l-13 coronary artery disease

8/2/2019 L-13 Coronary Artery Disease

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CORONARY

ARTERYDISEASE


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epidemiology

Leading cause of death in industrialized

world

Same risk factors as for atherosclerosis

Men more at risk than women; risk gap narrowsfor post-menopausal

Over last two decades, 30% decline


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topography

Epicardial

not intra-

myocardialvessels

End

circulation(with potentialcollaterals that may

develop).


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The unstable plaque

Ulceration, rupture or fissuring

Hemorrhage into plaque


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Fixed stenosis: stable angina

> 75 % = 1/16 flow!R4

Variables: Myocardium:

Work

Hypertrophy

O2 supply: BP

Hemoglobin


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Fixed stenosis: subendocardial

myocardial infarction

High-grade stenosis

+

Low flow or anemia

- involves more than one CAterritory


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High-grade stenosis

+

Low flow or anemia



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High-grade stenosis

+

Low flow or anemia


- if all three vessels are involved,

circumferential


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PLAQUE DISRUPTION WITH

COMPLETE CORONARY

OCCLUSION:

TRANSMURAL MYOCARDIAL

INARCTION


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Plaque disruption with complete

coronary occlusion:

Transmural myocardial infarct

Smaller (50-75% stenotic) more fatty

plaques prone to fissure, ulcerate or rupture Plaque disruption: thrombosis

Role for plaque hemorrhage in some

Complete transmural ischemia results(eventually) unless collaterals.


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Classic transmural infarcts

LAD: Anteroseptal

apex


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Classic transmural infarcts

Right coronary: Postero-septal transmural MI

Variable right ventricular infarction


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PLAQUE DISRUPTION WITH

INCOMPLETE CORONARY

OCCLUSION:

UNSTABLE ANGINA,

SUBENDOCARDIAL INFARCT,

AND SUDDEN CARDIAC DEATH


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UNSTABLE ANGINA

Onset of chest pain at rest

No EKG or biochemical evidence of MI

Incomplete occlusion by thrombus and role

for vasoconstriction

Thrombus embolizes to cause micro-infarct

May crescendo

May announce MI in evolution


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UNSTABLE ANGINA






May crescendo



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UNSTABLE ANGINA






May crescendo



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UNSTABLE ANGINA






May crescendo



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UNSTABLE ANGINA






May crescendo



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UNSTABLE ANGINA






May crescendo



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SUDDEN CARDIAC DEATH

Patients autopsied may have disruptedplaque but usually no occluding thrombus

Patients who survive do not always developinfarcts

Micro-emboli occasionally found in smallvessels at autopsy

Local ischemia can give electricalinstability and arrhythmia


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The Pathology of Myocardial Infarction

Macroscopic Findings


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Microscopic findings


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Microscopic Findings


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Microscopic Findings


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Subendocardial vs. Transmural

Myocardial Infarction


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Subendocardial vs. Transmural

Myocardial Infarction Inner 1/3 or 1/2

Extend past territory

of one artery May be

circumferential

Related to incomplete

occlusion +/- low flow

Non-Q wave

Distribution of one

artery

Related to completeocclusion

Q-wave


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Infarcts and Reperfusion


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Ischemic Cardiomyopathy

Chronic ischemic heart disease with or

without previous MI

Diffuse patchy scarring and high-gradecoronary stenosis

Some hypertrophy possible

Subendocardial myocytolysis

Heart failure


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Complications of Myocardial Infarction

Heart failure and cardiogenic shock

> 40% loss of myocardium = shock

Arrhythmia and conduction abnormalities

Ventricular tachyarrhythmias and asystole

Ventricular rupture

Mural thrombus and embolism


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Complications of Myocardial Infarction

Heart failure and cardiogenic shock

> 40% loss of myocardium = shock

Arrhythmia and conduction abnormalities

Ventricular tachyarrhythmias and asystole

Ventricular rupture

Cardiac tamponade

Mural thrombus and embolism


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Coronary Artery Disease

l-13 coronary artery disease

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