Coronary artery diseases,

Acute coronary syndrome,

Acute myocardial infarction

Final part II Theory Lecture

20 12 2021
Coronary artery disease
Atherosclerosis
Coronary circulation
Clinical Manifestation CAD
Mx CAD

Acute coronary syndromes/Acute myocardial infarction

Clinical presentation
Diagnostic algorithm
Management
Complication
• Ralston, S. H., Penman, I. D., Strachan, M. W. J., & Hobson, R. (Eds.). (2018).
Davidson's principles and practice of medicine (23rd ed.).
Coronary artery disease (CAD)
CAD is the most common cause of angina and acute coronary syndrome and the
most common cause of death worldwide.

CAD is mainly caused by atherosclerosis of the coronary vessels.

Heart Disease and Stroke Statistics —2021 Update Circulation. 2021;143:e254 –e743
 Definition of Atherosclerosis

Atherosclerosis is the thickening of the arterial wall and a loss of elasticity due to
variable pathogenesis.

‘atheroma’ (focal plaques)

‘sclerosis’ (overgrowth of fibrous tissue)

The changes in atherosclerosis take place in the intima and media of blood vessel
walls and lead to a stiffening of the vessel walls and narrowing of the vascular lumen.
Etiology of Atherosclerosis

Chronic inflammation in the walls of blood vessels

Oxidation of LDL cholesterol

Lipids, calcium and other cellular debris - stored within the intima of large and medium-sized
arteries
Vessel wall thickening and plaque formation

Causes of atherosclerosis

Dyslipidemia
Hypercholesterolemia (abetalipoproteinemia, lipoprotein lipase and apolipoprotein C -II
deficiency, or familial dysbetalipoproteinemia)
Hypertriglyceridemia
Pathophysiology
Stages of endothelial
dysfunction in atherosclerosis

Atherosclerotic plaque with cholesterol

crystal gaps, foam cells and fibrosis
Vulnerable Vs Stable plaque

Vulnerable plaque

- particularly susceptible to vessel wall

disruption.
- characterized with having a thin
inflamed fibrous cap over a very large
lipid core.

The vulnera b l e plaque : Current concept s and f ut urepers p e ct iv e s on

coronar y morpho l o g y, composi t i on and wall st ress imaging Rev Port
Cardio l . 2014 ;33(2):1 01 - -- 11 0
The v ulnerable and unstable atheros cl e r oti c plaque
Ca r diov a s Pa tho Ja n-Feb 2010;19( 1): 6 -1 1 .
Coronar y Ather os cl e r oti c Vulnerable Plaque: Current Perspec tive s
Jour na l of the Americ a n Hea r t As s oc ia tion . 2017;6:e 0 0 5 54 3
Risk factors of atherosclerosis (Modifiable and non-modifiable)
Non-modifiable risk factors
male gender, age, and family history of premature cardiovascular disease

Modifiable risk factors

• Nicotine abuse: Smoking promotes the early development and rapid progression of
atherosclerosis.
• Arterial hypertension: Due to the high-pressure load, endothelium damage occurs more
rapidly.
• Diabetes mellitus: Increased blood glucose levels cause reactive glycosylation, which in itself
causes increased phagocytosis and endothelial damage.
• Hyperlipoproteinemia: Excessive LDL cholesterol increases the risk of atherosclerosis,
especially if HDL cholesterol levels are concomitantly low
Coronary
Circulation

Davidson's principles and practice of medicine (23rd ed.).

The Netter Collection of Medical Illustrations, 2nd Edition, Vol 8: Cardiovascular System
 Left main coronary artery (LMCA) which supplies blood to the
(2) Main coronary left ventricle and left atrium.
arteries The left main coronary divides into branches:
1. The left anterior descending LAD artery which travels in the
anterior interventricular groove, gives rise to diagonal
1)Left main LM – LAD branches as well as septal branches, supplies the anterior,
& LCX lateral and apical walls of the LV.
2. The left circumflex artery LCX, supplies blood to the lateral
and posterior and inferior walls of LV, branches obtuse
2)Right coronary marginals branches.
artery RCA Right coronary artery (RCA) that supplies blood to the RV, the
RA, and the SA and AV nodes.
• The right coronary artery divides into smaller branches,
including the right posterior descending artery and the acute
marginal artery, and posterolateral branch.
Coronary Angiogram
Coronary blood flow in • Coronary blood flow in LV - greatest in diastole (when the
systole and diastole ventricle is not contracting)
• Systolic myocardial contraction or rapid HR - block LV
endocardial blood flow by compressing flow in the vessels
• In thinner-walled RV, coronary perfusion continues in
systole ( due to the lower pressures in the right heart)
 • Coronary blood flow - correlated to cardiac workload or
Coronary blood flow myocardial O2 demand
regulation • Coronary blood vessels - sympathetic & parasympathetic
supply.

• Symp – (α-adrenoceptors - vasoconstriction and β2-

adrenoceptors – vasodilatation), predominant effect of
sympathetic stimulation in coronary arteries - Vasodilatation.
• Parasymp - Vasodilatation of normal coronary arteries

• Because of these homeostatic mechanisms, narrowing or stenosis

in a coronary artery does not limit flow, even during exercise, until
the cross-sectional area of the vessel is reduced by at least 70%.
Supply- demand
mistmatch
Clinical Manifestations

Stable angina, unstable

angina

ACS – STEMI,NSTEMI

Stable IHD/Chronic CAD

Ischemic cardiomyopathy

Arrhythmia

SCD
Clinical presentation of
CAD • Angina pectoris

Chest pain on exertion

Index of Suspicion That Chest “Pain” Is Ischemic in Origin on the Basis of Commonly Used
Descriptors

Nature
Onset &Duration
Location & Radiation
Severity
Precipitating factors
Relieving factors
Associated symptoms
Determinants of the clinical likelihood
of obstructive coronary artery disease

European Heart Journal, Volume 41, Issue 3, 14 January 2020, Pages 407–
477, https://doi.org/10.1093/eurheartj/ehz425
CCS Angina score
Physical examination • Frequently unremarkable
• Hemodynamic stability
• left ventricular dysfunction (cardiomegaly, gallop
rhythm)
• evidence of valve disease (particularly aortic)
• important risk factors (hypertension, diabetes
mellitus)
• other manifestations of arterial disease (carotid
bruits, peripheral arterial disease)
• unrelated conditions that may exacerbate angina
(anaemia, thyrotoxicosis)
A scheme for the investigation and
treatment of stable angina on
effort.
Detection and Diagnosis of Angina

History/Physical exam
ECG
Echo
CT angio / MR angio
Stress tests
Angiogram
(IVUS, OCT)
Nuclear perfusion

Experimental:
PET-plaque imaging
Difference between
Angina Myocardial infarct
Angina & AMI
Does not involve cell death Involves cell death

ECG abnormalities are reversible ECG abnormalities are not

reversible

Cardiac biomarkers not raised Cardiac biomarkers are raised

Less severe chest discomfort More severe and prolonged

chest discomfort
 The principles of management involve:
Management
• Assessment of the extent and severity of CAD
• identification and treatment of risk factors
• advice on smoking cessation
• drug treatment for symptom control (antianginal)
• identification of high-risk patients for
revascularization treatment
 Mx of CAD
CAD

Pharmacological Tx Revascularization

Antithrombotics Anti Risk factor PCI CABG

▪ Antilplatelet angina modified drugs (percutaneous (Coronary artery
▪ Anticoagulants coronary bypass grafting)
interventions)
(PPCI – primary
Thrombolytics
PCI)
Pharmacological Mx

1. Antithromotics
2.Anti-anginal drug
therapy

3.Risk factor control

Antithrombotic
treatments

▪ Antiplatelet drugs
1.Aspirin
2.P2Y12 receptor inhibitors
Clopidogrel, Prasugrel, Ticagrelor, Cangrelor

3.GP IIb/IIIa receptor inhibitors

Abciximab, Eptifibatide, Tirofiban

▪Anticoagulant drugs
UFH, Enoxaparin, Enoxaparin, Fondaparinux

▪ Oral anticoagulant drugs

Rivaroxaban
Anti-anginal drug Anti anginal drugs

therapy
• Nitrates
• Betablockers (cardio selective)
• Calcium channel antagonists ( Verapamil,
diltiazem)
• Potassium channel activators : Nicorandil
• If channel antagonist : Ivabradine
• Ranolazine
 Nonpharmacological Mx
(Revascularization)
PCI (percutaneous coronary interventions)
(PPCI – primary PCI)
CABG ( Coronary artery bypass grafting)

Complication of PCI
Acute (2-5%) – coronary occlusion, coronary dissection, coronary rupture
Distal embolization, Access site complication
Long-term - Restenosis, Recurrent angina

Complication of CABG
Operative mortality -1-5%
Neuro complication – periop stroke risk 1-5%, Cognitive impairment
Recurrence of angina – Post op/ late
Indications of PCI Vs CABG

PCI
single or double vessel disease

CABG
Left main disease
Triple vessel disease
Acute coronary syndrome
(ACS)

ACS is characterized by
sudden onset severe chest
pain due to partial or
complete occlusion of a
coronary artery resulting
from unstable ruptured
plaque in the setting of
advanced ischemic heart
disease.
Universal definition MI
Detection of a rise and/or fall of cardiac
biomarker values (preferably (cTn)), with at
least one value above the 99th centile upper
reference limit (URL) and with at least one of
the following:
1. Symptoms of ischaemia
2. New or presumed new significant ST
segment–T wave (ST–T) changes or new
left bundle branch block (LBBB)
3. Development of pathological Q waves in
the ECG
4. Imaging evidence of new loss of viable
myocardium or new regional wall motion
abnormality
5. Identification of an intracoronary
thrombus by angiography or postmortem

Yader Sandoval. Circulation. The Universal Definition of Myocardial

Infarction, Volume: 141, Issue: 18, Pages: 1434-1436, DOI:
(10.1161/CIRCULATIONAHA.120.045708)
Clinical presentation and
classification of ACS

3 clinical entities:

1. ST-segment elevation
myocardial infarction (STEMI)
2. Non-ST-segment elevation
myocardial infarction
(NSTEMI)
3. Unstable angina pectoris
Clinical features of
ACS
Diagnostic algorithm for ACS
Signs & symptoms suggestive of ACS

ECG

1 ≥1 mm ST elevation in at least 2 1.ST changes that vary with onset

adjacent limb leads, e.g. II and III; I and offset of pain (‘dynamic’
and aVL OR changes)
2. ≥2 mm ST elevation in at least 2 2. ≥1 mm horizontal ST depression
adjacent praecordial leads, e.g. V2 in ≥2 adjacent leads
and V3; V5 and V6 OR 3. Deep symmetrical T wave
3. Left bundle branch block of new inversion
onset

STEMI Ask for cTn

If positive , NSTEMI If negative, Unstable angina

Macleod's Clinical Diagnosis 2nd Ed

Cardiac enzymes
Troponin T/I
CK MB
LDH
AST
Copeptin
 Schematic of myocytes and the
myocardial contraction process
Troponin – structural protein
(cardiomyocyte necrosis)

Cardiac troponin cTn (Troponin T,

Troponin I)

- proven to be associated with adverse

cardiovascular outcomes, including death
-rises 4 to 6 hours, and 12 hours for peak
level

high sensitivity Troponin (hscTn)

- hscTn assays - detect much lower

concentrations of the troponin protein
- higher sensitivity and higher Negative
predictive value NPV
 Rule-in/Rule-out of AMI with cTn

Recommended to use - hs-cTn

assays
0 h/1 h algorithm (best option,
blood draw at 0 h and 1 h) or the
0 h/2 h algorithm (second-best
option, blood draw at 0 h and 2
h).

Eur Heart J, Volume 33, Issue 5, March 2012, Pages 579–586, https://doi.org/10.1093/eurheartj/ehr492
The content of this slide may be subject to copyright: please see the slide notes for details.
Management

Oxygen
Nitroglycerines
Morphine

Antiplatelet

Anticoagulants
Thrombolytics

Beta blockers

Primary PCI/ Elective PCI

Emergency CABG/ Elective CABG
 Time is muscle

Mortality reduction as a benefit of

reperfusion therapy is greatest in the first
2 to 3 hours after the onset of
symptoms of AMI, due to a consequence
of myocardial salvage.

JAMA. 2005;293(8):979-986. doi:10.1001/jama.293.8.979

 PPCI

Treatment of choice in acute STEMI within

12 hours of symptom onset

➢ 90% reperfusion
➢ Mortality benefits -> 95% 1-year
survival rates
Benefits of PPCI – very time dependent

Risk -
<5% Reocclusion
<1% Stroke
Thrombolytics
( Fibrinolytics)
1.Tissue plasminogen activator (IV bolus)
▪ Tenecteplase (TNK) and reteplase (rPA)
In absence of contraindication and If PPCI cannot be
performed within 120 minutes from first medical
contact, thrombolysis is indicated in STEMI within
12 hours of symptom onset.

2. Streptokinase - polypeptide derived from

beta-hemolytic streptococci of Lancefield
group C bacteria (bind with plasminogen)

Greatest benefit in first hour

Minimal additional benefit after 3 hours

Risk – bleeding
1-2% Hemorrhagic stroke
10-20% Reinfarct after achieving reperfusion

Rescue PCI/Facilitated PCI

 Maximum target times
according to reperfusion
strategy selection

European Heart Journal, Volume 39, Issue 2, 07 January 2018, Pages 119–
177, https://doi.org/10.1093/eurheartj/ehx393
NSTEMI Mx

Risk stratification

Medical treatment Vs invasive

angioplasty

Timing of angioplasty

Antithrombotic treatment
Antiplatelet
Anticoagulants
 Risk stratification

TIMI Score

GRACE Score

109 140

JAMA. 2000;284(7):835-842. doi:10.1001/jama.284.7.835

BMJ 2006; 333 doi: https://doi.org/10.1136/bmj.38985.646481.55
Mx
TIMI score < 2
No ST segment deviation & negative biomarkers
Pt preference
Medical treatment
Recurrent chest pain
Invasive Angioplasty Heart failure symptoms EF < 40%
Stress test abnormal
Severe arrhythmia
Worsening MR

Invasive

All other patients - invasive

Timing of angioplasty
Summary of treatment for
acute coronary syndrome
(ACS).
Complications of AMI

• Arrhythmias
• Recurrent angina
• Acute heart failure
• Pericarditis
• Dressler’s syndrome
• Papillary muscle rupture
• Ventricular septum rupture
• Ventricular rupture
• Embolism
• Ventricular remodeling & ischemic
cardiomyopathy
Mx ACS
ACEI
Mineralocorticoid receptor antagonists
SGLT2inhibitors

Lipid-lowering therapy

Control of hypertension, Diabetes

Smoking cessation
Diet and exercise
Rehabilitation

ICD
Primary prevention
Post AMI 6 weeks, if the LVEF < 30%
Mild to moderate symptomatic heart failure on optimal
drug therapy, with LVEF < 35%
Secondary prevention
VT with hemodynamic compromise or significant LV
impairment (LVEF< 35%)
Prognosis • Number of diseased vessels
• Degree of left ventricular dysfunction

• Symptoms are a poor guide to prognosis, since

spontaneous improvement in angina due to the
development of collateral vessels is common
 Shared Decision-Making
Algorithm

J Am Coll Cardiol. Dec 09, 2021. Epublished DOI: 10.1016/j.jacc.2021.09.005

 THANK
YOU

J Am Coll Cardiol. 2021 Nov, 78 (22) e187–e285

Quick assessment
CAD ACS AMI

Final part II
20 12 2021

Quick assessment 20/12/2021 57