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EDITORIALS |
Department of Medicine; Division of Cardiovascular Medicine; University of Florida; Malcom Randall VA Medical Center; Gainesville, Florida (Sheps)
Department of Medicine; Section of Cardiovascular Medicine; Yale University; New Haven, Conneticut (Soufer)
Department of Psychiatry; Washington University School of Medicine; St. Louis, Missouri (Freedland)
With cardiovascular disease remaining the leading cause of death in the United States, there is intense interest in determining who is at risk and identifying opportunities to intervene to reduce the death toll. We have learned from previous research that mental stress-induced myocardial ischemia is an independent predictor of cardiac death (1). Indeed, the Psychophysiological Investigations of Myocardial Ischemia (PIMI) study indicated that patients with coronary disease who exhibited reduced cardiac blood flow in response to a mental stressor in the laboratory had triple the risk of death during the next 5 years.
Most studies of mental stress-induced ischemia have been conducted in a select group of patients—those with normal left ventricular function who have already demonstrated that they develop ischemia on exercise tests. We therefore have an incomplete understanding of whether anyone beyond this group may be at risk. In this issue of Psychosomatic Medicine, Holmes et al. offer another piece of the puzzle (2). They studied 58 patients with coronary artery disease; 22 had normal left ventricular function and 36 had varying degrees of left ventricular dysfunction characterized by an ejection faction of less than 50%. The patients underwent bicycle exercise and mental stress testing with myocardial perfusion imaging. The major findings were that heart rate response during mental stress is elevated in patients with severe left ventricular dysfunction, that it is similar to the response seen in patients with preserved left ventricular function, and that hemodynamic reactivity is not related to mental stress-induced ischemia.
Although not emphasized as a primary finding, patients with depressed left ventricular ejection fractions tended to have mental stress ischemia at least as frequently as those with normal left ventricular function. This finding was also reported in a previous study by the same group (3) and in a recent study by Hassan et al. (4). The finding that mental stress can provoke ischemia in patients with coronary disease but with depressed ejection faction is important for several reasons.
Previous studies had been done in a subset of patients (i.e., patients with a positive exercise test and a normal ejection fraction) that is declining as an overall percentage of the symptomatic coronary artery disease (CAD) population in the United States. This is due in part to the widespread use of aggressive, tailored pharmacotherapy and of reperfusion therapies. In addition, the population of patients with a depressed ejection fraction (with or without a positive exercise test) is increasing, with heart failure as one of the most common causes of hospitalization and death among patients with heart disease. In addition, a relatively recent study has shown that patients with negative exercise or adenosine stress tests can also have mental stress-induced ischemia (5).
Myocardial ischemia is a significant clinical burden in the United States today. According to the American Heart Association, 6.5 million to 16.5 million patients with stable angina account for more than $1.9 billion in annual direct costs in the United States (6). There is also a growing prevalence of chronic ischemia (angina and asymptomatic ischemia) due to residual CAD after percutaneous interventions or bypass surgery. According to an analysis of the National Heart, Lung, and Blood Institute (NHLBI) Dynamic registry, persistent ischemia occurs in 28% to 78% of patients within one year after intervention, depending on the type and number of medications employed (7). Given that 30% to 50% of those with inducible demand ischemia are vulnerable to mental stress ischemia (8), a significant number of patients would be at potential risk for adverse events due to mental stress-induced ischemia in the subgroup with documented exercise- or chemical-induced ischemia. If the evidence continues to build that mental stress-induced ischemia occurs in a percentage of patients with CAD but without exercise- or chemical-induced ischemia, the population at risk becomes even larger.
We do not yet know whether these recently identified populations face a similar level of risk for adverse cardiac events as patients with positive exercise tests. A fairly simple look at the numbers can demonstrate why it is so important that we find out.
The population at risk due to mental stress ischemia could be quite large depending on a number of factors. Even if one assumed a conservative estimate of the percent of CAD patients with mental stress-induced ischemia on top of exercise-induced ischemia (20%) and a risk ratio of 2.8 for adverse events (values taken from PIMI) the percent of events that could be attributed to the additional effect of mental stress is 26% (see Table 1).
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Thus, if mental stress ischemia can be effectively treated, it would be possible to prevent a large number of events including deaths. If the overall percentage of CAD patients with mental stress-induced ischemia is found to be higher than 20%, the preventive effect of successful treatment would be even greater. Of course, this depends on effective detection and treatment of the condition, and assumes that effective treatment will reverse the adverse prognosis. These points have yet to be demonstrated, but the possible public health implications are quite impressive.
It appears likely that in the near future, mental stress testing may become part of the clinical armamentarium of the practicing physician to identify patients at risk. If indeed those with mental stress-induced ischemia are at increased risk, it is incumbent on us to work in a multidisciplinary fashion to establish a suitable diagnostic approach. Interest is emerging in the nuclear cardiology community in establishing a mental stress testing procedure with an appropriate myocardial flow tracer, proper injection timing, and a reproducible mental stressor (8).
There have been several studies indicating that treatment strategies to reverse the adverse effects of mental stress on the myocardium can be effective, but much more work needs to be done. Blumenthal et al., for example, have shown that intensive exercise and behavioral programs can have significant physiologic effects, which in turn have been shown also to reduce the prevalence of mental stress-induced ischemia in this population (9). These findings need to be replicated by other investigators and long-term follow-up studies need to be done in these populations.
NOTES
The authors acknowledge the editorial assistance of Victoria White, MA, ELS.
DOI:10.1097/PSY.0b013e31814527c2
REFERENCES
This article has been cited by other articles:
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  L. Terre Behavioral Medicine Review: Psychological Risks for Metabolic Syndrome American Journal of Lifestyle Medicine, April 1, 2008; 2(2): 126 - 129. [Abstract] [PDF]
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