Physical, Psychological and Chemical Triggers of Acute Cardiovascular Events

Abstract

In addition to the impact of long-term stressors such as sedentary lifestyle and long-term exposure to high levels of air pollution, many studies have shown that there is an increased risk of acute cardiovascular events immediately after behavioral, psychosocial, and environmental triggers.1–8 After the landmark study documenting the increased rates of myocardial infarction (MI) related to the 1981 earthquake in Athens9 and the description of the circadian variation in the incidence of MI by Muller et al,10 various studies documented the frequency of potential triggers in the period immediately preceding MI onset. Although the observational studies examining physical, psychological, and chemical triggers of acute cardiovascular events are not without limitations, studies continue to show that short-term exposures appear to play a role in the occurrence of cardiovascular events. These triggers have been discussed in previous reviews,1–8 with a general consensus that different preventive strategies may be appropriate for particular triggers. The purpose of this review is to bring together the evidence of the association between several triggers and cardiovascular outcomes and to discuss the common underlying pathophysiology of these triggers. Rather than leading to slowly progressive atherosclerosis, triggers represent the final step in the pathophysiological process leading to cardiovascular outcomes among susceptible individuals, such as those with vulnerable atherosclerotic plaque, chronic atherosclerotic disease, disorders of the cardiac conduction system, and microvascular disease. In the presence of a vulnerable atherosclerotic plaque, chemical, physical, and psychological stressors may trigger transient vasoconstrictive and prothrombotic effects that ultimately cause plaque disruption and thrombosis. Even in the absence of an occlusive thrombus, triggers may lower the threshold for cardiac electric instability and increase cardiac sympathetic activation via centrally mediated release of catecholamines, thereby evoking primary ventricular fibrillation and sudden cardiac death.11 Figure 1 depicts several potential …