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Drugs: beta-blockers
- from Medical topics
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- By Sari D. Schwartz, Uniformed Services University of the Health Sciences, David S. Krantz, Uniformed Services University of the Health Sciences
- Edited by Susan Ayers, University of Sussex, Andrew Baum, University of Pittsburgh, Chris McManus, Stanton Newman, Kenneth Wallston, John Weinman, Robert West
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- Book:
- Cambridge Handbook of Psychology, Health and Medicine
- Published online:
- 18 December 2014
- Print publication:
- 23 August 2007, pp 683-685
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Summary
Beta-blockers are a class of drugs that selectively compete for and inhibit binding at the beta-adrenergic subset of receptors of the sympathetic nervous system (Middlemiss et al., 1981; Patel & Turner, 1981). Beta-adrenergic receptors are primarily located in the heart and in the smooth muscle of the blood vessels and the lungs, but also exert metabolic and other effects. The beta-blockers are structurally similar to the body's adrenergic neurotransmitters, norepinephrine and epinephrine, and they exhibit their greatest effects during periods of intense sympathetic nervous system (SNS) activation. Therefore, the most common clinical use of these drugs is for the treatment of cardiovascular disorders, including hypertension and manifestations of ischaemic heart disease such as angina pectoris and cardiac arrhythmias (Frishman, 1980; Patel & Turner, 1981; Weiner, 1985).
However, since the introduction of these drugs and their wide therapeutic use, a variety of both desirable and unwanted psychological effects have been observed. One of the most frequently noted beneficial effects has been the reduction of reported anxiety by individuals in certain acutely stressful situations (e.g. performing before an audience or dental surgery) that are normally accompanied by several somatic manifestations of arousal (Frishman et al., 1981; Noyes, 1982; Elman et al., 1998). There have also been some reports that chronic beta-blocker therapy might lessen anger and irritability or ‘coronary-prone’ behaviour pattern (Schmeider et al., 1983; Krantz & Durel, 1983; Fedorets et al., 2004).
Mental stress and the induction of silent myocardial ischemia in patients with coronary artery disease
- from Section 2 - Psychophysiological processes in disease
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- By A. Rozanski, University of California at Los Angeles School of Medicine, C. N. Bairey, University of California at Los Angeles School of Medicine, D. S. Krantz, University of California at Los Angeles School of Medicine, J. Friedman, University of California at Los Angeles School of Medicine, K. J. Resser, University of California at Los Angeles School of Medicine, M. Morell, University of California at Los Angeles School of Medicine, S. Hilton-Chalfen, University of California at Los Angeles School of Medicine, L. Hestrin, University of California at Los Angeles School of Medicine, J. Bietendorf, University of California at Los Angeles School of Medicine, D. S. Berman, University of California at Los Angeles
- Edited by Andrew Steptoe, St George's Hospital Medical School, University of London, Jane Wardle, Imperial Cancer Research Fund, London
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- Book:
- Psychosocial Processes and Health
- Published online:
- 05 August 2016
- Print publication:
- 24 November 1994, pp 147-165
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Summary
Abstract
To assess the causal relation between acute mental stress and myocardial ischemia, we evaluated cardiac function in selected patients during a series of mental tasks (arithmetic, the Stroop color-word task, simulated public speaking, and reading) and compared the responses with those induced by exercise. Thirty-nine patients with coronary artery disease and 12 controls were studied by radionuclide ventriculography.
Of the patients with coronary artery disease, 23 (59 percent) had wall-motion abnormalities during periods of mental stress and 14 (36 percent) had a fall in ejection fraction of more than 5 percentage points. Ischemia induced by mental stress was symptomatically “silent” in 19 of the 23 patients with wall-motion abnormalities (83 percent) and occurred at lower heart rates than exerciseinduced ischemia (P<0.05). In contrast, we observed comparable elevations in arterial pressure during ischemia induced by mental stress and ischemia induced by exercise. A personally relevant, emotionally arousing speaking task induced more frequent and greater regional wall-motion abnormalities than did less specific cognitive tasks causing mental stress (P < 0.05). The magnitude of cardiac dysfunction induced by the speaking task was similar to that induced by exercise.
Personally relevant mental stress may be an important precipitant of myocardial ischemia - often silent - in patients with coronary artery disease. Further examination of the pathophysiologic mechanisms responsible for myocardial ischemia induced by mental stress could have important implications for the treatment of transient myocardial ischemia. (N Engl J Med 1988; 318:1005-12.)
Recent research indicates that transient myocardial ischemia is common in patients with coronary artery disease. It usually occurs without symptoms, at low heart rates, and has a circadian rhythm that parallels changes in heart rate, blood, pressure, and the release of catecholamines. Other evidence suggests that mental stress - like physical stress - may be associated with myocardial ischemia. It is currently unknown whether ischemia is a direct consequence of mental activities or a spontaneous or independent phenomenon. Laboratory studies involving the provocation of myocardial ischemia by mental stress are needed to confirm such a causal relation.
Studies involving positron-emission tomography have demonstrated that a wide variety of physiologic stimuli, including physical exercise, exposure to cold temperature, smoking, and nonspecific forms of mental stress, can induce transient ischemia in selected patients with coronary artery disease.