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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Physical and mental stressors result in increased inflammation markers in populations free of coronary artery disease (CAD). However, inflammatory responses to mental and exercise challenges have not been established in patients with CAD. This study investigated the responses of inflammatory markers, including C-reactive protein (CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule-1, in patients with CAD after successful elective percutaneous coronary intervention (n = 36, 59 +/- 8 years of age, 33% women) and healthy controls without a history of CAD (n = 28, 54 +/- 10 years of age, 36% women). Increases in inflammatory markers were examined in response to mental challenge tasks (anger recall and mental arithmetic) and treadmill exercise. Stress echocardiography was used to rule out stress-induced ischemia as a possible confounding factor. Results showed that CRP increased significantly to mental challenge and exercise (p values <0.01), and CRP responses were higher in patients with CAD than in controls (change in mental arithmetic 0.19 +/- 0.11 vs 0.01 +/- 0.03 mg/L, p = 0.003; change in exercise 0.57 +/- 0.11 vs 0.08 +/- 0.0.03 mg/L, p = 0.001). Increased norepinephrine responses were related to larger CRP and IL-6 increases to mental challenge tasks (p values <0.05). Exercise elicited increased CRP, IL-6, and soluble intercellular adhesion molecule-1 levels (p values <0.01), and these responses were larger than with mental challenge tasks (p values <0.05). In conclusion, mental stress and exercise induce increased levels of inflammatory markers in patients with CAD. These stress-induced increases are larger than in healthy subjects, occur in the absence of myocardial ischemia, and are related to the neurohormonal stress response.
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PMID:Effects of acute mental stress and exercise on inflammatory markers in patients with coronary artery disease and healthy controls. 1832 37

Heart failure affects millions of Americans and new diagnosis rates are expected to almost triple over the next 30 years as our population ages. Affective disorders including clinical depression and anxiety are common in patients with congestive heart failure. Furthermore, the presence of these disorders significantly impacts quality of life, medical outcomes, and healthcare service utilization. In recent years, the literature has attempted to describe potential pathophysiologic mechanisms relating affective disorders and psychosocial stress to heart failure. Several potential mechanisms have been proposed including autonomic nervous system dysfunction, inflammation, cardiac arrhythmias, and altered platelet function. These mechanisms are reviewed in this article. Additional novel mechanisms such as mental stress-induced myocardial ischemia are also discussed.
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PMID:Psychobiology of depression/distress in congestive heart failure. 1836 81

There is an enormous amount of literature on psychological stress and cardiovascular disease. This report reviews conceptual issues in defining stress and then explores the ramifications of stress in terms of the effects of acute versus long-term stressors on cardiac functioning. Examples of acute stressor studies are discussed in terms of disasters (earthquakes) and in the context of experimental stress physiology studies, which offer a more detailed perspective on underlying physiology. Studies of chronic stressors are discussed in terms of job stress, marital unhappiness, and burden of caregiving. From all of these studies there are extensive data concerning stressors' contributions to diverse pathophysiological changes including sudden death, myocardial infarction, myocardial ischemia, and wall motion abnormalities, as well as to alterations in cardiac regulation as indexed by changes in sympathetic nervous system activity and hemostasis. Although stressors trigger events, it is less clear that stress "causes" the events. There is nonetheless overwhelming evidence both for the deleterious effects of stress on the heart and for the fact that vulnerability and resilience factors play a role in amplifying or dampening those effects. Numerous approaches are available for stress management that can decrease patients' suffering and enhance their quality of life.
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PMID:Psychological stress and cardiovascular disease. 1935 51

The authors assessed the effect of psychological stress on total and cause-specific mortality among men and women. In 1981-1983, the 12,128 Danish participants in the Copenhagen City Heart Study were asked two questions on stress intensity and frequency and were followed in a nationwide registry until 2004, with <0.1% loss to follow-up. Sex differences were found in the relations between stress and mortality (p = 0.02). After adjustments, men with high stress versus low stress had higher all-cause mortality (hazard ratio (HR) = 1.32, 95% confidence interval (CI): 1.15, 1.52). This finding was most pronounced for deaths due to respiratory diseases (high vs. low stress: HR = 1.79, 95% CI: 1.10, 2.91), external causes (HR = 3.07, 95% CI: 1.65, 5.71), and suicide (HR = 5.91, 95% CI: 2.47, 14.16). High stress was related to a 2.59 (95% CI: 1.20, 5.61) higher risk of ischemic heart disease mortality for younger, but not older, men. In general, the effects of stress were most pronounced among younger and healthier men. No associations were found between stress and mortality among women, except among younger women with high stress, who experienced lower cancer mortality (HR = 0.51, 95% CI: 0.28, 0.92). Future preventive strategies may be targeted toward stress as a risk factor for premature death among middle-aged, presumably healthy men.
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PMID:Perceived stress and cause-specific mortality among men and women: results from a prospective cohort study. 1861 55

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.
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PMID:Comparison of peripheral arterial response to mental stress in men versus women with coronary artery disease. 1892 95

Myocardial ischemia that results from emotional provocation occurs in as many as 30% to 50% of patients with coronary artery disease during the discourse of their lives. This emotionally provoked or mental stress ischemia is associated with poor prognosis, with emerging treatment strategies. This article outlines the conceptual constructs that support the pathophysiologic underpinnings, and biobehavioral aspects associated with this mental stress ischemia. We review a biobehavioral model in which cognitive stress is transduced in the brain. The response of the brain to psychosocial stress is a highly sophisticated and integrated process by which sensory inputs are evaluated and appraised for their importance in relation to previous experience and current goals. The biologic consequences of such stress transduced in the central nervous system has its effect on cardiovascular flow and function through changes in autonomic balance, which result in various biologic processes that culminate in the perturbation of flow and function of the heart.
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PMID:Heart-brain interactions in mental stress-induced myocardial ischemia. 1923 29

Detection of microvolt levels of T-wave alternans (TWA) has been shown to be useful in identifying individuals at heightened risk for sudden cardiac death. The mechanistic bases for TWA are complex, at the cellular level involving multiple mechanisms, particularly instabilities in membrane voltage (i.e., steep action potential duration restitution slope) and disruptions in intracellular calcium cycling dynamics. The integrative factors influencing TWA at the systemic level are also multifold. We focus on three main variables: heart rate, autonomic nervous system activity, and myocardial ischemia. Clinically, there is growing interest in extending TWA testing to include ambulatory ECG monitoring as well as exercise. The former modality permits assessment of the influence of diverse provocative stimuli of daily life, including physical activity, circadian factors, mental stress, and sleep-state related disturbances in respiratory and cardiovascular function. Two major emerging concepts in clinical TWA testing are discussed: quantitative analysis of TWA level to complement the current binary classification scheme, and risk stratification of patients with preserved left ventricular function, the population with the largest absolute number of sudden cardiac deaths.
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PMID:Basis for sudden cardiac death prediction by T-wave alternans from an integrative physiology perspective. 1925 Dec 21

Stress can be a primary or secondary contributor to ill health via excessive and sustained sympathetic arousal leading to ischemic heart disease, hypertension, stroke, obesity, and mental ill health, or through related behaviors such as smoking, substance abuse, and over or inappropriate eating; or as a contextual variable in terms of risk factor and lifestyle outcome. In addition, psychosocial stress can impair recovery from any pathological insult or injury. Most assessments of stress relate to life events, and both past and current life stressors, acute and chronic, play a major role. However, beyond the impact of stressors, it is the reported state of feeling stressed that is the critical predictor of ill health. This article describes stress and its correlates, discusses models of stress, and presents the nine-item Psychological Stress Measure (PSM-9). This tool is aimed directly at the state of feeling stressed, is suited for assessing stress clinically in the general population and serving as an outcome measure. The tool is valid and reliable and easy to administer in health care settings; it has a normal distribution, which makes it a very sensitive-to-change instrument in repeated measures to document progress.
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PMID:Psychological Stress Measure (PSM-9): integration of an evidence-based approach to assessment, monitoring, and evaluation of stress in physical therapy practice. 1984 68

Thoracic pain is a common symptom in emergency services, and stress radionuclide imaging represents one of the phases of risk stratification in these individuals. However, a group of patients with negative functional exams after physical or pharmacological stress develops myocardial ischemia during this psychological stress. Alterations in vascular tonus as a response to endogenous mechanisms are the physiopathologic basis for such alterations. We report a case that illustrates how mental stress radionuclide imaging has the potential to be used in the assessment of myocardial ischemia non-detected by conventional methods in patients with suspicion of ischemic thoracic pain.
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PMID:Radionuclide imaging of myocardium with mental stress in the investigation of thoracic pain. 1993 45

Post stress neurovascular responses induced by physical and mental stress are poorly understood. We investigated the time course of cardiovascular and autonomic recovery, induced by orthostatic and mental challenge, using passive head up tilt (HUT) and mental arithmetic (MA), respectively, when applied singly (MA, HUT) or in combination (MA+HUT). Fifteen healthy males participated in three protocols: HUT, MA and combined MA+HUT, with sessions randomized and 2 weeks apart. Post stress responses were studied in the first 10 min (early; cardiovascular only) and 30 min (late), in 2.5 min epochs. A detailed analysis of early period was done in 30s epochs. Within the first 2.5 min recovery, time courses of heart rate, stroke volume and cardiac output differed significantly, particularly when comparing HUT vs. MA and MA+HUT vs. MA. Additionally, heart rate response differed in HUT vs. MA+HUT. No differences in hemodynamic recovery were seen during the next 2.5 min. Late responses of heart rate and cardiac output showed significantly lower values as compared to baseline, especially for HUT and MA+HUT. Recovery of hemodynamic responses, either due to single or combined stress challenges, showed stressor- and time-dependent patterns. Our data provide useful information regarding why longer recovery periods must be assessed and provide novel insights regarding recovery of physical and mental stressors. This may have clinical implications in the development of cardiovascular diseases such as hypertension or myocardial ischemia.
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PMID:Rate of cardiovascular recovery to combined or separate orthostatic and mental challenges. 1996 11


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