The American Journal of Cardiology

1993

DOI: 10.1016/0002-9149(93)90180-k

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Anger report predicts coronary artery vasomotor response to mental stress in atherosclerotic segments

Michael D. Boltwood

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²

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Michelle Boutté Burke

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et al.

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Discussion1

Induction Of Myocardial Ischemia1

Psychosocial Stress and Endothelial Function1

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Cited by 123 publications

(60 citation statements)

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“…24 At present, it is unknown whether increases in coronary vascular resistance, either involving epicardial vessels or smaller vessels in the coronary microcirculation, correlate with changes in systemic vascular resistance. 25,26 If so, this association could account for the effects of mental stress on myocardial oxygen supply.…”

Section: Discussionmentioning

confidence: 99%

Mental Stress–Induced Ischemia and All-Cause Mortality in Patients With Coronary Artery Disease

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et al. 2002

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Background-Ischemia during laboratory mental stress tests has been linked to significantly higher rates of adverse cardiac events. Previous studies have not been designed to detect differences in mortality rates. Methods and Results-To determine whether mental stress-induced ischemia predicts death, we evaluated 196 patients from the Psychophysiological Investigations of Myocardial Ischemia (PIMI) study who had documented coronary artery disease and exercise-induced ischemia. Participants underwent bicycle exercise and psychological stress testing with radionuclide imaging. Cardiac function data and psychological test results were collected. Vital status was ascertained by telephone and by querying Social Security records 3.5Ϯ0.4 years and 5.2Ϯ0.4 years later. Of the 17 participants who had died, new or worsened wall motion abnormalities during the speech test were present in 40% compared with 19% of survivors (Pϭ0.04) and significantly predicted death (rate ratioϭ3.0; 95% CI, 1.04 to 8.36; Pϭ0.04). Ejection fraction changes during the speech test were similar in patients who died and in survivors (Pϭ0.9) and did not predict death even after adjusting for resting ejection fraction (Pϭ0.63), which was similar in both groups (mean, 56.4 versus 59.7; Pϭ0.24). Other indicators of ischemia during the speech test (ST-segment depression, chest pain) did not predict death, nor did psychological traits, hemodynamic responses to the speech test, or markers of the presence and severity of ischemia during daily life and exercise. Conclusions-In patients with coronary artery disease and exercise-induced ischemia, the presence of mental stressinduced ischemia predicts subsequent death.

“…24 At present, it is unknown whether increases in coronary vascular resistance, either involving epicardial vessels or smaller vessels in the coronary microcirculation, correlate with changes in systemic vascular resistance. 25,26 If so, this association could account for the effects of mental stress on myocardial oxygen supply.…”

Section: Discussionmentioning

confidence: 99%

Mental Stress–Induced Ischemia and All-Cause Mortality in Patients With Coronary Artery Disease

¹

,

²

,

³

et al. 2002

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Background-Ischemia during laboratory mental stress tests has been linked to significantly higher rates of adverse cardiac events. Previous studies have not been designed to detect differences in mortality rates. Methods and Results-To determine whether mental stress-induced ischemia predicts death, we evaluated 196 patients from the Psychophysiological Investigations of Myocardial Ischemia (PIMI) study who had documented coronary artery disease and exercise-induced ischemia. Participants underwent bicycle exercise and psychological stress testing with radionuclide imaging. Cardiac function data and psychological test results were collected. Vital status was ascertained by telephone and by querying Social Security records 3.5Ϯ0.4 years and 5.2Ϯ0.4 years later. Of the 17 participants who had died, new or worsened wall motion abnormalities during the speech test were present in 40% compared with 19% of survivors (Pϭ0.04) and significantly predicted death (rate ratioϭ3.0; 95% CI, 1.04 to 8.36; Pϭ0.04). Ejection fraction changes during the speech test were similar in patients who died and in survivors (Pϭ0.9) and did not predict death even after adjusting for resting ejection fraction (Pϭ0.63), which was similar in both groups (mean, 56.4 versus 59.7; Pϭ0.24). Other indicators of ischemia during the speech test (ST-segment depression, chest pain) did not predict death, nor did psychological traits, hemodynamic responses to the speech test, or markers of the presence and severity of ischemia during daily life and exercise. Conclusions-In patients with coronary artery disease and exercise-induced ischemia, the presence of mental stressinduced ischemia predicts subsequent death.

“…One mechanism is mental stress-induced coronary vasoconstriction. 213,214 During mental stress, significant coronary vasoconstriction may occur in CAD patients at sites manifesting vasoconstriction during acetylcholine infusion. 213 Because acetylcholine is used to test for endothelium-dependent coronary vasoconstriction, these findings sug- gest that neurohumoral stimulation during mental stress induces coronary vasoconstriction through an endotheliumdependent mechanism.…”

Section: Induction Of Myocardial Ischemiamentioning

confidence: 99%

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

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1999

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Abstract-Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis.Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys.Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. ...

“…31 Previous work evaluating a possible surrogate of endothelial function, peripheral vascular reactivity, has demonstrated links to psychosocial stress in monkeys, 29 hostility in humans, 32 and progression of atherosclerosis in humans. 33 Pathophysiologic links between psychosocial stress and endothelial function may involve direct endothelial damage because of catecholamine and blood pressure surges, resulting in intimal damage, inflammatory-induced free radicals blocking nitric oxide synthesis, and increased endothelial reactivity triggered by activated platelets.…”

Section: Psychosocial Stress and Endothelial Functionmentioning

confidence: 99%

Psychosocial Stress and Cardiovascular Disease: Pathophysiological Links

Merz¹,

et al. 2002

Behavioral Medicine

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The remarkable decline in cardiovascular disease (CVD) experienced in developed countries over the last 40 years appears to have abated. Currently, many CVD patients continue to show cardiac events despite optimal treatment of traditional risk factors. This evidence suggests that additional interventions, particularly those aimed at nontraditional factors, might be useful for continuing the decline. Psychosocial stress is a newly recognized (nontraditional) risk factor that appears to contribute to all recognized mechanisms underlying cardiac events, specifically, (a) clustering of traditional cardiovascular risk factors, (b) endothelial dysfunction, (c) myocardial ischemia, (d) plaque rupture, (e) thrombosis, and (f) malignant arrhythmias. A better understanding of the behavioral and physiologic associations between psychosocial stress and CVD will assist researchers in identifying effective approaches for reducing or reversing the damaging effects of stress and may lead to further reductions of CVD morbidity and mortality. Index Termscardiovascular disease; psychosocial interventions; psychosocial stress; review Cardiovascular disease (CVD) remains the largest contributor to morbidity and mortality in developed countries. 1 Advances in prevention and treatment in the last 40 years have resulted in a 40% decline in mortality from this disease. 1 Despite this remarkable success, it is sobering to note that the decline has abated recently,2 paradoxically despite continued reductions in traditional risk factors.3 Up to 50% of patients with established coronary artery disease have recurrent cardiac events, such as myocardial infarction and cardiac death, even with aggressive

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