial reserve capacity. In healthy
BLSA individuals, a 30 mmHg increase in systolic blood
pressure induced by phenylephrine infusion in the pres-
ence of β-adrenergic blockade induced significant echo-
cardiographic LV dilatation at end diastole in healthy older
(60–68 years), but not in younger (18–34 years), men: the
cardiac dilatation occurred in older men despite a smaller
reduction in heart rate (106), analogous to the handgrip
response. Thus, an apparent age-associated decrease in
intrinsic myocardial contractile reserve occurs in response
to an acute increase in afterload; the senescent heart dilates
to preserve SV via the Frank–Starling mechanism.
Aerobic exercise capacity
The ability to perform oxygen-utilizing (i.e., aerobic) activi-
ties is a fundamental requirement of independent living
and is probably the best-studied CV stressor. The accepted
standard for aerobic fitness is maximum oxygen consump-
tion rate (VO2max), the product of cardiac output (the
central component) and arteriovenous oxygen difference
(the peripheral component) during exhaustive exercise. In
healthy adults, VO2max is up to 15 times greater than rest-
ing VO2. This huge increase is accomplished by a four- to
fivefold augmentation of cardiac output and up to a three-
fold widening of the arteriovenous oxygen difference; the
latter is due to both a dramatic increase in the relative pro-
portion of cardiac output delivered to working muscles and
increased oxygen extraction by these muscles. Because the
total body VO2max is strongly influenced by muscle mass,
VO2max is typically compared across individuals by nor-
malizing for body weight.
Multiple studies have documented that treadmill
VO2max, adjusted for body weight, declines with age. In
cross-sectional studies, the decline typically approximates
50% across the adult age span (107,108). However, the extent
of the VO2max decline with aging varies among studies,
depending on age ranges, differences in body weight and
composition, and differences in habitual physical activity
among the individuals studied. Longitudinal studies gen-
erally report a more pronounced age-associated decline
in VO2max than do cross-sectional studies. In BLSA vol-
unteers rigorously screened to exclude CV or lung disease,
VO2max declines by ~50% between the third and ninth
decades by cross-sectional analysis (107,108). Although
such cross-sectional studies are usually interpreted to indi-
cate that VO2max declines linearly with age, a more detailed
analysis in this same BLSA population demonstrated that
 CV response to stress 11

Men healthy BLSA volunteers represent a best-case scenario. The

Longitudinal % change per decade
15
10 superimposition of CV or pulmonary disease as well as the
5 deconditioning and loss of muscle mass commonly seen in
0 the elderly because of their sedentary lifestyle accentuate
–5 this decline in VO2max. Because activities of daily living
–10 typically require a fixed aerobic expenditure, they require
–15 a significantly larger percent of VO2max in an older than
Peak VO2/mL a younger person. Once the energy required of an activity
–20
O2 pulse
–25 Maximum heart rate
approaches or exceeds the aerobic capacity of an elderly
–30 individual, he/she will likely be unable to perform it. Thus, it
10 20 30 40 50 60 70 80 is not surprising that a low aerobic capacity, represented by
(a) Age (years) slow walking speed, comprises one of the five components
Women of the “frailty phenotype” (110).
Longitudinal % change per decade

15
10
Another potential contributor to exercise intolerance with
5 aging is a greater metabolic debt incurred during exercise
0 that persists during recovery. For several minutes after a bout
–5 of aerobic exercise, the body continues to consume o ­ xygen
–10 at a higher rate than at rest. This “oxygen debt” incurred
–15 during recovery can comprise 14%–20% of the total aero-
–20 Peak VO2/mL bic expenditure. In one study, the VO2 consumed by healthy
O2 pulse older persons during recovery from exercise exceeded that
–25
Maximum heart rate
–30 in the young by more than 30% (111). Although the precise
10 20 30 40 50 60 70 80 causes of this greater VO2 use during recovery in the elderly
(b) Age (years) is unclear, increased circulating catecholamine levels (112)
and the higher core temperature that occur during exercise
Figure 1.8 Longitudinal change in peak VO2 and its and early recovery in deconditioned older adults (113) may
components (maximal heart rate and O2 pulse) in healthy be contributory.
BLSA male (a) and female (b) volunteers. In both sexes,
Because of the difficulty in imaging the heart during
the decline in maximal heart rate is only ~5% per decade
and is relatively constant across age. However, the
treadmill exercise, cycle ergometry has been used to dis-
decline in O2 pulse, encompassing both stroke volume sect the relative contributions of cardiac and peripheral
and peripheral oxygen delivery and utilization, declines factors in the age-associated decline in aerobic capac-
more rapidly in older adults, paralleling the decline in ity (Table 1.2). During upright cycle ergometry, the peak
peak VO2. Abbreviation: BLSA, Baltimore Longitudinal VO2 of healthy BLSA participants averages about 80% of
Study of Aging. (From Fleg, J.L. et al., Circulation, 112, that during treadmill exercise, regardless of age, usually
674–682, 2005.) limited by leg fatigue. Peak cycle work rate and VO2 decline

the longitudinal decline in aerobic capacity is not con- Table 1.2 Changes in maximal aerobic capacity and its
stant across adulthood as assumed by cross-sectional stud- determinants between ages 20 and 80 years in healthy
ies, but accelerates markedly with successive age decades, volunteers
especially in men, regardless of physical activity levels Oxygen consumption ⇓ (50%)
(Figure 1.8) (109). When the components of VO2max were (A-V)O2 difference ⇓ (20%)
examined, the longitudinal decline in oxygen pulse (VO2 Cardiac output ⇓ (30%)
per heartbeat) mirrored that of VO2max, whereas maximal
Heart rate ⇓ (25%)
heart rate decreased only 4%–6% per decade regardless of
Stroke volume no change
starting age (Figure 1.8). Although age-associated loss of
EDV ⇑ (30%)
muscle mass and increase in body fat also contribute to the
reduction in VO2max with aging, the pattern of accelerated ESV ⇑ (275%)
VO2max decline with age persists even after normalizing it Contractility ⇓ (60%)
for fat-free mass rather than body weight (109). Despite the Ejection fraction ⇓ (15%)
similar rates of decline in VO2max with age regardless of Vascular (SVR) ⇑ (30%)
physical activity level, it should be emphasized that at any Plasma catecholamines ⇑
age the more active quartiles maintain a higher VO2max Cardiac and vascular
than their sedentary peers. Responses to β-adrenergic stimulation ⇓
The accelerated decline of aerobic capacity has impor- Abbreviations: 
AV, arteriovenous; EDV, end-diastolic volume;
tant implications regarding functional independence and ESV, end-systolic volume; SVR, systemic vascular
quality of life. It should be emphasized that the data in resistance.
12 Cardiovascular changes with aging

End-diastolic volume index (mL.m–2)

140 70

End-systolic volume index (mL.m–2)

Female Female
Male r = 0.34, p = 0.0003
120 r = 0.11, p = 0.23 60 Male
r = 0.43, p = 0.0001
50
100
40
80
30
60
20
40 10

20 0
20 40 60 80 100 20 40 60 80 100
(a) Age (years) (b) Age (years)

110 100

Stroke volume index (mL.m2)

100 90
Ejection fraction (%)

80
90
70
80
60
70
50
60 Female 40 Female
r = –0.34, p = 0.0002 r = – 0.063, p = 0.49
50 Male 30 Male
r = –0.44, p = 0.0001 r = – 0.034, p = 0.66
40 20
20 40 60 80 100 20 40 60 80 100
(c) Age (years) (d) Age (years)

220 18 Female
r = – 0.46, p = 0.0001
200 16
Cardiac index (L.min–2.m–1)

Male
Heart rate (beats/min)

180 14 r = – 0.43, p = 0.0001

160 12
140 10
120 8
Female
100 6
r = – 0.64, p = 0.0001
80 Male 4
r = – 0.68, p = 0.0001
60 2
20 40 60 80 100 20 40 60 80 100
(e) Age (years) (f) Age (years)

Figure 1.9 Scatter plots of left ventricular volumes (a, b), ejection fraction (c), stroke volume (d), heart rate (e), and cardiac
index (f) during maximal graded upright cycle exercise in healthy BLSA volunteers, carefully screened to exclude silent
coronary artery disease. Note the similar age changes in men and women and the increasing heterogeneity with age
in the end-systolic volume index, ejection fraction, and heart rate. Abbreviation: BLSA, Baltimore Longitudinal Study of
Aging. (From Fleg, J.L. et al., J. Appl. Physiol., 78, 890–900, 1995.)

by ~50% between ages 20 and 90 years in healthy, non- LV ­ejection ­fraction (Figure 1.9c), this deficit is offset by a
athletic BLSA men and women, attributable to declines of larger end-­ diastolic ­
volume index (EDVI) (Figure 1.9a)
~30% in cardiac output and 20% in arteriovenous oxygen (115). Thus, a “stiff heart” that prohibits sufficient filling
difference (Table 1.2) (114). between beats during exercise does not characterize aging in
The age-associated decrease in cardiac index at ­maximal healthy individuals. The larger EDVI in healthy older ver-
effort during upright cycle exercise (Figure 1.9f) is due entirely sus younger individuals during vigorous aerobic exercise is
to a reduction in heart rate (Figure 1.9e), as the LVSV index due in part to a longer ­diastolic interval (i.e., slower heart
(LVSVI) does not decline with age in either gender (Figure 1.9d) rate) and to a greater amount of blood ­remaining in the
(115). However, the manner in which SVI is achieved during heart at end systole (Figure 1.9b) (115). However, an exag-
­maximal exercise changes importantly with aging. Although gerated rise in p­ ulmonary ­capillary wedge pressure occurs
older individuals have a blunted capacity to reduce end-­ during ­aerobic exercise in older adults, p
­ erhaps contributing
systolic volume index (ESVI) (Figure 1.9b) and to increase to exercise intolerance (97).
Another random document with
no related content on Scribd:
Habedin. During this short journey my body swelled prodigiously,
without giving any other sign of life. The village sheik having placed
me on a mattress, sent to Hems for a surgeon. For nine whole hours
I remained perfectly insensible; and at the end of that time opened
my eyes without the smallest perception of the objects around me, or
recollection of what had befallen me. I felt as if under the influence of
a dream, but without being sensible of pain. In this state I lay for
four-and-twenty hours, and recovered from my lethargy only to suffer
such indescribable agonies that I fancied it would have been better a
hundredfold to have remained at the bottom of the precipice.
Sheik Ibrahim never quitted me for an instant, and offered the
highest rewards to the surgeon in case he should succeed in saving
me. The latter was zealous, but by no means skilful; and no
amendment appearing at the expiration of thirty days, gangrene was
apprehended. The Drayhy had visited me immediately on being
informed of my accident; and he also wept over me, and offered rich
presents to stimulate the surgeon’s efforts: but at the highest point of
his sensibility he could not suppress his regret for the loss of his
mare Abaige, who was of pure blood, and worth ten thousand
piastres. Nevertheless, he was in real distress, as was Ibrahim; for
they not only feared my loss, but foresaw in it the miscarriage of all
their operations. I endeavoured to encourage them, telling them that
I did not believe myself dying. But it was too true, that though, I
should be spared, there was no probability of my being for a long
while in a condition to travel.
The Drayhy was obliged to take leave of us to pursue his migration
eastwards; and Sheik Ibrahim was in despair at seeing me grow
daily worse. Hearing at length that a more skilful surgeon resided at
El Dair Attia, he sent for him. The surgeon refused to come, requiring
that the patient should be taken to him. I was therefore put upon a
sort of litter in the best manner that could be contrived, and carried to
him, at the hazard of expiring on the road. The new surgeon entirely
changed the dressing of my wounds, and washed them with warm
wine. Three months I stayed with him, suffering martyrdom, and a
thousand times regretting the death I had escaped. I was then
transported to the village of Nabek, where for three months longer I
kept my bed. From that period I may date the actual commencement
of my recovery, though it was retarded by frequent relapses. Upon
the sight of a horse, for example, I fainted, and continued for a
month in a state of extreme nervousness, which at length, and by
degrees, I conquered: but I am bound to confess that to this moment
the presence of that animal causes me a shudder; and I made a
resolution never again to mount a horse, except in a case of
absolute necessity.
My illness cost Sheik Ibrahim five hundred tallarins. But how shall I
estimate his attentions, his paternal care! I am assuredly indebted to
him for my life.
During my convalescence he learnt that our friend the Pacha of
Damascus had been replaced by another, Soliman Selim. This news
greatly disconcerted us, as it appeared indicative of the loss of our
credit with the Turks.
Ten months had elapsed—a second spring was come, and we were
expecting with impatience the arrival of the Bedouins, our allies,
when, to our great joy, a courier announced their approach. We
forwarded him in haste to the Drayhy, who liberally rewarded him for
the good news he brought of my recovery, which produced universal
joy in the camp, where I had long been supposed dead. We waited
some days longer, till the tribe advanced nearer; and in the interval a
singular story came to my knowledge, which I think worthy of
insertion, as an illustration of Arab manners.
A merchant of Anatolia, escorted by fifty men, was leading ten
thousand sheep to be sold at Damascus. On the road he made
acquaintance with three Arabs, with one of whom he formed a close
intimacy, and at parting was desired to swear fraternity with him. The
merchant could not discover in what respect he, who was the
proprietor of ten thousand sheep, and was escorted by fifty soldiers,
could be benefitted by having a brother amongst the poor Bedouins;
but the Bedouin, whose name was Chatti, was so importunate, that,
to satisfy him, he consented to give him two piastres and a handful
of tobacco as pledges of fraternity. Chatti divided the two piastres
between his companions, saying, “Be ye witnesses that this man is
become my brother.” They then separated, and the merchant
thought no more of the matter, till, at a place called Ain el Alak, a
party of Bedouins, superior in number to his escort, attacked and
routed them, took possession of his sheep, and stripped him to his
shirt; in which pitiable condition he arrived at Damascus, imprecating
curses upon the Bedouins, and especially upon his pretended
brother Chatti, whom he accused of betraying and selling him.
Meanwhile the news of so rich a capture was quickly spread in the
desert, and reached the ears of Chatti, who, having with some
difficulty found his two witnesses, brought them before Soultan el
Brrak, chief of the tribe of El Ammour, to whom he declared that he
was brother to the merchant who had just been robbed, and called
upon the chief to enable him to fulfil the duties of fraternity, by
restoring the property. Soultan, having taken the depositions of the
two witnesses, was obliged to accompany Chatti to El Nahimen, the
sheik of the tribe which had carried off the sheep, and to reclaim
them in conformity with their laws. The sheik was under the
necessity of restoring them; and Chatti, having first ascertained that
none were missing, took the road to Damascus, with the flocks and
their shepherds.
Leaving them outside the town, he entered it in search of his brother,
whom he found seated in a melancholy mood in front of a coffee-
room of the Bazaar. He went straight to him with a joyful air; but the
other turned angrily away, and Chatti had great difficulty in obtaining
a hearing, and still greater in persuading him to believe that his
sheep were waiting for him outside the walls. He apprehended a new
snare, and would not for a long while consent to follow the Bedouin.
Convinced at last by the sight of his sheep, he threw himself on
Chatti’s neck, and after giving full expression to his gratitude, vainly
exerted himself to induce him to accept a recompense proportioned
to such a service. The Bedouin could only be persuaded to receive a
pair of boots and a cafia (handkerchief), not worth above a tallarin at
the utmost, and, after partaking of his brother’s bread, returned to his
tribe.
Our first interview with the Drayhy was truly affecting. He came
himself, with the principal members of his tribe, to seek us at the
village of Nabek, and took us back in a sort of triumph to the camp.
By the way he gave us the history of the wars he had waged in the
territory of Samarcand, and his good fortune in vanquishing four of
the principal tribes,[P] and afterwards inducing them to sign the
treaty. It was important to have detached these tribes in time from
their alliance with the Wahabees, to whom they were formerly
tributary; for it was reported that our enemies were preparing a
formidable army, and flattered themselves with obtaining the
supremacy of all Syria. Soon afterwards we heard that the army was
on its march, spreading terror and devastation everywhere on its
passage.
The Pacha of Damascus despatched orders to the governors of
Hems and Hama, to keep guard day and night, and to hold their
troops in readiness for battle: while the inhabitants fled towards the
coast, to escape the sanguinary Wahabees, whose name alone
sufficed to drive them from their homes.
The Drayhy was invited by the pacha to a conference with him at
Damascus; but fearing some treason, he excused himself under
pretence of the impossibility of deserting his post at so critical a
moment. He even requested from him some auxiliary troops, hoping
by their assistance to be able to keep the enemy in check.
While waiting for the expected reinforcement, the Drayhy caused a
solemn declaration of war to be made, according to the custom of
the Bedouins on very particular occasions, in the following form:—A
white female camel was selected, and blackened all over with soot
and oil; reins made of black hair were then put over her, and she was
mounted by a young maiden dressed in black, with her face and
hands also blackened. Ten men led her from tribe to tribe, and on
reaching each she proclaimed aloud three times,—“Succour!
succour! succour! Which of you will make this camel white? she is a
relic from the tent of the Drayhy menacing ruin. Fly, fly, noble and
generous defenders! The Wahabees are coming! they will carry
away your allies and your brothers: all you who hear me, address
your prayers to the prophets Mahomet and Ali, the first and the last!”
Saying which, she distributed amongst the tribe handfuls of black
hair, and letters from the Drayhy, indicating the place of rendezvous
on the banks of the Orontes. Our camp was in a short time
augmented by the coalition of thirty tribes, assembled in the same
plain, and so thickly encamped that the ropes of our tents touched.
The Pacha of Damascus sent ten thousand men to Hama,
commanded by his nephew Ibrahim Pacha, there to wait for other
troops which the Pachas of Acre and Aleppo were to furnish.
Scarcely had they met, when the arrival of the Wahabees at Palmyra
was announced by the inhabitants, who fled to take refuge in Hama.
Ibrahim Pacha wrote to the Drayhy, who repaired to him, and they
arranged together their plan of defence. The Drayhy, who took me
with him as his counsellor, acquainted me with the stipulations
agreed upon; when I pointed out to him the danger of uniting
Bedouins and Turks in the same camp, the latter having no means of
distinguishing in the confusion of battle their friends from their
enemies. The Bedouins themselves, indeed, recognize each other in
the heat of the fight only by their war-cries, each tribe incessantly
repeating its own,—“Khrail el allia Doualli,—Khrail el bionda Hassny,
—Khrail el hamra Daffiry,” &c.;—Khrail signifying horsemen; allia,
bionda, hamra, indicating the colour of their favourite mare; Doualli,
Hassny, Daffiry, are the names of the tribes. This war-cry, therefore,
is equivalent to the words, horsemen of the red mare of Daffir, &c.
Others invoke their sister, or some other beauty; hence the Drayhy’s
war-cry is, Ana Akhron Rabda,—I the brother of Rabda; that of
Mehanna,—I the brother of Fodda: both have sisters renowned for
their beauty. The Bedouins pride themselves greatly in their war-
cries, and would consider that man a coward who should hesitate to
pronounce it in the moment of danger. The Drayhy saw the force of
my argument, and persuaded Ibrahim Pacha, though with difficulty,
to consent to a division of their forces.
The next day we returned to the camp, followed by the Mussulman
army, composed of Dalatis, Albanese, Mogrebins, Houaras, and
Arabs; in all, fifteen thousand men. They had with them some pieces
of ordnance, a few mortars and bombs, and pitched their tents half
an hour’s march from ours: the pride of their bearing, the variety and
richness of their costumes, and their banners, altogether formed a
magnificent spectacle; but, in spite of their fine appearance, the
Bedouins jested upon them, and asserted that they would be the first
to fly.
In the afternoon of the second day a broad cloud was observable
towards the desert, spreading itself like a thick fog as far as the eye
could reach: by degrees the cloud cleared up, and the enemy’s army
appeared in view.
This time they brought their wives, their children, and their camels,
and established their camp, composed of fifty tribes, forming
seventy-five thousand tents, at an hour’s march from ours. About
each tent, camels and a great number of sheep were tied;
presenting, together with the horses and warriors, a formidable mass
to the eye. Ibrahim Pacha was in consternation, and sent in great
haste in search of the Drayhy, who, having succeeded in reanimating
his courage a little, returned to the camp, to order the necessary
entrenchments. For this purpose all the camels were assembled,
bound together by their knees, and placed in double files in front of
the tents; and, to complete the rampart, a trench was dug behind
them. The enemy on his part did the same, and the Drayhy ordered
the hatfé to be prepared. This singular ceremony consists in
selecting the most beautiful amongst the Bedouin girls, to be placed
in a houdah, richly ornamented, borne by a tall white camel. The
choice of the maiden who is destined to occupy this honourable but
perilous post is very important, for the success of the battle depends
almost entirely upon her. Placed opposite to the enemy, and
surrounded by the bravest warriors, it is her duty to excite them to
the combat: the principal action always takes place around her, and
prodigies of valour defend her. All would be lost should the hatfé fall
into the enemy’s hands; and, to avoid so irreparable a misfortune,
half the army must always be stationed about her. Warriors succeed
each other on this point, where the battle is always hottest, and each
comes to gather enthusiasm from her looks. A girl named Arkia,
uniting in an eminent degree courage, eloquence and beauty, was
chosen for our hatfé. The enemy also prepared his, and the battle
soon afterwards commenced. The Wahabees divided their army into
two corps: the first and most considerable, commanded by Abdallah
el Hedal, the general-in-chief, was opposed to us; the second, under
the command of Abou Nocta, to the Turks. Both the character of the
latter, and their mode of fighting, are totally different from those of
the Bedouins, who, prudent and cool headed, begin the action
calmly, but growing gradually animated, become at last furious and
irresistible. The Turk, on the contrary, proud and arrogant, rushes
impetuously upon the enemy, and fancies he has only to appear and
conquer: his whole energy is thus expended on the first shock.
The Pacha Ibrahim, seeing the Wahabees attack coldly, deemed
himself sufficiently strong to disperse their entire army without
assistance; but, before the end of the day, he had learned by dear-
bought experience to respect his enemy, and was forced to permit
his troops to fall back, leaving us to sustain the whole weight of the
action.
Sunset suspended the engagement, but not till both parties had
suffered a severe loss.
The next morning brought us a reinforcement, in the tribe of El
Hadidi, four thousand strong, all mounted on asses, and armed with
muskets. We numbered our forces, which amounted to eighty
thousand men; but the Wahabees had a hundred and fifty thousand,
and this day’s battle terminated in their favour. Our defeat,
exaggerated, as always happens in similar cases, was reported at
Hama, and filled the inhabitants with dismay; but two days
afterwards their fears for us were removed, and for three weeks we
were alternately discomfited and successful. The actions became
daily more sanguinary; and on the fifteenth day of this trying
campaign, a new enemy, more formidable than the Wahabees, arose
in the shape of famine. The town of Hama, which alone could furnish
subsistence to either army, was exhausted, or concealed its
resources. The Turks took to flight; our allies dispersed, to avoid
perishing with hunger; the camels, forming the rampart of our camp,
began to devour one another. Amidst such frightful calamities, the
courage of Arkia never for an instant wavered. The bravest of our
warriors were slain by her side; but she ceased not to encourage
them, and to excite and applaud their efforts. She animated the old
by extolling their valour and experience; the young, by the promise of
marrying him who should bring her the head of Abdallah el Hedal.
Keeping my station near her houdah, I saw all the warriors present
themselves to her for some words of encouragement, and then rush
to the combat, excited to enthusiasm by her eloquence. I confess I
preferred hearing these compliments to receiving them myself, for
they were almost uniformly the forerunners of death.
I one day saw a fine young man, one of our bravest soldiers, present
himself before the houdah: “Arkia,” said he, “O thou fairest amongst
the fair, allow me a sight of thy face, for I go to fight for thee!” Arkia,
unveiling, replied: “Behold, O thou most valiant! Thou knowest my
price; it is the head of Abdallah!” The young man brandished his
spear, put spurs to his courser, and rushed into the midst of the
enemy. In less than two hours he sank covered with wounds.
“Heaven preserve you!” said I to Arkia, “this brave man is
killed.”—“He is not the only one who has never returned,” she
sorrowfully replied. At this moment a warrior made his appearance,
armed from head to foot; even his boots were defended with steel,
and his horse covered with a coat of mail, (the Wahabees reckoned
twenty such warriors amongst them; we had twelve.) He advanced
towards our camp, challenging the Drayhy to single combat: this has
been the custom amongst the Bedouins from time immemorial; he
who is thus defied, cannot without forfeiting his honour refuse to
fight. The Drayhy, hearing his name, prepared to answer to the
challenge: but his kinsmen joined with us to prevent it. His life was of
too much importance to be thus risked; for the loss of it would have
entailed the total ruin of our cause, and the destruction of the two
allied armies. Persuasion becoming useless, we were obliged to
have recourse to coercion. We bound him with cords hand and foot
to stakes driven into the ground in the middle of his tent: the most
influential chiefs supported him, and entreated him to calm himself,
urging the imprudence of risking the welfare of the army for the
purpose of answering the insolent bravado of a savage Wahabee.
Meanwhile, the latter incessantly exclaimed: “Let the Drayhy come
forth! this shall be his last day; I am waiting to terminate his career.”
The Drayhy, who heard him, becoming more and more furious,
foamed with rage and roared like a lion; his blood-shot eyes almost
starting from his head, while he fought with terrible strength to
disencumber himself of his bonds. This tumult attracted a
considerable multitude around the tent, when suddenly a Bedouin,
making his way through the crowd, presented himself before the
Drayhy. His sole clothing was a shirt bound round his loins with a
leathern girdle, and a turban on his head; he was mounted upon a
bay horse, and armed only with a spear; and thus singularly
equipped, he came to ask, in the following metrical style, permission
to fight the Wahabee instead of the sheik: “This day, I, Tehaisson,
have become master of the horse Hadidi: it has long been the object
of my ambition; I wished to receive upon his back the praises due to
my valour. I am about to fight and to vanquish the Wahabee, for the
beautiful eyes of my betrothed, and to render myself worthy of his
daughter who was always conqueror.” So saying, he rushed to
combat the hostile warrior. No one imagined that he could for one
half hour resist his formidable antagonist, whose armour rendered
him invulnerable; but if the blows he dealt were thus robbed of their
murderous power, he avoided with wonderful dexterity those that
were aimed at himself during the two hours that the struggle lasted.
Meanwhile, all was suspense; the deepest interest was manifested
on both sides. At length our champion turned round, and apparently
took to flight. All hope was now lost; the enemy was about to
proclaim his triumph. The Wahabee pursued, and, with a hand
strengthened by the assurance of success, flung his lance; but
Tehaisson, foreseeing the blow, stooped even to his saddle-bow, and
the weapon flew whizzing above his head; then, suddenly returning,
he thrust his spear into the throat of his adversary, taking advantage
of the moment when the latter, being obliged to curb his horse hastily
before him, was in the act of raising his head. This movement
leaving a space between the helmet and the cuirass, the spear
passed through from side to side, and killed him on the spot: but his
armour supporting him in the saddle, he was carried by his horse
into the midst of his followers; and Tehaisson returned in triumph to
the tent of the Drayhy, where he was enthusiastically received. All
the chiefs embraced him, loading him with eulogies and presents;
and Sheik Ibrahim was not backward in testifying his gratitude.
Meanwhile, the war and the famine continued to rage: even in the
Drayhy’s tent we were two days without food; on the third, he
received a considerable supply of rice, which Mola Ismael, chief of
the Dallatis, sent him as a present. Instead of husbanding it as a last
resource, he ordered that the whole should be dressed, and invited
all present to sup with him. His son Saher would not sit down to
table; but, being importuned by his father, he requested that his
portion might be given to him, and carried it to his mare, declaring
that he had rather suffer himself, than see her die for want of food.
We had now arrived at the thirty-seventh day from the
commencement of the war: on the thirty-eighth, the battle was
terrible. The camp of the Osmanlis was taken and pillaged: the
pacha had scarcely time to escape to Hama, whither he was
pursued by the Wahabee, who there besieged him.
The defeat of the Turks was the more fatal to us, as it left the second
corps of the hostile army, commanded by the famous Negro Abou
Nocta, at liberty to unite with Abdallah, and make a combined attack
upon us. The following day witnessed the commencement of a
frightful struggle, which lasted eight days without intermission. The
combatants were so intermingled together, that it was impossible to
distinguish one party from another. They fought with the sabre man
to man; the entire plain was deluged with blood, the colour of the
ground being totally invisible: never perhaps was such a battle
fought. The inhabitants of Hama, fully persuaded that we were utterly
exterminated, no longer sent us those occasional supplies of
provisions which, coming at our utmost need, had hitherto preserved
us from starvation. At length the Drayhy, finding his misfortunes
accumulate, assembled his chiefs, and addressed them thus: “My
friends, it now becomes necessary that we should make a last effort.
To-morrow we must either conquer or die. To-morrow, by God’s
permission, I will destroy the enemy’s camp: to-morrow we will feast
upon its spoils.” This harangue was received with a smile of
incredulity; until one, more daring than the rest, replied: “Give but the
word, and we will obey.”—“This night,” he continued, “you must
noisely transplant your tents, your wives, and your children, to the
other side of the Orontes. The whole must have disappeared before
sunrise, without the cognisance of the enemy. Then, having no
longer any care to trouble us, we will make a desperate attack upon
them, and will exterminate them, or perish ourselves in the attempt:
but God will be on our side, and we shall conquer.” Every one
hastened to execute the commands thus given, with incredible order,
celerity, and silence. The next day, the efficient warriors alone
remained. The Drayhy divided them into four corps, ordering a
simultaneous attack upon the four sides of the enemy’s camp. The
troops, in desperation, threw themselves upon their prey like hungry
lions; and the impetuous but well-concerted onset was attended with
all the success which could have been wished. Confusion and
disorder spreading rapidly amongst their unexpectedly enclosed
ranks, the Wahabees took to flight, abandoning their women and
children, their tents and their baggage. The Drayhy, without allowing
his men time to seize upon the booty, obliged them to pursue the
fugitives to Palmyra, and gave them no respite until they had
accomplished the total dispersion of the enemy.
No sooner had victory declared itself in our favour, than I departed
with Sheik Ibrahim to announce the joyful intelligence at Hama; but
nobody there would give credit to it, and the inhabitants would fain
have treated ourselves as fugitives. They exhibited the utmost
perturbation: some climbed the heights, whence they could perceive
nothing but clouds of dust; others prepared their mules for flight
towards the coast. The defeat of the Wahabees being, however,
speedily confirmed, the most extravagant demonstrations of joy
succeeded to this terrible alarm. A Tartar was despatched to
Damascus, and brought back with him forty loads of wheat, twenty-
five thousand piastres, and a sabre and a robe of honour for the
Drayhy, who made his triumphal entry into Hama, escorted by all the
chiefs of the allied tribes. He was received by the governor, the agas,
the pacha, and all his court, in the most splendid manner.
After four days of rejoicings we quitted Hama, to rejoin our tribes,
and conduct them to the east before the approach of winter. The
Drayhy was personally attended by a company of twelve; the others,
in groups of five or six, dispersed themselves in the desert of
Damascus. Our first stay was at Tall el Dehab, in the territory of
Aleppo, where we encountered four tribes who had taken no part in
the war. The chiefs came forward to meet the Drayhy, penetrated
with respect for his recent exploits, and soliciting the favour of being
admitted to sign the treaty of alliance with us.[Q] From thence we
marched without interruption to join our friend, the Emir Faher, who
received us with the most lively demonstrations of joy. In company
with his, and several other tribes, proceeding like ourselves to
Mesopotamia, we crossed the Euphrates, some establishing
themselves in the neighbourhood of Hamad, others in the desert of
Bussora.
On the road we received a letter from Fares el Harba, announcing
that six considerable tribes, who had fought on the side of the
Wahabees against us, were encamped in the Hebassia, near
Machadali, and were well disposed to enter into alliance with us; and
that if the Drayhy would send me to him furnished with full powers to
treat, he believed himself certain of success. I lost not a moment in
availing myself of this invitation, and, after a journey of six hours,
reached him without accident. Fares el Harba immediately broke up
his camp, and conducted me to the distance of a day’s journey from
the tribes.[R] I then wrote in his name to the Emir Douackhry, chief of
the tribe El Fedhan, exhorting him to make an alliance with the
Drayhy, and promising oblivion of the past. Douackhry came in
person to Fares el Harba, and we were soon agreed; but he
disclaimed answering for more than his own tribe, considering that it
would be extremely difficult to succeed with the others. He proposed,
however, that I should accompany him back, when he would
assemble the chiefs of all the tribes, and exert his utmost influence
with them. I accepted the invitation, and departed with him; but when
arrived in the centre of what ought to have been an encampment, I
was painfully affected to behold hordes of Arabs crouching on the
ground under the full blaze of the sun: having lost their tents and
baggage in the battle, their only bed was the bare ground, their only
canopy the sky. A few rags suspended here and there upon pikes
did indeed afford a semblance of shade to these unfortunate beings,
who, having stripped themselves of their only garments to furnish
this slender shelter from the fervent heat of the sun, were exposed to
the sting of insects, and to the thorny points of the plants on which
their camels browse. Many were wholly destitute of any defence
either from the heat of day or the cold of night, at that autumnal
season, when the contrasts of temperature are most fatal.
Never had I conceived an idea of wretchedness so complete: the
sad spectacle oppressed my heart and drew tears from my eyes,
and it was some time before I could recover from the agitation it
occasioned me.
The next day Douackhry assembled the chiefs and old men to the
number of five hundred. Alone in the midst of them, I despaired of
making myself heard, and especially of being able to unite them in
one counsel. Independent in their character and manners, and
irritated by misfortune, they all mooted different opinions; and if
neither hoped to make his own prevail, at least each made it a point
of honour to maintain it obstinately, leaving all the others at liberty to
do the like. Some proposed removing to the Nedgde country, others
to retire to Samarcand: these vociferated imprecations against
Abdallah, chief of the Wahabee army; those denounced the Drayhy
as the author of all their misfortunes. Amid the conflict of voices, I
armed myself with patience, and endeavoured to conciliate all
parties. I began by shaking their confidence in the Wahabees;
showing them that Abdallah must necessarily have become their
enemy, since they had abandoned him on the last day of the battle,
and that he was now seeking vengeance upon them: that in going to
Nedgde they voluntarily threw themselves under the domination of
Ebn Sihoud, who would extort from them oppressive contributions,
and compel them to bear the whole burden of a disastrous war: that
having once deserted his cause, and effected their withdrawal from
his power, they should not follow the example of the foolish bird, who
no sooner escapes the sportsman’s shot than he falls into the
fowler’s net. At last, the fable of the bundle of sticks occurred to my
mind; and thinking so simple a demonstration would make an
impression on their unsophisticated minds, I determined to make a
practical application of it before their eyes. Having exhorted them to
be united, and by their union to resist all oppression, I took from the
hands of the sheiks about thirty djerids, and presented one to the
Emir Fares, requesting he would break it, which he effected with
ease. I then presented him with two, and afterwards with three, all of
which he broke in the same manner, for he was a man of great
muscular strength. I then placed in his hand the whole bundle, which
he could neither break nor bend. “Machala,” said I, “thy strength is
not sufficient;” and I then passed the united spears to another, who
succeeded no better. A general murmur now arose in the assembly:
“Who could split such a mass?” cried they unanimously. “I take you
at your word,” said I; and in the most energetic language I could
command, I applied the apologue to their reasoning faculties,—
adding, that so powerfully had I been affected by their destitute
condition, without clothing or shelter, that I pledged myself to solicit
from the Drayhy the restitution of their baggage and tents, and that I
was sufficiently acquainted with his magnanimity to answer for the
success of my application, if they entered heartily into the alliance, of
which I had just proved the advantages. Upon this they all exclaimed
with one voice: “Thou hast conquered, Abdallah; we are thine in life
and in death!” and all ran forward to embrace me. It was then
determined that they should give the Drayhy the rendezvous in the
plain of Halla, to affix their seal to the treaty.
Recrossing the Euphrates the next morning, I rejoined our tribe on
the fifth day, and found my friends uneasy at my protracted absence;
but the report of my fortunate negotiation filled them with joy. I have
already so frequently detailed meetings, feasts, and rejoicings of
every kind, that I shall not repeat the same narrative by describing
those which took place on this occasion.
The Emir Douackhry buried the seven stones, and thus
consummated the alliance; and after dinner I witnessed for the first
time the ceremony of swearing fidelity over bread and salt. The
Drayhy then declared that he was ready to fulfil the engagement I
had contracted in his name, by restoring the booty taken from the six
tribes who had just united their cause with his. But the generous will
was insufficient—the means of its execution were still to be provided.
In the pillage of the Wahabee and allied camp, the plunder of fifty
tribes was confounded, and to identify the property of each was no
easy matter. It was decided that the women alone were competent to
the task; and it would be impossible to form an idea of the exertion
and fatigue of the five days employed by them in recognising the
cattle, tents, and baggage of the various tribes. Every camel and
sheep has two ciphers stamped with a hot iron on the leg, those of
the tribe and the proprietor. But when, as it often happens, the
ciphers are similar, or half effaced, the difficulty of identifying them is
extreme; and under the exhausting task of reconciling such various
pretensions, and deciding such harassing controversies, which it
required something more than generosity to endure with patience, I
was sometimes tempted to repent my momentary impulse of
compassion and my imprudent promise.
At this time a great caravan from Bagdad to Aleppo passed, and was
plundered by the Fedans and Sabhas. It was very richly laden with
indigo, coffee, spices, Persian carpets, Cashmires, pearls, and other
valuable articles, which we estimated at ten millions of piastres. No
sooner was the capture known, than merchants flocked to the
desert, some from a great distance, to purchase these treasures
from the Arabs, who sold, bartered, or rather gave them away almost
for nothing. For instance, they exchanged a measure of spices
against an equal measure of dates; a Cashmire shawl, worth a
thousand francs, against a black saddle-cloth; a chest of indigo for a
linen dress; entire pieces of India muslin for a pair of boots. A
merchant from Moussoul bought, for a shirt, a saddle-cloth, and a
pair of boots, goods worth fifteen thousand piastres; and a diamond
ring was sold for a roll of tobacco. I might have made my fortune on
the occasion, but M. Lascaris prohibited my either purchasing or
receiving any thing as a gift, and I scrupulously obeyed. Every day
tribes arrived from the Nedgde country, deserting the Wahabees to
join us; some attracted by the Drayhy’s extraordinary reputation,
others driven by dissensions with King Ebn Sihoud. One
circumstance of that nature brought us five tribes in a body. The emir
of the tribe Beny Tay had a very beautiful daughter, named Camara
(the moon); Fehrab, son of the chief of a neighbouring tribe, and a
relative of the Wahabee, became enamoured of her, and contrived to
gain her affection; but the girl’s father discovering their passion,
forbade her speaking to the prince, and himself refused to receive
him or listen to his proposals, designing Camara for her cousin
Tamer; for it is a custom amongst the Bedouins, which reminds one
of those transmitted to us by the Bible, for the nearest kinsman to be
preferred to all other suitors when a maiden’s marriage is in
question.
Camara, however, neither swayed by the usages of her people, nor
intimidated by her father’s menaces, positively refused to espouse
her cousin; and her attachment acquiring strength in proportion to
the obstacles opposed to it, she lost no opportunity of corresponding
with her lover. The latter, seeing no hope of obtaining her parent’s
consent, resolved to run away with her, and opened the proposition
to her through an old woman whom he had gained. She gave her
consent; and he introduced himself into the tribe Beny Tay in the
disguise of a mendicant, and arranged with her the hour and
circumstances of the elopement. In the middle of the night the
maiden stole fearfully out of her father’s tent, to the prince, who was
waiting for her at the entrance of the camp. He placed her behind
him on his mare, and dashed across the plain; but the celerity of
their flight could not conceal them from the jealous eye of Tamer:
enamoured of his cousin, and determined to maintain his right, he
had long watched the proceedings of his rival, and every night
mounted guard near Camara’s tent. At the moment the lovers
escaped, he was making his circuit; but immediately perceiving
them, he galloped in pursuit. Fehrab’s mare, endowed by nature with
all the fleetness of the Nedgdian race, and stimulated to greater
exertions by her master’s impatience, urged her course to its highest
speed; but, pressed by a double burden, she could at length no
longer give her wonted aid to her master—she fell; and Fehrab,
seeing himself on the point of being overtaken by Tamer, lifted his
beloved from the horse, and prepared for her defence. The combat
was terrible, and its sequel tragical. Tamer was victor, slew Fehrab,
and seized his cousin; but, exhausted by fatigue, and now in full
security, he fell asleep for a moment by her side. Camara, who had
watched the influence of slumber stealing over his senses, snatched
up his sabre, stained with the blood of her lover, and cut off the head
of her ravisher; then precipitating herself upon the point of his lance,
pierced her own heart. The three dead bodies alone were found by
those who went in search of them.
A murderous war between the two tribes was the consequence of
this melancholy event;—that of Fehrab, supported by the Wahabees,
forced Beny Tay to a retreat; and the latter, with four other tribes,[S]
its allies, came to solicit protection from the Drayhy, whose power
was henceforth unrivalled. Five hundred thousand Bedouins, allied in
our cause, formed but one camp, and overspread Mesopotamia like
a cloud of locusts.
While we remained in the neighbourhood of Bagdad, our allies
pillaged another caravan coming from Aleppo, laden with
productions of European manufacture; cloths, velvets, satins, amber,
coral, &c.; and although the Drayhy took no part in these spoliations,
he was too well versed in Bedouin habits to think of offering any
opposition. The Pacha of Bagdad demanded satisfaction, but
obtained none; and perceiving that to enforce justice would require
an army of at least fifteen thousand men, he renounced his claim,
happy to continue in friendship with the Bedouins at any sacrifice.
Sheik Ibrahim now saw his hopes realized beyond even his most
sanguine anticipations; but as long as any thing remained to be
done, he would allow himself no repose: crossing the Tigris,
therefore, at Abou el Ali, we continued our march, and entered
Persia. Here, also, the reputation of the Drayhy had preceded him,
and the tribes of the country came continually to fraternize with us;
but in our vast plan of operations, these partial alliances were
insignificant,—we required the co-operation of the great prince, chief
of all the Persian tribes, the Emir Sahid el Bokhrani, whose
command extends to the frontiers of India. The family of this prince
has for many years reigned over the errant tribes of Persia, and
claims its descent from the kings Beni el Abass, who conquered
Spain, and whose descendants still call themselves the Bokhrani.
We learned that he was in a very distant province. The Drayhy
having convoked all the chiefs to a general council, it was decided to
traverse Persia, keeping as near as possible to the sea-coast,
notwithstanding the probable scarcity of water, in order to avoid the
mountains which intersect the interior of this country, and to find
pasturage. In the itinerary of a tribe, a plentiful supply of grass is
more important than water: the latter may be transported, but nothing
can remedy a deficiency of food for the cattle, on which the very
existence of the tribe itself depends.
This march occupied fifty-one days. During the whole time we
encountered no obstacle on the part of the inhabitants, but were
often seriously incommoded by the scarcity of water. On one of
these occasions, Sheik Ibrahim, having observed the nature of the
soil and the freshness of the grass, advised the Drayhy to dig for
water. The Bedouins of the country treated the attempt as madness,
saying that no water had ever been known in those parts, and that it
was necessary to send for it to a distance of six hours. But the
Drayhy persevered: “Sheik Ibrahim is a prophet,” said he, “and must
be obeyed.”
Holes were accordingly dug in several places, and at the depth of
four feet excellent water was found. Seeing this happy result, the
Bedouins by acclamation proclaimed Sheik Ibrahim a true prophet,
his discovery a miracle, and, in the excess of their gratitude, had well
nigh adored him as a god.
After journeying several days among the mountains and valleys of
the Karman, we reached the deep and rapid river Karassan; and
having crossed it, proceeded in the direction of the coast, where the
road was less difficult. We made acquaintance with the Bedouins of
the Agiam Estan, who received us in a very friendly manner; and on
the forty-second day after entering Persia, we arrived at El
Hendouan, where one of their greatest tribes was encamped,
commanded by Hebiek el Mahdan. We hoped that our long
pilgrimage was drawing towards its close; but the sheik informed us
that we were still distant nine long days’ journeys from Merah
Fames, the present residence of the Emir Sahid, on the frontiers of
India. He offered us guides to conduct us thither, and described the
points where it would be necessary to lay in a provision of water;
without which information, we should have been exposed to great
danger in this last expedition.
We despatched couriers before us, to give notice to the grand prince
of our approach, and of our pacific intentions. On the ninth day he
came to meet us, at the head of a formidable army. It did not at first
appear very clear whether this demonstration of strength was to do
us honour or to intimidate us. The Drayhy began to repent of having
ventured so far from his allies. However, he showed no symptom of
fear, but placing the women and the baggage behind the troops, he
advanced with the choicest of his cavalry, accompanied by his friend
the Sheik Saker,—the same to whom in the preceding year he had
delegated the command of the desert of Bassora, and who had
negotiated all our alliances there during our stay in Syria.
The prince soon satisfied them respecting his intentions; for,
detaching himself from this numerous host, he advanced with a
small train of horsemen to the middle of the plain which separated
the two armies; the Drayhy did the same; and the two chiefs, on
meeting, alighted and embraced with every expression of cordiality.
If I had not so frequently described the hospitality of the desert, I
should have much to say on the reception we experienced from the
Emir Sahid, and the three days’ festivities with which he welcomed
us: but, to avoid repetitions, I shall pass over this scene, only
remarking, that the Bedouins of Persia, more pacific than those of
Arabia, entered readily into our views, and fully understood the
importance of the commercial intercourse we were desirous of
establishing with India. This was all that it was needful to explain to
them of the nature of our enterprise. The emir promised us the co-
operation of all the tribes of Persia under his dominion, and offered
his influence with those of India, who hold him in high consideration,
on account of the antiquity of his race, and of his personal reputation
for wisdom and generosity. He entered into a distinct treaty with us,
which was drawn up in the following terms:—
“In the name of the clement and merciful God, I, Sahid, son of Bader,
son of Abdallah, son of Barakat, son of Ali, son of Bokhrani, of
blessed memory: I hereby make a declaration of having given my
sacred word to the powerful Drayhy Ebn Chahllan, to Sheik Ibrahim,
and to Abdallah el Katib. I declare myself their faithful ally; I accept
all the conditions which are specified in the general treaty now in
their hands. I engage to assist and support them in all their projects,
and to keep their secrets inviolably. Their enemies shall be my
enemies; their friends, my friends. I invoke the great Ali, the first of
men, and the well-beloved of God, to bear witness to my word.
“Health.”
(Signed and sealed.)
We remained six days encamped with the tribe of Sahid, and had
thus an opportunity of observing the difference between the customs
of these Bedouins and those of our provinces. The Persians are
milder, more sober, and more patient; but less brave, less generous,
and less respectful to the women: they have more religious
prejudices, and follow the precepts of the sect of Ali. Besides the
lance, the gun, and the sabre, they use the battle-axe.
Prince Sahid sent to the Drayhy two beautiful Persian mares, led by
two negroes: the latter, in return, made him a present of a black
mare of great value, of the race of Nedgdie, named Houban Neggir,
and added some ornaments for his wives.
We were encamped not far from Menouna, the last town of Persia,
twenty leagues from the frontiers of India, on the banks of a river
which the Bedouins call El Gitan.
On the seventh day we took leave of Sahid, and recommenced our
march, in order to reach Syria again before the heats of summer set
in. We marched rapidly, and without precautions, till one day, while
we were passing through the province of Karman, our beasts were
carried off; and the next day we were ourselves attacked by a
powerful tribe, commanded by the Emir Redaini, an imperious man,
and jealous of his authority, who constitutes himself the guardian of
the caliphate of Persia. These Bedouins, very superior in number,
were as much our inferiors in courage and tactics: our troops were
vastly better commanded. Our position was, however, extremely
critical—we were lost if the enemy gained the smallest advantage;
for all the Bedouins of the Karman would at once have surrounded
us, and hemmed us in as with a net, from which there would have
been no possibility of escaping. The necessity, then, of inspiring
them with respect by a decisive victory, which should at once cure
them of any inclination to try their strength with us for the future, was