Pathophysiology of Cardiac Pain

Abstract

Almost invariably angina pectoris occurs in the presence of obstructive coronary artery disease or of myocardial hypertrophy. Ischemia can be precipitated by any set of circumstances which disturbs the balance between O2 supply and O2 demand. Oxygen demand can be chronically augmented by any disease process chronically increasing cardiac activity. This demand can be acutely increased by any stress which acutely increased cardiac pressure, contraction or rate. Emotion, through autonomic stimuli to the heart can even be more detrimental than effort in provoking ischemia. Conversely, the reserve mechanism of O2 supply can be chronically compromised by disease processes chronically affecting O2 transport (anemia). Oxygen supply can be acutely compromised by reduction in perfusion pressure or time and, more important, by acute coronary vasoconstriction (or coronary spasm if it occurs clinically). Acting as a resistance in series with arterial obstruction, constriction can readily induce ischemia in the diseased heart. Thus, the potential exists for ischemia to occur with varying degrees of morphologic coronary disease, depending solely on what other influences play upon the heart. For example, severe coronary disease may be decompensated by even a mild anemia or mild physical effort By contrast, a single moderate coronary stenosis can be made highly significant by the simultaneous effect of increased cardiac effort and coronary vasoconstriction. Special emphasis must be given to reflexes from the central nervous system in changing cardiac activity. The response to an emotional stress or to external stimuli, such as environmental cold, may involve acute hypertension, tachycardia and augmented vigor of contraction. Such stimulation may be poorly tolerated in the damaged and potentially ischemia heart. In addition, active coronary vasoconstriction, an "inappropriate" sympathetic nervous system response, may be a major factor in many attacks of angina. Vasoconstriction further compromises coronary supply in areas distal to arterial obstruction or narrowing, particularly under circumstances demanding augmented cardiac performance. The interplay of all these factors may well explain some hitherto confusing aspects of clinical angina. The occurrence of ischemia is not necessarily a good yardstick for the significance of morphologic coronary disease. Not only is there the anatomic variable of collateral flow, but there is the functional variable of load on the heart and antagonistic reflexes to modify the ischemic resultant of any given degree of coronary disease.