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Full download Cardiology Secrets, 6th Edition Glenn N. Levine file pdf all chapter on 2024
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N. Levine
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CARDIOLOGY
SECRETS
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Practitioners and researchers must always rely on their own experience and knowledge in evaluating
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Printed in India
“You think dogs will not be in heaven? I tell you, they will be there long before any of us”.
–Robert Louis Stevenson
CONTRIBUTORS
vi
CONTRIBUTORS vii
This is now the sixth edition of Cardiology Secrets and the fourth edition I have edited. Among the 16 books I have
authored or edited, this series of books is the most satisfying and rewarding; from the feedback that we receive, it is
clear that we, to at least some extent, achieve our objectives of trying to educate readers and disseminate knowledge
on the optimal evaluation and management of patients of cardiovascular disease, and do so in a concise, digestible,
and entertaining manner. As always, we have updated all chapters to bring readers the most up-to-date information
and recommendations to the extent that a format such as this allows.
I am again deeply indebted to the hundreds of national and international experts and thought leaders in cardio-
vascular disease who over the years have taken time from their many academic and clinical responsibilities, as well
as family time, to contribute to the Cardiology Secrets series of books. I am similarly appreciative to the many persons
at Elsevier who I have worked with to bring this book in both hardcopy and electronic format to fruition.
It is my hope that you find this edition of the book both educational and enjoyable and that it in some small
way serves to improve the care of the patients that entrust their health and wellbeing to us. As always, I welcome
comments and suggestions from readers; my email is glevine@bcm.tmc.edu.
Glenn N. Levine, MD, FACC, FAHA
xii
CONTENTS
CHAPTER 3 ELECTROCARDIOGRAPHY 19
Gilad Birnbaum, Glenn N. Levine, Yochai Birnbaum
CHAPTER 7 ECHOCARDIOGRAPHY 49
Xiaoming Jia, Arunima Misra
xiii
xiv contents
V Arrhythmias
CHAPTER 35 ATRIAL FIBRILLATION 307
Michael E. Field
INDEX 604
TOP 100 SECRETS
1. The four conditions identified as having the highest risk of adverse outcome from endocarditis for which
prophylaxis with dental procedures is still recommended by the American Heart Association are prosthetic cardiac
valve, previous infective endocarditis, certain cases of congenital heart disease, and cardiac transplantation
recipients who develop cardiac valvulopathy.
2. Causes of ST-segment elevation include acute myocardial infarction (MI) as a result of thrombotic occlusion of a
coronary artery, Prinzmetal’s angina, cocaine-induced myocardial infarction, pericarditis, left ventricular aneurysm,
left bundle branch block (LBBB), left ventricular hypertrophy with repolarization abnormalities, J point elevation,
and severe hyperkalemia.
3. During pregnancy, maternal heart rate (HR) increases throughout the 40 weeks, mediated partially by increased
sympathetic tone and heat production. Hormonal changes cause an increase in both plasma volume (from water
and sodium retention) and red blood cell volume (from erythrocytosis) during a normal pregnancy. Stroke volume
subsequently continues to increase until the third trimester, when inferior vena cava (IVC) return may be
compromised by the gravid uterus. Maternal cardiac output (CO) increases by 30% to 50% during a normal
pregnancy. Systolic blood pressure drops during the first half of pregnancy and returns to normal levels by
delivery.
4. The major risk factors for coronary artery disease (CAD) are family history of premature coronary artery disease
(father, mother, brother, or sister who first developed clinical CAD at age younger than 45–55 for males and at age
younger than 55–60 for females), hypercholesterolemia, hypertension, cigarette smoking, and diabetes mellitus.
5. Coronary flow reserve (the increase in coronary blood flow in response to agents that lead to microvascular
dilation) begins to decrease when a coronary artery stenosis is 50% or more luminal diameter. However, basal
coronary flow does not begin to decrease until the lesion is 80% to 90% luminal diameter.
6. Important causes of chest pain not related to atherosclerotic coronary artery disease include aortic dissection,
pneumothorax, pulmonary embolism, pneumonia, hypertensive crisis, Prinzmetal’s angina, cardiac syndrome X,
anomalous origin of the coronary artery, pericarditis, esophageal spasm or esophageal rupture (Boerhaave’s
syndrome), and shingles.
7. Sinus node dysfunction, commonly referred to as sick sinus syndrome, refers to a broad array of abnormalities of
the sinus node ranging from atrial impulse formation through propagation of the depolarization impulse. Sick
sinus syndrome can manifest as sinus bradycardia, paroxysmal sinus arrest, sinus node exit block or chronotropic
insufficiency. Tachycardia-bradycardia (“tachy-brady”) syndrome is a common appearance of sick sinus syndrome
in patients with an atrial fibrillation or atrial flutter.
8. Other causes of elevated cardiac troponin besides acute coronary syndrome and myocardial infarction that should
be considered in patients with chest pains include pulmonary embolism, aortic dissection, myopericarditis, severe
aortic stenosis, and severe chronic kidney disease.
9. Causes of pericarditis include infectious (viral, bacterial, fungal, mycobacterial, human immunodeficiency virus
[HIV] associated), neoplastic (usually metastatic from lung or breast; melanoma, lymphoma, or acute leukemia),
myocardial infarction, injury (postpericardiotomy, traumatic), radiation, metabolic (myxedema, uremia), and
connective tissue disease. In the developed world, the most common cause remains viral etiologies, whereas
tuberculosis is the most frequent cause in developing countries.
10. Prinzmetal’s angina, also called variant angina, is an unusual cause of angina caused by coronary vasospasm.
Patients with Prinzmetal’s angina are typically younger and often female. Treatment is based primarily on the use
of calcium channel blockers and nitrates.
11. Microvascular angina appears to play a major role in the underlying mechanisms of ischemia with nonobstructive
coronary arteries (INOCA) and is defined as the occurrence of chest pain based on abnormal coronary flow
reserve due to coronary microvascular dysfunction in the absence of obstructive coronary artery disease. This
condition was prior referred to as “syndrome X.” Microvascular angina is more common in women and likely
underdiagnosed. Abnormal coronary flow reserve is diagnosed as a coronary flow reserve of less than 2.5, which
requires measurement using invasive (flow wire) or noninvasive (positron emission tomography, echo Doppler, or
cardiac magnetic resonance imaging) techniques. Standardized criteria for diagnosis of microvascular angina
have been proposed. However, many uncertainties about the underlying pathophysiological mechanisms of
microvascular angina persist, and further studies are needed to develop the evidence base for diagnosis and
especially for the treatment of this condition. For now, potential therapies include beta-blockers, short-acting
nitrates, calcium antagonists, and angiotensin-converting enzyme inhibitors for symptom relief.
12. The three main types of ASDs are secundum (80%), primum (15%), and sinus venosus (5%). The secundum ASD
is a defect involving the floor of the fossa ovalis of the atrial septum. It usually presents as an isolated anomaly.
xvii
xviii TOP 100 SECRETS
The primum ASD is a defect at the base of the atrial septum adjacent to the atrioventricular valves. It is invariably
part of an atrioventricular septal defect (endocardial cushion defect), and a cleft mitral valve is almost always
present. The sinus venosus ASD is a defect of the posterior part of the septum, usually located in the superior
part. In the majority of cases, a sinus venosus ASD is associated with anomalous connections or drainage of the
right-sided pulmonary veins
13. Numerous cardiovascular medications are associated with drug-induced lupus erythematosus. Those with a
definitive causative relationship include procainamide, hydralazine, diltiazem, quinidine, and methyldopa. Those
with a probable causative relationship include beta-blockers, captopril, hydrochlorothiazide, amiodarone, and
ticlopidine.
14. Subarachnoid hemorrhage due to aneurysm rupture classically presents with the worst headache of one’s life;
loss of consciousness, nausea/vomiting, nuchal rigidity, and focal neurologic signs are also common. Although
large amounts of subarachnoid blood are readily apparent on CT, even small amounts of subarachnoid blood can
provoke symptoms. Detection of these small “sentinel bleeds” is vital, as they herald aneurysm rupture.
15. Findings that suggest a heart murmur is pathologic and requires further evaluation include the presence of
symptoms, extra heart sounds, thrills, abnormal ECG or chest radiography, diminished or absent S2, holosystolic
(or late systolic) murmur, any diastolic murmur, and all continuous murmurs.
16. In the early- and pre-ART eras (early 2000s and prior), common CVD manifestations of HIV/AIDS included
pericardial effusion/tamponade, dilated cardiomyopathy and severe systolic dysfunction, myocarditis, marantic
(thrombotic) or infectious endocarditis, cardiac tumors (Kaposi’s sarcoma, lymphoma), pulmonary arterial
hypertension, and sudden cardiac death. These complications may still occur in the present era, especially in the
setting of poor HIV control, although now common CVD complications tend to be more subacute and chronic,
including coronary artery disease and MI, heart failure with preserved and reduced ejection fraction, and sudden
cardiac death
17. The major categories of ischemic stroke are large vessel atherosclerosis (including embolization from carotid to
cerebral arteries), small vessel vasculopathy or lacunar type, and cardioembolic. Hemorrhagic strokes are
classified by their location: subcortical (associated with uncontrolled hypertension in 60% of cases) versus cortical
(more concerning for underlying mass, arteriovenous malformation, or amyloidosis).
18. Acute MI remains the leading cause of cardiogenic shock in the United States. In fact, despite the decline in its
incidence with progressive use of timely primary PCI, cardiogenic shock still occurs in 5% to 8% of hospitalized
patients with ST-segment elevation myocardial infarction (STEMI). Unlike what is commonly believed, cardiogenic
shock may also occur in up to 2% to 3% of patients with non–ST-segment-elevation myocardial infarction
(NSTEMI). Overall, 40,000 to 50,000 cases of cardiogenic shock occur annually in the United States. Chronic
congestive heart failure may decompensate into cardiogenic shock and is the second most common etiology for
cardiogenic shock after acute MI. Ventricular septal rupture and papillary muscle rupture, both usually occurring
within days of a transmural MI, are less common causes.
19. Cardiomyopathy in COVID-19 may occur as a result of direct viral damage, myocarditis, microvasculature
dysfunction secondary to endothelial cell damage or systemic inflammatory response syndrome in response to
SARS-CoV-2 infection. Other potential etiologies include thrombotic myocardial infarction or severe myocardial
ischemia in patients with preexisting coronary artery disease, stress-mediated myocardial dysfunction,
tachycardia-induced cardiomyopathy, and myocardial stunning after resuscitation or prolonged hypotension. The
mainstay of management of COVID-19–related cardiomyopathy is supportive care.
20. Findings that should raise the suspicion for endocarditis include bacteremia/sepsis of unknown cause, fever,
constitutional symptoms, hematuria/glomerulonephritis/suspected renal infarction, embolic event of unknown
origin, new heart murmurs, unexplained new atrioventricular (AV) nodal conduction abnormality, multifocal or rapid
changing pulmonic infiltrates, peripheral abscesses, certain cutaneous lesions (Osler’s nodes, Janeway’s lesions),
and specific ophthalmic manifestations (Roth’s spots).
21. Common radiographic signs of congestive heart failure include enlarged cardiac silhouette, left atrial enlargement,
hilar fullness, vascular redistribution, linear interstitial opacities (Kerley’s lines), bilateral alveolar infiltrates, and
pleural effusions (right . left).
22. Classic ECG criteria for the diagnosis of ST-segment elevation myocardial infarction (STEMI), warranting
thrombolytic therapy, are ST-segment elevation greater than 0.1 mV in at least two contiguous leads (e.g., leads III
and aVF or leads V2 and V3) or new or presumably new left bundle branch block (LBBB).
23. Perioperative cardiac morbidity occurs most commonly during the first 3 postoperative days and includes
perioperative myocardial infarction (PMI), unstable angina, congestive heart failure, cardiac death, and nonfatal
cardiac arrests. Studies suggest a peak incidence of PMI within the first 48 hours or earlier. Among patients with
known ischemic heart disease, incidence of PMI is approximately 5%, with incidence decreasing to 2% to 4%
among patients with risk factors but no history of ischemic heart disease and decreasing still among patients with
no risk factors. Additionally, mortality from PMI has decreased from previous rates of 30% to 50% to
approximately 12%. A more recently described but separate syndrome from PMI is myocardial injury after
noncardiac surgery (MINS). MINS is defined by elevated troponin in the perioperative period due to cardiac
ischemia that does not meet criteria for MI set by the Fourth Universal Definition of Myocardial Infarction. While
seemingly more benign, MINS is independently associated with risk of death and cardiovascular complications in
the year following surgery.
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