Disruption Plaque-Associated Thrombus

Stable angina >75% No No

Unstable angina Variable Frequent Nonocclusive, often with thromboemboli

Transmural myocardial infarction Variable Frequent Occlusive

Subendocardial myocardial infarction Variable Variable Widely variable, may be absent, partial/complete, or lysed

Sudden death Usually severe Frequent Often small platelet aggregates or thrombi and/or thromboemboli

ANGINA PECTORIS

Angina pectoris is a symptom complex of IHD characterized by paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort (variously described as constricting,

squeezing, choking, or knifelike) caused by transient (15 seconds to 15 minutes) myocardial ischemia that falls short of inducing the cellular necrosis that defines infarction. There are

three overlapping patterns of angina pectoris: (1) stable or typical angina, (2) Prinzmetal or variant angina, and (3) unstable or crescendo angina. They are caused by varying combinations

of increased myocardial demand and decreased myocardial perfusion, owing to fixed stenosing plaques, disrupted plaques, vasospasm, thrombosis, platelet aggregation, and embolization.

Moreover, it is being increasingly recognized that not all ischemic events are perceived by patients, even though such events may have adverse prognostic implications (silent ischemia).

Stable angina, the most common form and therefore called typical angina pectoris, appears to be caused by the 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. Typical angina pectoris is usually relieved by rest (thereby decreasing demand) or nitroglycerin, a strong vasodilator. Although the coronary

arteries are usually maximally dilated by intrinsic regulatory influences, nitroglycerin also decreases cardiac work by dilating the peripheral vasculature. In particular instances, local

vasospasm may contribute to the imbalance between supply and demand.

Prinzmetal variant angina is an uncommon pattern of episodic angina that occurs at rest and is due to coronary artery spasm. Usually there is an elevated ST segment on the

electrocardiogram (ECG), indicative of transmural ischemia. Although individuals with this form of angina may well have significant coronary atherosclerosis, the anginal attacks are

unrelated to physical activity, heart rate, or blood pressure. Prinzmetal angina generally responds promptly to vasodilators, such as nitroglycerin and calcium channel blockers.

Unstable or crescendo 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 more prolonged duration. As discussed above, in most patients, unstable angina is induced by disruption of an atherosclerotic plaque with superimposed partial (mural) thrombosis

and possibly embolization or vasospasm (or both). Although the ischemia that occurs in unstable angina falls precariously close to inducing clinically detectable infarction, unstable angina

is often the prodrome of subsequent acute MI. Thus this syndrome is sometimes referred to as preinfarction angina, and in the spectrum of IHD, unstable angina lies intermediate between

stable angina on the one hand and MI on the other.

MYOCARDIAL INFARCTION (MI)

MI, also known as "heart attack," is the death of cardiac muscle resulting from ischemia. It is by far the most important form of IHD and alone is the leading cause of death in the United

States and industrialized nations. About 1.5 million individuals in the United States suffer an acute MI annually and approximately one third of them die. At least 250,000 people a year die

of a heart attack before they reach the hospital.

Date: 2016-04-22; view: 844