Acute Ischemic Heart Disease (AIHD)

Acute Ischemic Heart Disease (AIHD)

Angina pectoris

It is a symptom complex of IHD characterized by paroxysmal attacks of substernal or pericordial chest discomfort (variously described as constricting, squeezing, choking, or knife-like) caused by transient (15 sec. to 15 min.) myocardial ischemia that falls short of inducing the cellular necrosis that defines infarction.

There are three somewhat distinctive patterns of angina pectoris, differentiated on the basis of the provocation and severity of the pain:

1. Stable (typical) angina pectoris appears to be reduction of coronary perfusion to a critical level by chronic stenosing coronary atherosclerosis; this renders the heart vulnerable to further ischemia whenever there is increased demand, such as that produced by physical activity, emotional excitement, or any other cause of increased cardiac workload.
2. Prinzmetal’s variant refers to a pattern of episodic angina that occurs at rest and has been documented to be due to coronary artery spasm.
3. Unstable angina refers to a pattern of pain that occurs with progressively increasing frequency, is precipitated with progressively less effort, often occurs at rest, and tends to be of prolonged duration. This syndrome is sometimes referred to as preinfarction or acute coronary insufficiency. Unstable angina is induced by fissuri

Acute myocardial infarction (MI)

Acute myocardial infarction also known as “heart attack”, is overwhelmingly the most important form of IHD in industrial nations.

Pathogenesis. At least 90% of transmural acute MI are caused by an occlusive intracoronary thrombus overlying an ulcerated or fissured stenotic plaque. Occlusion of a major coronary artery results in ischemia throughout the anatomic region supplied by that artery, most pronounced in the subendocardium. The function becomes strikingly abnormal within 1 min after ischemia, but myocardial coagulation necrosis occurs only after 20 to 40 min of severe ischemia.

Classification of Myocardial infarction

I. According to localization: left ventricle, right ventricle, and right atrium, left atrium.

Infarctions are most frequently located in the left ventricle. Besides it may be located in other parts of heart, but this is observed rarely. The region of infarction depends upon the area of obstructed blood supply by one or more of the three coronary arterial trunks:

1) Stenosis of the left anterior descending coronary artery is the most common (40-50%) - the infarctions of the anterior wall of left ventricle near apex or anterior two-thirds of interventricle septum.

2) Stenosis of the right coronary artery is the next most frequent (30-40%) - interior/posterior wall of left ventricle; posterior one-third of interventricular septum, posterior right ventricular free wall in some cases.

3) Stenosis of the left circumflex coronary artery is seen least frequently (15-20%) - lateral wall of left ventricle.

II. According to the anatomic region of the left ventricle: anterior, posterior, lateral, septal and circumferential.

III. According to the degree of thickness of the ventricular wall:

1. Full-thickness or transmural, in which the ischemic necrosis involves the full or nearly full thickness of the ventrical wall in the distribution of a single coronary artery. As a result the rupture of cardiac wall, endocarditis with thrombus and fibrinous pericarditis can develop.
2. Subendocardial or lamina constitutes an area of ischemic necrosis limited to the inner one-third or at most one-half of the ventricular walls, often extending laterally beyond the perfusion territory of a single coronary artery.
3. Subepicardial is rare infarction. In region of it fibrinous inflammation of pericardium develops. It is called reactive pericarditis.

IV. According to the duration of infarctions:

1. Acute myocardial infarction develops in the first time (during 8 weeks from beginning of ischemic necrosis).

2.       Repeated myocardial infarction develops after 8 weeks of acute infarction.

3.       Recurring (recidivic) myocardial infarction develops during 8 weeks of acute infarction.

Morphology

·        The macroscopic and microscopic changes in the myocardial infarction correspond to the age of the infarct.

·        In 6-12 hours the lesion may have a slight pallor but may be inapparent; however, changes in as early as 3 to 6 hours may be accentuated by use histochemical techniques.

·        By 18-24 hours infracted tissue is pale to cyanotic.

·        During first week the lesion becomes progressively more sharply defined, the color of infarction is charged from cyanotic red to bright yellow or yellow-green. The consistency of infarct in this period is soft.

·        A circumferential rim of hyperemic granulation tissue that progressively expends may be seen by 7 to10 days.

·        Fibrous scar is well established by 6 weeks. It is thin, gray-white, hard, shrunken fibrous scar.

Microscopically, within one hour of ischemic injury, there is intercellular edema, and myocytes become wavy and buckled. This is attributable to stretching of noncontractile dead fibers by adjacent viable contracting myocytes. In addition, border-zone viable cells show fine lipid droplets and large cytoplasmic vacuoles called vacuolar degeneration or myocytolysis. At this stage, typical coagulative necrosis is not yet evident.

·        In 12 to 72 hours a neutrophilic infiltrate into necrotic tissue with progressive evolution of characteristic eosinophilic coagulative necrosis can occurs.

·        Between 3 and 7 days dead myocytes begin to disintegrate and are resorbed by macrophages and enzyme proteolysis.

·        At 7 to 10 days granulation tissue appears and progressively replaces necrotic tissue, ultimately generating a dens fibrous scar.

·        In fourth to sixth week increased fibrous tissue, decreased blood supply, fewer pigmented macrophages, lymphocytes and plasma cells are seen.

Complications of infarction

Complications of infarction depend on the size and location of the necrosis, as well as the reserve of functional myocardium.

1. Arrhythmias are the most common form of complication in acute myocardial infarction (75 to 95%).
2. Left ventricular congestive failure and mild-to-severe pulmonary edema (60%).
3. Cardiogenic shock (10%).
4. During the first weak the heart rupture may develop, which is often fatal. Rupture of the free wall causes pericardial hemorrhage and tamponade. Rupture of the septum produces a left-to right shunt with right heart volume overload.
5. Fibrinous pericarditis appears on the second day of myocardial infarction.
6. About 3 - 4% of patients who suffered from acute myocardial infarction develop post-myocardial infarction syndrome, which is characterized by pneumonitis.
7. Mural thrombosis and thromboembolism from intracardiac thrombi and thrombosis in the leg veins is observed in 15-45% cases of acute myocardial infarction.
8. Cardiac aneurysm often occurs in the left ventricle, it impairs the function of the heart and is the site for mural thrombi.
9. Dressler’s syndrome. It is immunocomplexis reaction to decomposition’s products of the necrotic tissue with formation pericarditis and right-side pleurisy.

The main causes of death in this case are complications

1. Cardiogenic shock.
2. Tamponade of heart.
3. Thromboembolism.
4. Acute cardiac insufficiency.