Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Major depression is a common comorbidity associated with ischemic heart disease (IHD). There is growing evidence that psychological stress in general and depression in particular predispose to cardiovascular disease. Persons who have mental stress during daily life are at twice the risk of myocardial ischemia, and patients with post-myocardial infarction depression have higher mortality rates than nondepressed controls. These data suggest a psychophysiologic mechanism underlying the vulnerability of depressed patients to IHD. Clinical studies have demonstrated that depression is associated with a much higher risk of both cardiovascular morbidity and mortality, which could be caused by platelet activation. Physicians should maintain a heightened level of clinical suspicion for depression and depressive disorders in persons with IHD, particularly those individuals who are recovering from an acute ischemic event, such as myocardial infarction. Furthermore, depression may complicate the recovery of IHD, but in most cases depression can be effectively treated with antidepressant agents.
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PMID:Depression and ischemic heart disease. 1101 50

The risk of ischemic heart disease is connected with the definite mode of life. Improper nourishment, smoking, alcohol abuse, sedentary lifestyle and excessive mental stress cause disturbances leading to development of atherosclerosis. The change of the lifestyle may prevent from coronary heart disease and may play a main role in secondary prevention, making the prognosis after myocardial infarction much better. The epidemiological and clinical studies have shown the significance of particular risk factors reduction on survival after myocardial infarction and allowed to create the optimal preventive mode of life. Therefore the change of lifestyle should become the priority in the postinfarction therapy.
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PMID:[Change of lifestyle as a relevant therapy after myocardial infarction]. 1119 67

Mental stress has been shown to induce myocardial ischemia in people with coronary heart disease (CHD), both in the laboratory and in daily life. In order to investigate the role of the endothelium in the regulation of blood flow during stress, the endothelium-dependent (EDV) and endothelium-independent (EIDV) vasodilation was examined in the forearms of healthy people during a mental arithmetic test (MAT), a cold pressor test (CP) and an isometric handgrip test (ISO). A total of 10 young healthy volunteers (four men and six women, aged 20-25 years) underwent measurements of forearm vascular resistance (FVR) during local intraarterial infusions of methacholine (MCh; inducing EDV) and sodium nitroprusside (SNP; inducing EIDV) at rest and during the different forms of stress by the use of venous occlusion plethysmography. MAT induced a significant increase in FVR during MCh infusion (4 microg/min, from 3.5 +/- 0.7 at rest to 4.2 +/- 1.4 mmHg/ml per min per 100 ml tissue during MAT; p < 0.01), while FVR during SNP infusion was unchanged by MAT. CP induced a significant increase in FVR during infusions with both MCh and SNP compared to resting levels (p < 0.01 for both), while ISO induced a significant increase in FVR during MCh infusion (p < 0.05) and a smaller increase in FVR during SNP infusion. When the SNP to MCh FVR ratio was used as an index of endothelial function, only MAT impaired endothelial function significantly (p < 0.01). In conclusion, mental stress induced by an arithmetic task selectively opposed EDV in the forearms of young healthy people, while cold pressor and isometric handgrip tests induced a more general attenuation in vasodilatation.
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PMID:Mental stress opposes endothelium-dependent vasodilation in young healthy individuals. 1135 57

Sympathetic overactivity is a common feature of certain cardiovascular diseases. An acute activation of the sympathetic nervous system can provoke angina pectoris attacks through the increase of myocardial oxygen demand, frequently associated to coronary arterial constriction. It can also promote cardiac arrhythmias leading, in some cases, to cardiac sudden death. The aim of the present study was to evaluate the cardiovascular effects of a single oral dose of baclofen or ifenprodil (two drugs modulating central glutamatergic relays) at rest and during three laboratory stressors (a cold pressor test, a mental arithmetic stress test and an exercise test on a cycloergometer), in human healthy volunteers. Ifenprodil increased resting heart rate and did not reduce the cardiovascular response to any test. In contrast, baclofen reduced the tachycardic response to mental stress test and so limited the increase of myocardial oxygen demand during the test. Nevertheless, this drug was not able to affect the cardiovascular response to exercise. Finally, we have shown in this study that baclofen exhibits a profile of a central sympathomodulator without cardiodepression. Its activity towards mental stress induced cardiovascular responses leads us to proposing this compound for testing after a chronic treatment, in patients with silent myocardial ischemia and mental stress test induced ischemia.
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PMID:Effects of centrally-acting glutamatergic modulators on cardiovascular responses to stress in humans. 1143 32

This study examined the effects of exercise and stress management training on clinical outcomes and medical expenditures over a 5-year follow-up period in 94 male patients with established coronary artery disease (CAD) and evidence of ambulatory or mental stress-induced myocardial ischemia. Patients were randomly assigned to 4 months of aerobic exercise 3 times per week or to a 1.5-hour weekly class on stress management; patients who lived too far from Duke to participate in the weekly treatments formed the usual care control group. Follow-up was performed at the end of treatment and annually thereafter for 5 years. Stress management was associated with a significant reduction in clinical CAD events relative to usual care over each of the first 2 years of follow-up and after 5 years. Economic analyses revealed that stress management was associated with lower medical costs than usual care and exercise in the first 2 years, and that the cumulative cost over 5 years was also lower for stress management relative to usual care. These results suggest that there may be clinical and economic benefit to offering the type of preventive stress management and exercise interventions provided to patients with myocardial ischemia. Moreover, these findings suggest that the financial benefits that accrue from an appropriately targeted intervention may be substantial and immediate.
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PMID:Usefulness of psychosocial treatment of mental stress-induced myocardial ischemia in men. 1208 93

We examined the association between social status, assessed by education and occupational categories and risk of myocardial infarction. We conducted a case-control study among 35-64 year-old women of Kaunas. Cases were 191 women with first myocardial infarction treated in hospitals in 1997-2000, and controls were 482 women in the same age group, randomly selected, without ischemic heart disease. We used multiple logistic regression to estimate the adjusted odds ratios of developing myocardial infarction in relation to social status and psychological stress. The study results indicated that stress, arterial hypertension, smoking, overweight and low education increased the risk of first myocardial infarction among 35-64 years old women. Managers and service, market sales workers had about twice higher risk for myocardial infarction than associate professionals (OR = 2.64; 95% CI 1.17-6.62 and OR = 2.18; 95% CI 1.03-4.63 correspondingly).
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PMID:[Social status, psychological stress and myocardial infarction risk among 35-64-year-old women]. 1247 76

Recent studies provide relevant evidence that psychological stress significantly influences the pathogenesis of sudden cardiac death. Psychological stress expresses a situation of imbalance, derived from a real or perceived disparity between environmental demands and the individual's ability to cope with these demands. A situation of psychological stress may include different components: personality factors and character traits, anxiety and depression, social isolation and acute or chronic adverse life events. In particular, it has been documented that a sudden extremely hard event, such as an earthquake or a war strike, can significantly increase the incidence of sudden death. Nevertheless, each one of these factors, if not present, can balance a partially unfavorable situation; this overview suggests a multifactorial situation where almost all elements are present and in which the relative influence of each one varies according to the individual examined. Sudden death occurs when a transient disruption (such as acute myocardial ischemia, platelet activation or neuroendocrine variations), occurring in a patient with a diseased myocardium (such as one with a post-necrotic scar or hypertrophy), triggers a malignant arrhythmia. Psychological stress acts at both levels: by means of a "chronic" action it contributes to create the myocardial background, while by means of an acute action it can create the transient trigger precipitating sudden death. In the chronic action two possible mechanisms can be detected: the first is a direct interaction, which contributes to cause a hypertension status or to exacerbate coronary atherosclerosis consequent to endothelial dysfunction; the second one acts through adverse health behaviors, such as a poor diet, alcohol consumption or smoking. In case of acute psychological stress, the mechanisms involved are mainly the ability to trigger myocardial ischemia, to promote arrhythmogenesis, to stimulate platelet function, and to increase blood viscosity. Finally, some individuals have a sympathetic nervous system hyper-responsitivity, manifesting as exaggerated heart rate and blood pressure responses which result in accelerated atherosclerosis.
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PMID:[Psychological stress and sudden death]. 1247 27

The immune system plays a role in the progression of coronary artery diseases and its clinical manifestations as acute coronary syndromes. It is well established that psychological factors can act as risk factors for acute coronary syndromes. This review describes psychoneuroimmunological pathways involved in coronary disease progression and documents that the stage of coronary disease is a major determinant of pathophysiological mechanisms accounting for the association between psychological risk factors, immune system parameters, and acute coronary syndromes. Chronic psychological risk factors (e.g., hostility and low socioeconomic status) are important at early disease stages, episodic factors (e.g., depression and exhaustion) are involved in the transition from stable to unstable atherosclerotic plaques, and acute psychological triggers (e.g., mental stress and anger) can promote myocardial ischemia and plaque rupture. The psychoneuroimmunological pathways are described for each of these three types of psychological risk factors for acute coronary syndromes.
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PMID:The integration of cardiovascular behavioral medicine and psychoneuroimmunology: new developments based on converging research fields. 1283 24

Fear, anger, and grief may precipitate myocardial ischemia and infarction. The prognosis of patients with inducible ischemia during mental stress is worse than in those without inducible ischemia. The sympathetic nervous system plays an important role in stress-associated changes in cardiovascular regulation and contributes to cardiovascular morbidity and mortality by inducing vasoconstriction and tachycardia, as well as arrhythmia. Hostility--previously termed type A personality--is often associated with sympathetic hyperreactivity to mental stress and carries an increased risk for atherosclerotic vascular disease. As endothelial dysfunction is an early manifestation of atherosclerosis, the impact of mental stress on endothelial function is also important. Acute mental stress induces prolonged endothelial dysfunction in healthy volunteers, which is prevented by selective endothelin A receptor antagonism. This represents an important link between mental stress and atherosclerotic vascular disease. In addition, patients with depression show hypercortisolemia, and changes in platelet function leading to a prothrombotic state. These findings help to explain the increased cardiovascular risk in patients with depression.
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PMID:[Pathophysiologic cardiovascular changes in stress and depression]. 1466 4

Depression represents an independent risk factor for developing ischemic heart disease, with platelet hyperactivity possibly serving as an important mediator of this association. In this pilot study we analyzed platelet surface activation markers in response to two stimuli, mental stress and physical activity. Using flow cytometry, we quantified the presence of two functional activation-dependent glycoprotein receptors on platelets' surface (P-selectin, GP53). Platelet reactivity was assessed as the difference in markers' fluorescence intensity before and after stimulation. We included 10 depressed psychiatric inpatients and 10 age- and sex-matched healthy subjects in our study. There was a significant rise in platelet activation markers in both groups associated with the stress protocol. When the effect of stressors was analyzed separately, strenuous physical activity was found to lead to a significant rise in platelet activation markers in depressed patients but not in healthy subjects, although values indicated a higher baseline level of activation in healthy subjects. These preliminary results lend partial support to the hypothesis of an exaggerated platelet reactivity after physical activity in depression, thus possibly contributing to an increased cardiovascular risk in this disorder.
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PMID:Effect of mental and physical stress on platelet activation markers in depressed patients and healthy subjects: a pilot study. 1526 5


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