Angina pectoris (literally chest pain), wherein the ischemia causes pain but is insufficient to lead to death of myocardium; as we will discuss, angina may be stable (occurring reliably after certain levels of exertion), may be due to vessel spasm (variant angina or Prinzmetal angina), or may be unstable (occurring with progressively less exertion or even at rest).
Ischemic heart disease_Myocardial infarction_
Ischemic Heart Disease
DPT-student 3rd year
• Coronary Artery Disease (CAD).
IHD is also frequently called coronary
artery disease (CAD).
• The clinical manifestations of IHD are a direct consequence of
insufficient blood supply to the heart.
There are four basic clinical syndromes
Angina pectoris (literally chest pain), wherein the ischemia causes
pain but is insufficient to lead to death of myocardium;
II. Acute myocardial infarction (MI), wherein the severity or duration of
ischemia is enough to cause cardiac muscle death.
III. Chronic IHD refers to progressive cardiac decomposition (heart
failure) following MI.
IV. Sudden cardiac death (SCD), can result from a lethal arrhythmia
following myocardial ischemia.
• In most cases IHD occurs because of inadequate coronary perfusion
relative to myocardial demand. This may result from a combination
of pre-existing ("fixed") atherosclerotic occlusion of coronary arteries
and new superimposed thrombosis and/or vasospasm
• MI, popularly called heart attack, is necrosis of heart muscle
resulting from ischemia.
• The major underlying cause of IHD is atherosclerosis.
• The frequency of MIs rises progressively with increasing age and
presence of other risk factors such as
Myocardial Infarction Cont…
• Approximately 10% of MIs occur in people younger than 40 years,
and 45% occur in people younger than age 65. Blacks and whites
are equally affected.
• Men are at significantly greater risk than women, although the gap
progressively narrows with age.
• In general, women are remarkably protected against MI during their
reproductive years. Nevertheless, menopause-and presumably
declining estrogen production-is associated with exacerbation of
• Although any form of coronary artery occlusion can cause acute MI,
angiographic studies demonstrate that most MIs are caused by
acute coronary artery thrombosis.
• In most cases, disruption of an atherosclerotic plaque results in the
formation of thrombus. Vasospasm and/or platelet aggregation can
contribute but are infrequently the sole cause of an occlusion.
• Sometimes, particularly with infarcts limited to the innermost
(subendocardial) myocardium, thrombi may be absent. In these
cases, severe diffuse coronary atherosclerosis significantly limits
coronary vessel perfusion, and a prolonged period of increased
demand (e.g., due to tachycardia or hypertension) may be sufficient
to cause necrosis of myocytes most distal to the epicardial vessels.
Coronary Artery Occlusion
• In a typical MI, the following sequence of events transpires:
• There is a sudden disruption of an atheromatous plaque
-for example, intraplaque hemorrhage, erosion or ulceration, or
rupture or fissuring-exposing subendothelial collagen and necrotic
plaque contents.Platelets adhere, aggregate, become activated, and
release potent secondary aggregators including thromboxane A2,
• Vasospasm is stimulated by platelet aggregation and mediator
• Other mediators activate the extrinsic pathway of coagulation,
adding to the bulk of the thrombus.Within minutes the thrombus can
evolve to completely occlude the coronary lumen of the coronary
Myocardial Response to Ischemia
Coronary artery obstruction blocks the myocardial blood supply, leading to
profound functional, biochemical, and morphologic consequences. Within
seconds of vascular obstruction, cardiac myocyte aerobic glycolysis ceases,
leading to inadequate production of adenosinetriphosphate (ATP) and
accumulation of potentially noxious breakdown products (e.g., lactic acid).
The functional consequence is a striking loss of contractility, occurring
within a minute or so of the onset of ischemia.
Ultrastructural changes including myofibrillar relaxation, glycogen depletion,
and cell and mitochondrial swelling also become rapidly apparent. However,
these early changes are potentially reversible, and myocardial cell death is
Only severe ischemia lasting at least 20 to 40 minutes causes irreversible
injury and myocyte death.
The final location, size, and specific morphologic
features of an acute MI depend on:
rate of development of the coronary occlusion
Size of the vascular bed perfused by the obstructed vessels
Duration of the occlusion
Metabolic demands of the myocardium (affected, e.g., by blood
pressure and heart rate).
• Extent of collateral supply.
An MI is usually heralded by severe, crushing substernal chest pain or discomfort that
can radiate to the neck, jaw, epigastrium, or left arm.
In contrast to the pain of angina pectoris, the pain of an MI typically lasts from 20
minutes to several hours and is not significantly relieved by or rest. In a substantial
minority of patients (10% to 15%) MIs can be entirely asymptomatic. Such "silent"
infarcts are particularly common in patients with underlying diabetes mellitus (with
peripheral neuropathies) and in the elderly.
With MIs the pulse is generally rapid and weak, and patients can be diaphoretic and
nauseated particularly with posterior-wall MIs. Dyspnea is common and is caused by
impaired myocardial contractility and dysfunction of the mitral valve apparatus, with
resultant pulmonary congestion and edema.
Electrocardiographic abnormalities are important markers of MIs;
Laboratory evaluation of MI is based on measuring the blood levels of intracellular
macromolecules that leak out of injured myocardial cells through damaged cell
Consequences and Complications
• Unfortunately, half of the deaths associated with acute MI occur in
individuals who never reach the hospital; such patients generally die
within 1 hour of symptom onset-usually as a result of arrhythmias.
The variables associated with a poor prognosis include
and previous MI.
Figure 11-12 Complications of MI. A-C, Cardiac rupture. A, Anterior myocardial rupture in an acute infarct (arrow). B,
Rupture of the ventricular septum (arrow). C, Complete rupture of a necrotic papillary muscle. D, Fibrinous pericarditis,
showing a dark, roughened epicardial surface overlying an acute infarct. E, Early expansion of anteroapical infarct with
wall thinning (arrow) and mural thrombus. F, Large apical left ventricular aneurysm (arrow). (A-E, From Schoen FJ:
Interventional and Surgical Cardiovascular Pathology: Clinical Correlations and Basic Principles. Philadelphia, WB
Saunders, 1989. F, Courtesy of Dr. William D. Edwards, Mayo Clinic, Rochester, Minnesota.)
• The risk of developing complications and the prognosis after MI
iii. fractional thickness of the myocardial wall that is damaged.