Triggering of Acute Cardiovascular Disease and Potential Preventive Strategies

The last 2 decades have seen major advances in understanding of the mechanism of onset and treatment of acute coronary syndromes. It has become accepted that acute myocardial infarction (MI), sudden cardiac death, and stroke can be triggered by stressors such as heavy physical exertion and severe emotional stress; the clinical implications that can be derived from the findings of triggering remain uncertain, however.The triggering studies were stimulated by observations of a circadian variation and morning peak in MI, sudden cardiac death, and stroke that indicated that events did not occur randomly.1 In a 1989 review in Circulation ,1 we stated that although the primary value of recognizing the circadian variation of acute coronary events was the emphasis that could be placed on pharmacological protection during the morning hours, the main significance was the support it provided for the broader concept that the onset of coronary thrombosis at any time of the day is frequently triggered by activities of the patient.The aim of the present review is to update current knowledge about triggering of acute cardiovascular disease (CVD), place it in the context of advances in understanding of the mechanisms of onset, and suggest a 5-faceted strategy to protect against the pathophysiological effects of triggering. The rationale for such a strategy is discussed, with areas for further research highlighted.The treatment of hyperlipidemia and hypertension illustrates long-term risk factor management, in which an individual may take a daily lipid-lowering or antihypertensive agent for several years to reduce the risk of MI. Although the relative risk reduction with treatment may be 30%, the absolute risk reduction varies considerably, depending on the overall risk profile of a particular individual. For instance, in a moderately high-risk person with a 10% to 15% 5-year CVD event rate, a 30% risk …