Stable and Variant Angina Pectoris
Classic angina pectoris, as described above, behaves in a predictable and reproducible manner: it is brought on by physical activity or emotional stress, which increases myocardial oxygen demands, and is relieved promptly by rest, which decreases oxygen requirements. This established pain pattern is called stable angina pectoris. It is associated with fixed narrowing of the coronary arteries, resulting from advanced atherosclerosis. Coronary arteriograms usually show at least 75% narrowing of one or more of the arteries; most often, two or three vessels are involved.
Angina pectoris may also result from coronary artery spasm. The arterial spasm reduces coronary blood flow sufficiently to produce ischemic artery disease. Coronary artery spasm may be manifested clinically in several ways, but its most typical form is described as variant angina, or Prinzmetal’s angina. The pain pattern of variant angina differs greatly from stable angina; indeed, it is almost the opposite in many of its characteristics. The main feature of variant angina is that the pain occurs with rest and not with activity. In fact, patients with variant angina do not develop chest pain or characteristic clectrocardio-: graphic signs of ischemia even during exercise testing. Also, the pain has an unusual cyclic pattern, often awakening the patient each night at about the same time. Furthermore, the electrocardiographic changes that accompany variant angina are entirely different than those associated with stable angina. The cause of coronary artery spasm is still unknown, but it is related somehow to abnormal contraction of the smooth muscles in the walls of arteries.
Although variant angina is very uncommon compared to stable angina, it has commanded increasing attention in recent years. Part of this interest can be attributed to a new class of drugs, called calcium antagonists or calcium blocking agents, that have proved very effective in inhibiting or releasing coronary spasm and relieving variant angina. Much more important is that these drugs also seem to benefit certain patients with fixed coronary artery obstruction. This implies that coronary spasm may contribute to the classic anginal syndrome even when the dominant cause of ischemia is advanced coronary atherosclerosis. However, the mechanism of action of these drugs in controlling stable angina is not known with certainty, but the very fact that calcium antagonists are effective for this purpose has caused a reevaluation of the causes and treatment of ischemic heart disease. Clinical research now in progress is likely to produce many new concepts about an old disease.
Intermediate Coronary Syndrome (Unstable Angina)
The term intermediate coronary syndrome has been used to characterize a clinical state that lies between stable angina pectoris and acute myocardial infarction. The syndrome has several different patterns, which accounts for the variety of names given to this condition in the past. Among the older (but still used) terms are: impending myocardial infarction, preinfarction angina, crescendo angina, accelerated angina, and acute coronary insufficiency. At present the preferred term is unstable angina, connoting that the common feature of the syndrome is its clinical instability.
Unstable angina may occur as the initial symptom of CHID or, more often, as a sudden worsening of stable angina. The chest pain, instead of lasting briefly as with stable angina, usually persists for 1020 minutes or longer. It develops with increasing frequency and is provoked by less effort, often occurring at rest. Nitroglycerin provides incomplete or no relief in most cases of unstable angina. Electrocardiographic signs of ischemic are common but without definite evidence of acute myocardial infarction.
The mechanism of unstable angina is not entirely clear but progressive narrowing of the coronary arteries probably plays a major role, especially in patients with stable angina previously. In any case, unstable angina is more serious than stable angina since frequently it is an immediate forerunner of acute myocardial infarction.
The diagnosis of unstable angina implies, theoretically, that despite prolonged ischemic adequate oxygenation was restored before actual myocardial destruction occurred. However from a clinical standpoint it is often difficult to rule out the possibility that small areas of the myocardium were in fact injured or destroyed during the ischemic episodes. For this reason and because of the changing and unpredictable course of the condition, patients with unstable angina are admitted to a coronary care unit, at least until the diagnosis of acute myocardial infarction has been excluded.
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