The pathophysiology of mental stress-induced myocardial ischemia, which occurs at lower heart rates than during physical stress, is not well understood.
The Psychophysiological Investigations of ...Myocardial Ischemia Study (PIMI) evaluated the physiological and neuroendocrine functioning in unmedicated patients with stable coronary artery disease and exercise-induced ischemia. Hemodynamic and neurohormonal responses to bicycle exercise, public speaking, and the Stroop test were measured by radionuclide ventriculography, ECG, and blood pressure and catecholamine monitoring. With mental stress, there were increases in heart rate, systolic blood pressure, cardiac output, and systemic vascular resistance that were correlated with increases in plasma epinephrine. During exercise, systemic vascular resistance fell, and there was no relationship between the hemodynamic changes and epinephrine levels. The fall in ejection fraction was greater with mental stress than exercise. During mental stress, the changes in ejection fraction were inversely correlated with the changes in systemic vascular resistance. Evidence for myocardial ischemia was present in 92% of patients during bicycle exercise and in 58% of patients during mental stress. Greater increases in plasma epinephrine and norepinephrine occurred with ischemia during exercise, and greater increases in systemic vascular resistance occurred with ischemia during mental stress.
Mental stress-induced myocardial ischemia is associated with a significant increase in systemic vascular resistance and a relatively minor increase in heart rate and rate-pressure product compared with ischemia induced by exercise. These hemodynamic responses to mental stress can be mediated by the adrenal secretion of epinephrine. The pathophysiological mechanism involved are important in the understanding of the etiology of myocardial ischemia and perhaps in the selection of appropriate anti-ischemic therapy.
To describe factors influencing chest pain expression in patients with cardiac or noncardiac disease.
The authors conducted a case presentation and review of literature.
Causes of chest pain are ...diverse. Psychologic factors influence chest pain expression commonly in patients with or without cardiac disease.
Physicians and other therapists must be aware of psychologic influences on chest pain expression to provide optimal treatment to their patients.
OBJECTIVES
The purposes of this database study were to determine: 1) the relationship between mental stress–induced ischemia and ischemia during daily life and during exercise; 2) whether patients ...who exhibited daily life ischemia experienced greater hemodynamic and catecholamine responses to mental or physical stress than patients who did not exhibit daily life ischemia, and 3) whether patients who experienced daily life ischemia could be identified on the basis of laboratory-induced ischemia using mental or exercise stress testing.
BACKGROUND
The relationships between mental stress–induced ischemia in the laboratory and ischemia during daily life and during exercise are unclear.
METHODS
One hundred ninety-six stable patients with documented coronary disease and a positive exercise test underwent mental stress testing and bicycle exercise testing. Radionuclide ventriculography and electrocardiographic (ECG) monitoring were performed during the mental stress and bicycle tests. Patients underwent 48 h of ambulatory ECG monitoring. Hemodynamic and catecholamine responses were obtained during mental stress and bicycle tests.
RESULTS
Ischemia (reversible left ventricular dysfunction or ST segment depression ≥1 mm) developed in 106 of 183 patients (58%) during the mental stress test. There were no significant differences in clinical characteristics of patients with, compared with those without, mental stress–induced ischemia. Patients with mental stress ischemia more often had daily life ischemia than patients without mental stress ischemia, but their exercise tests were similar. Patients with daily life ischemia had higher ejection fraction and cardiac output, and lower systemic vascular resistance during mental stress than patients without daily life ischemia. Blood pressure and catecholamine levels at rest and during the mental stress tests were not different in patients with, compared with those without, daily life ischemia. Patients with daily life ischemia had a higher ejection fraction at rest and at peak bicycle exercise compared with patients without daily life ischemia, but there were no other differences in peak hemodynamic or catecholamine responses to exercise. The presence of ST segment depression during routine daily activities was best predicted by ST segment depression during mental or bicycle exercise stress, although ST segment depression was rare during mental stress.
CONCLUSIONS
Patients with daily life ischemia exhibit a heightened generalized response to mental stress. ST segment depression in response to mental or exercise stress is more predictive of ST segment depression during routine daily activities than other laboratory-based ischemic markers. Therapeutic management strategies might therefore focus on patients with these physiologic responses to stress and on whether lessening such responses reduces ischemia.
Coronary artery disease (CAD) is the leading cause of death in the United States and other developed countries. Along with a number of other factors thought to contribute to the high prevalence of ...CAD in developed societies (longer life expectancy, obesity, sedentary lifestyles), various psychological and social factors appear to promote the development or worsening of heart disease. It is well recognized that stress can be harmful to the cardiovascular system. The combination of the preexisting vulnerability and the major stressor are believed to result in cardiac arrhythmias and/or plaque rupture leading to death.
Recently, the epidemiologic evidence of a link between stress and CAD is very convincing, yet the biopsychosocial pathway that would explain how stress can lead to disease is less clear. Different types of psychological stress have been found to be associated with increased cardiovascular events. Evidence regarding the efficacy of psychosocial interventions is also presented.
It is suggested that, taken as a whole, evidence for a psychological and social impact on CAD morbidity and mortality is convincing.
There are profound gender-related differences in the incidence, presentation, and outcomes of coronary artery disease (CAD). These differences are not entirely explained by traditional cardiovascular ...risk factors. Nontraditional risk factors, such as psychological traits, have increasingly been recognized as important contributors to the genesis and outcomes of CAD. Mental stress induces significant peripheral arterial vasoconstriction, with consequent increases in heart rate and blood pressure. These changes are thought to underlie the development of myocardial ischemia and other mental stress–induced adverse cardiac events in patients with CAD. This study examined for gender-related differences in peripheral arterial response to mental stress in a cohort of patients with CAD using a novel peripheral arterial tonometric (PAT) technique. There were 211 patients (77 women; 37%) with a documented history of CAD and a mean age of 64 ± 9 years. Patients were enrolled from August 18, 2004, to February 21, 2007. Mental stress was induced using a public speaking task. Hemodynamic and PAT measurements were recorded during rest and mental stress. The PAT response was calculated as a ratio of pulse wave amplitude during stress to at rest. PAT responses were compared between men and women. The PAT ratio (during stress to at rest) was significantly higher in women compared with men. Mean PAT ratio was 0.80 ± 0.72 in women compared with 0.59 ± 0.48 in men (p = 0.032). This finding remained significant after controlling for possible confounding factors (p = 0.037). In conclusion, peripheral vasoconstrictive response to mental stress was more pronounced in men compared with women. This finding may suggest that men have higher susceptibility to mental stress–related adverse effects. Additional studies are needed to determine the significance of this finding.
Depression is common in patients with acute myocardial infarction (AMI) and is associated with adverse health outcomes. However, the extent to which clinical depression is related to comorbid medical ...conditions is unknown. This study examined the degree of association between clinical depression and medical comorbidity in patients hospitalized with AMI.
Two thousand four hundred and eighty-one depressed or socially isolated patients with AMI were enrolled, as part of the National Heart, Lung, and Blood Institute-sponsored Enhancing Recovery in Coronary Heart Disease clinical trial. A structured interview was used to diagnose major and minor depression and dysthymia; severity of depression was measured by the Hamilton Rating Scale for Depression and the Beck Depression Inventory. Level of social support was measured by the ENRICHD Social Support Instrument. A modified version of the Charlson Comorbidity Index was used to measure the cumulative burden of medical comorbidity.
The adjusted odds ratios (ORs) for having major depression increased linearly with medical comorbidity (ORs 1.6, 2.2, 2.7 for each increasing medical comorbidity category). This relationship remained after adjusting for coronary heart disease severity (ORs 1.4, 1.7, 1.9,
P < .001). The relationship between severity of depression and medical comorbidity was also maintained after excluding somatic symptoms of depression (F = 21.5,
P < .0001).
Patients with AMI and clinical depression have significantly greater levels of medical comorbidity than nondepressed, socially isolated patients. Further research is needed to determine whether comorbid medical illness contributes to the more frequent rehospitalizations and increased risk of mortality associated with depression.
Methods We performed a multicenter randomized controlled trial with 150 patients with elevated depressive symptoms (Beck Depression Inventory score >10) 2 to 6 months after an ACS who were recruited ...and randomized from 7 private and academic ambulatory centers across the United States between March 18, 2010 and January 9, 2012.
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