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The likelihood that acute myocardial infarction is triggered by a specific event has been a subject of debate since the earliest description of this disorder, which incorporated the belief that specific physical or mental events precipitated the attack (1). Controversy concerning the events precipitating acute myocardial infarction continued for decades (2,3), until 1960 when Master published a retrospective study of over 2600 patients with acute myocardial infarction (4). This study was the largest to that date addressing the triggering of myocardial infarction. While no formal statistical analysis was applied, it was concluded from the data that the onset of myocardial infarction was unrelated to physical effort, to time of day, to day of the week, or to the occupation of the patient. In the last 15 yr, as knowledge of the pathological processes underlying acute coronary syndromes has advanced, the possibility of the existence of specific triggers of the onset of acute myocardial infarction and related syndromes has been reconsidered.

The current concept holds that acute coronary syndromes result from a breach in the surface of an atherosclerotic plaque, either by frank rupture of the fibrous cap overlying the plaque or, less commonly, by endothelial denudation of the cap (5-12). This event exposes collagen, tissue factor, and the lipid material underlying the luminal surface of the plaque to blood. The interaction between the inner constituents of the plaque and its cap and blood where platelets and clotting factor proteins are available for activation, initiates

From: Contemporary Cardiology: Management of Acute Coronary Syndromes, Second Edition Edited by: C. P. Cannon © Humana Press Inc., Totowa, NJ

the formation of intracoronary thrombus. The competition between thrombosis and intrinsic fibrinolytic processes determines the natural history of the plaque rupture. One possible outcome is a voluminous thrombus little diminished by fibrinolysis, causing total coronary occlusion, extensive myocardial ischemia with electrocardiographic ST segment elevation, and myocardial infarction. A different clinical syndrome might be expected to result from a smaller thrombus mass that is spontaneously lysed—transient symptoms, with or without ischemic electrocardiographic changes, and without myocar-dial infarction. Another acute presentation of coronary artery disease is sudden cardiac death. There is evidence that acute changes in plaque morphology can be found in a majority of such cases (13), and mechanisms, including ischemia and reperfusion, hemodynamic factors, metabolic alterations, and autonomic influences, are implicated (14).

The triggering of acute coronary syndromes requires two elements: a substrate and the triggering events or circumstances. The substrate is an atherosclerotic plaque with features predisposing it to superficial erosion or rupture. The plaque exists in a microenvironment which includes the physical forces that stress or deform the plaque, coronary vasomotor tone and endothelial function, circulating catecholamines and other vasoac-tive substances, and the state of the intracoronary hemostatic environment. The activities and circumstances that may be recognized as triggering events for acute coronary syndromes produce their effects through alterations in the microenvironment, which favor plaque erosion or rupture and intracoronary thrombus formation (Fig. 1).

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