We read with interest the report by Fiuzat et al, using the Duke Databank for Cardiovascular Disease, suggesting an increase in acute myocardial infarction (AMI) associated with the downturn in stock market values from October 2008 to April 2009. In their discussion, the investigators cited the New Orleans experience relative to the incidence of AMI during the Hurricane Katrina era. They referenced Gautam et al’s report (from Tulane Medical Center), which demonstrated a dramatic, threefold increase in the number of patients who presented with AMI after February 2006 (when Tulane Medical Center reopened with complete onsite catheterization services); the increased incidence of acute cardiovascular (CV) events persisted during the entire 2-year study period. However, our experience (C.J. Lavie and R.V. Milani, unpublished observations) was inaccurately linked to the Tulane Medical Center as opposed to Ochsner Medical Center. They correctly stated that unlike Gautam et al, we found no increase in the incidence of acute coronary syndromes (ACS) or the absolute number of ACS treated before or after Hurricane Katrina at an institution that remained opened before, during, and after the storm. Nevertheless, we noted that patients who presented with ACS after Hurricane Katrina were on average 3 years younger (p <0.01), with a greater percentage of patients aged <55 years (p <0.01) and a small proportion aged >65 years (p <0.01), supporting the notion that a major disaster may increase the risk for AMI or ACS, especially in younger patients. Fiuzat et al presented evidence from several trials, as we did, suggesting that there are physical, psychological, chemical, and environmental triggers of acute CV events.

Unlike the findings from the Duke Databank for Cardiovascular Disease, which are limited to the analysis and interpretation of their data, we and others have suggested measures that may reduce the risk for AMI with various triggers. Exposures that transiently increase sympathetic activity have the potential to trigger acute CV events. For example, there is a peak of AMI and cardiac arrest in the early morning hours, and β-blocker therapy reduces this morning increase in risk. Although Tofler and Muller suggested several methods to attenuate the risk of potential triggers and the associated mortality, our discussion also emphasized the role of regular physical activity, exercise training, and improvements in cardiorespiratory fitness (CRF).

Mechanisms by which regular physical activity or improved CRF, or both, may provide protection against the triggering of acute CV events are multiple. One possible mechanism might be through adaptations in autonomic control. As a consequence of aerobic training, sympathetic drive at rest is reduced and vagal tone is increased, with potential cardioprotective effects on blood pressure, thrombosis, and other factors associated with coronary risk.

In many coronary patients, exercise-based cardiac rehabilitation produces significant reductions (>50%) in major psychological risk factors, including depression, anxiety, and hostility. In fact, small improvements in exercise capacity and overall CRF were associated with marked reductions in depression and depression-related increased mortality risk. In a recent study, almost all the benefits from exercise training in a coronary heart disease cohort after major coronary events were derived from improving CRF in groups with high psychosocial stress. Although no such intervention data are available for natural disasters (or stock market crashes), it seems likely that prophylaxis against the triggering of acute CV events should include regular exercise, because it is readily accessible and beneficial for physical and mental health.