Ischemic Heart Diseases - 37

Question 1

Ischemic heart disease

Answer 1

Ischemic heart disease is a constellation of disorders in
which myocardial ischemia is the common
pathophysiologic mechanism

Question 2

. These disorders are:

Answer 2

1. Angina pectoris,
2. Myocardial infarction,
3. Chronic ischemic heart disease, and
4. Sudden cardiac death.

Question 3

CAUSES OF ISCHEMIC HEART DISEASE:

Answer 3

1. Complicated atherosclerosis (most common cause),
2. Coronary artery spasm,
3. Coronary thrombosis,
4. Coronary embolism,
5. Coronary arteritis.

Question 4

MYOCARDIAL INFARCTION

Answer 4

Myocardial infarction is a discrete focus of ischemic necrosis (coagulation necrosis) in the heart that
occurs when myocardial ischemia is prolonged for more than 20 or 30 minutes.

Question 5

Gross morphology:

Answer 5

become visible after 4
hours as a discrete, dark, mottled area in the
myocardium.
- Over the next 3 days, the infarct
becomes more clearly defined with a pale
center.
- Over the next week, the infarct is sharply
outlined with a central pale yellowish center
(coagulation necrosis and neutrophilic infiltrate)
bordered by a hyperemic zone composed of
granulation tissue.
Over the course of months, the infarcted region
progresses to an organized gray-white scar

Question 6

Microscopic morphology:

Answer 6

~ one day Coagulative necrosis and early infiltration by neutrophils.
~ one week Disintegration of necrotic myofibrils and minimal blood vessel proliferation at
periphery of infarct.
~ one month Granulation tissue peak and minimal collagen fibers.
Later Increased collagen and decreased cellularity (scarring)

Question 7

he clinical diagnosis of transmural myocardial infarction:

Answer 7

biomarkers. Elevation of these
cardiac biomarkers (Treponin, Creatinin Kinase-MB and LDH) results from release of cytoplasmic
proteins into the bloodstream by necrotic myocytes

Question 8

Complications of myocardial infarction:

Answer 8

1. Ventricular arrhythmias,
2. Cardiac rupture and hemopericardium,
3. Rupture of papillary muscle or septal rupture,
4. Ventricular thrombosis,
5. Systemic or pulmonary embolization,
6. Ventricular aneurysm (weeks to months postinfarct).
7. Chronic ischemic heart disease (months to years postinfarct).

Question 9

ANGINA PECTORIS

Answer 9

Angina pectoris is a symptom complex characterized by recurrent attacks of crushing substernal chest
pain, which often radiates to the left arm and jaw. Three variants are recognized, but they have
overlapping features.

Question 10

Stable (Typical) Angina:

Answer 10

Stable (typical) angina is characterized by chest pain and shortness of breath precipitated by exertion
and relieved by rest or nitroglycerin. Pathologically stable angina usually corresponds to a fixed coronary
obstruction

Question 11

Unstable (Crescendo) Angina

Answer 11

Unstable (crescendo) angina is characterized by chest pain and shortness of breath that occur either at
rest, with progressively less exertion, or with increasing frequency. Pathologically, unstable angina is
associated with acute plaque change and often with microscopic foci of infarction secondary to
embolization of microthrombi. Unstable angina is associated with a significant risk of acute transmural
myocardial infarction.

Question 12

Prinzmetal’s (Variant) Angina

Answer 12

Prinzmetal’s (variant) angina is uncommon, with pain occurring at rest as a result of primary coronary
vasospasm (contraction of medial smooth muscle resulting in luminal narrowing). This syndrome
typically responds to calcium channel blockers, distinguishing it from other forms of angina.

Question 13

CHRONIC ISCHEMIC HEART DISEASE:

Answer 13

Chronic ischemic heart disease typically occurs in elderly patients with a previous history of myocardial
ischemia/infarction who have progressive congestive heart failure.
-subendocardial fibrosis
secondary to severe fixed coronary obstruction is almost always present, with focal discrete scars
corresponding to prior acute transmural infarcts.
There is usually moderate to marked left ventricular
hypertrophy and dilatation. Histologically, there is myocardial hypertrophy and interstitial fibrosis
resulting from loss of individual myofibers.