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)

The central nervous system (CNS) effects of mental stress in patients with coronary artery disease (CAD) are unexplored. The present study used positron emission tomography (PET) to measure brain correlates of mental stress induced by an arithmetic serial subtraction task in CAD and healthy subjects. Mental stress resulted in hyperactivation in CAD patients compared with healthy subjects in several brain areas including the left parietal cortex [angular gyrus/parallel sulcus (area 39)], left anterior cingulate (area 32), right visual association cortex (area 18), left fusiform gyrus, and cerebellum. These same regions were activated within the CAD patient group during mental stress versus control conditions. In the group of healthy subjects, activation was significant only in the left inferior frontal gyrus during mental stress compared with counting control. Decreases in blood flow also were produced by mental stress in CAD versus healthy subjects in right thalamus (lateral dorsal, lateral posterior), right superior frontal gyrus (areas 32, 24, and 10), and right middle temporal gyrus (area 21) (in the region of the auditory association cortex). Of particular interest, a subgroup of CAD patients that developed painless myocardial ischemia during mental stress had hyperactivation in the left hippocampus and inferior parietal lobule (area 40), left middle (area 10) and superior frontal gyrus (area 8), temporal pole, and visual association cortex (area 18), and a concomitant decrease in activation observed in the anterior cingulate bilaterally, right middle and superior frontal gyri, and right visual association cortex (area 18) compared with CAD patients without myocardial ischemia. These findings demonstrate an exaggerated cerebral cortical response and exaggerated asymmetry to mental stress in individuals with CAD.
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PMID:Cerebral cortical hyperactivation in response to mental stress in patients with coronary artery disease. 960 Sep 87

The objectives of this study were to compare and contrast indicators of ischemia in a well-characterized group of 196 patients with coronary artery disease, documented angiographically or by verified history of myocardial infarction, and a positive exercise test result. Myocardial ischemia occurs frequently in response to everyday stressors in patients with coronary artery disease. The Psychophysiological Interventions in Myocardial Ischemia study provides a unique opportunity to study neuroendocrine and psychological manifestations of ischemia. Patients with exercise-induced ischemia underwent exercise radionuclide ventriculography and electrocardiographic monitoring and 2 laboratory mental stressors (Speech and Stroop) after being withdrawn from cardiac medications. In addition, 48-hour ambulatory electrocardiograms were recorded during routine daily activities. Patients with a history of angina within the past 3 months reported angina during the bicycle or treadmill test with a much higher frequency than patients without such an anginal history (77% vs 26%). Ejection fraction (EF) responses to the Stroop test were abnormal in 48% of patients with an abnormal EF response to the Speech task, versus 17% in patients with a normal EF response (p <0.01). Seventy-six percent of patients had an abnormal EF response to bicycle exercise. Three indicators of ischemia (ST-segment depression, wall motion abnormality, and EF response) were compared during the same laboratory stressor and across different types of stress tests. Presence of the 3 indicators was only moderately associated during exercise, and only weak or nonsignificant associations occurred among the presence of the 3 ischemic markers during mental stress. Occurrence of the same ischemic markers was moderately associated between the 2 mental stress tasks, but few associations were found between the occurrence of the same ischemic marker during exercise and mental stress. There is a marked heterogeneity of responses to psychological and exercise stress testing using electrocardiography, ambulatory electrocardiography, or radionuclide criteria for ischemia during stress. The heterogeneity may be related to differences in the magnitude or types of physiologic responses provoked and to differences in the sensitivity and specificity of the different tests used to identify ischemia.
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PMID:Heterogeneity among cardiac ischemic and anginal responses to exercise, mental stress, and daily life. 967 Sep 99

The hypothesis that addition of mental stress to physical exercise would modify the circulation response to stress and improve noninvasive detection of myocardial ischemia was tested in a randomized, crossover radionuclide angiocardiographic study. Compared with physical exercise or mental stress alone, combined stress led to higher heart rates and rate-pressure products in early stress stages, to more pronounced symptoms, and to a better discrimination of subjects with and without coronary artery disease by radionuclide angiography.
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PMID:Improved myocardial ischemia detection by combined physical and mental stress testing. 967 Oct 17

Nitric oxide is a soluble gas continuously synthesized by the endothelium. This substance has a wide range of biological properties that maintain vascular homeostasis, including modulation of vascular dilator tone, regulation of local cell growth, and protection of the vessel from injurious consequences of platelets and cells circulating in blood. A growing list of conditions, including those commonly associated as risk factors for atherosclerosis such as hypertension and hypercholesterolemia, are associated with diminished release of nitric oxide into the arterial wall either because of impaired synthesis or excessive oxidative degradation. Diminished nitric oxide bioactivity may cause constriction of coronary arteries during exercise or during mental stress and contribute to provocation of myocardial ischemia in patients with coronary artery disease. Additionally, diminished nitric oxide bioactivity may facilitate vascular inflammation that could lead to oxidation of lipoproteins and foam cell formation, the precursor of the atherosclerotic plaque. Numerous therapies have been investigated to assess the possibility of reversing endothelial dysfunction by enhancing the release of nitric oxide from the endothelium, either through stimulation of nitric oxide synthesis or protection of nitric oxide from oxidative inactivation and conversion to toxic molecules such as peroxynitrite. Accordingly, causal relationships between improved endothelial function and reduction in myocardial ischemia and acute coronary events can now be investigated.
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PMID:Role of nitric oxide in cardiovascular disease: focus on the endothelium. 970 90

Stress worsens certain disorders such as migraines or asthma, and has also been implicated in sudden myocardial arrest. It was previously shown that acute psychological stress by immobilization results in dura mast cell degranulation, an effect blocked by pretreatment with antiserum against corticotropin-releasing hormone (CRH). Moreover, CRH was recently shown to induce skin mast cell degranulation. The effect of psychological stress was investigated on rat cardiac mast cells, because their release of coronary constrictive and proinflammatory molecules contributes to myocardial ischemia and possibly arrhythmias. Immobilization of rats for 30 min induced maximal cardiac mast cell degranulation as evidenced by light and electron microscopy. This effect was inhibited by pretreatment with the "antiallergic" drug sodium cromoglycate (cromolyn), which is thought to act primarily through mast cell stabilization. Mast cell degranulation was also blocked by preincubation with antiserum against CRH and was partially inhibited by a CRH type-1 receptor selective antagonist. Sensory neuropeptides did not appear to influence this effect, but a nonpeptide neurotensin receptor antagonist blocked stress-induced cardiac mast cell degranulation. This finding supports the involvement of neuropeptide neurotensin which is present in the heart and is known to trigger mast cell degranulation. These results indicate acute stress could result in local CRH and nonpeptide neurotensin release which could contribute to myocardial pathophysiology through direct or indirect release of cardiac mast cell mediators.
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PMID:A neurotensin receptor antagonist inhibits acute immobilization stress-induced cardiac mast cell degranulation, a corticotropin-releasing hormone-dependent process. 976 51

In this paper a theoretical framework is offered for mental stress as a risk factor for the development of ischaemic heart disease (IHD). The development of IHD related to mental stress can be described as dependent on interaction between the following factors: (1) the presence of stressors, (2) activation of a receptor and transformation system (i.e. the central nervous system) and (3) physiological effector systems. Stressors are defined as external or internal, nomothetic or idiosyncratic and are exemplified. A prerequisite for the psychological stress reaction is the existence of a central nervous system in which stimuli are perceived, interpreted and responded to. The interaction between neocortex and paleocortex is discussed as well as the initiation of the cerebral stress reaction. Four physiological effector systems seem to be related to mental stress: (1) the autonomic nervous system (ANS), (2) the hypothalamic-pituitary-adrenal (HPA) axis, (3) the peripheral nervous system (PNS) and (4) the endorphin system. In the development of cardiovascular diseases the pathophysiological changes in the ANS and in the HPA axis play the most important roles.
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PMID:Mental stress and ischaemic heart disease: an underestimated connection. 985 45

Mental stress may induce myocardial ischemia and ventricular arrhythmia in patients with coronary artery disease, and cholinergic stimulation is a potential protective mechanism. The purpose of this study was to determine the effect of pyridostigmine bromide (PYR), a reversible cholinesterase inhibitor, on the cardiac responses to a mental stress challenge. Twelve healthy young volunteers were submitted to a mental stress test (arithmetic test) 2 hours after the oral administration of either placebo or PYR (45 mg) on two separate days, following a randomized crossover double-blind protocol. Heart rate was reduced after both placebo and PYR (p < 0.05), but the cardiac responses to the mental stress were lower with PYR (p < 0.05): mean RR interval (mean +/- SE)-placebo: 730 +/- 19 msec; PYR: 769 +/- 21 msec; Peak systolic pressure-placebo: 129 +/- 4 mmHg; PYR: 124 +/- 3 mmHg; Peak diastolic pressure-placebo: 92 +/- 3 mmHg; PYR: 89 +/- 4 mmHg; Mean rate-pressure product-placebo: 10,496 +/- 412 bpm x mmHg; PYR: 9,746 +/- 383 bpm x mmHg. In conclusion, 45 mg of pyridostigmine blunted the pressor and chronotropic responses to mental stress in healthy young subjects.
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PMID:Cholinergic stimulation with pyridostigmine blunts the cardiac responses to mental stress. 1021 43

This study examined the relationship between "emotional responsivity" (i.e., individuals who exhibit relatively large variations of self-reported tension levels) and myocardial ischemia. One hundred thirty-six patients with coronary artery disease underwent 48 hr ambulatory electrocardiographic (ECG) monitoring and laboratory mental stress testing using radionuclide angiocardiography. Compared with individuals characterized as low emotional responders, a higher proportion of individuals characterized as high emotional responders exhibited wall motion abnormalities in response to laboratory mental stress testing and were more likely to exhibit ECG ST-segment depression (> or = 1 mm for > or = 1 min) during routine daily activities. These results suggest that emotional responsivity may represent an individual difference characteristic that is associated with an increased likelihood of exhibiting myocardial ischemia in both the laboratory and the real-world setting.
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PMID:Emotional responsivity and transient myocardial ischemia. 1045 Jun 34

Twenty years ago, I became an "unstable patient", starting with a short episode of precordial discomfort and tiredness, ischemic ECG without enzymes, hypokinetic apex and no other signs. Following a week in bed and a lot of sleep, I went back to my usual lifestyle, refusing to undergo cineangiography or any hydraulic intervention. For ten years, the periodic controls showed no changes and I continued my intense activity under adequate therapy until another more severe episode occurred. Again, during a stressful and psychologically negative period, I experienced more severe precordial discomfort that was accentuated after minor psychological tension, whereas long and intense physical exercise was instead asymptomatic. The hypokinetic area was more extensive--no enzymes again--with a more severe ischemic ECG. My inability to face my psychological stress suggested surgical bypass, given the fact that since the Fifties, any type of intervention--even if nothing is vascularized--would nevertheless block pain and allow me to return to a normal lifestyle (denervation). At that time, cineangiography showed the occlusion of all three main coronary arteries. These occlusions had been there for years without an infarct and were obviously already compensated by adequate collateral circulation, as demonstrated by the normal lifestyle I had led with intense and long-lasting physical exercise. I returned to my regular activity, again mainly under anti-adrenergic stress therapy, and now, another ten years after surgery, I am still waiting for a third episode or something else. What have I learned from studying myself? I've learned that every ischemic patient has his own history and must learn how to face his own risks, the different patterns of so-called ischemic heart disease can not be theorized in a unique etiopathogenesis, the adrenergic system plays a major role in this disease, the "plumbing" vision is supported by reasons which have little to do with the knowledge--as yet incomplete--of the natural history of this disease, and the data obtained in years of research have been confirmed.
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PMID:[What I have learned by monitoring my own ischemia]. 1054 37

Mental stress testing has been proposed as a noninvasive tool to evaluate endothelium-dependent coronary vasomotion. In patients with coronary artery disease, mental stress can induce myocardial ischemia. However, even the determinants of the physiological myocardial blood flow (MBF) response to mental stress are poorly understood. Twenty-four individuals (12 males/12 females, mean age 49 +/- 13 yr, range 31-74 yr) with a low likelihood for coronary artery disease were studied. Serum catecholamines, cardiac work, and MBF (measured quantitatively with N-13 ammonia and positron emission tomography) were assessed. During mental stress (arithmetic calculation) MBF increased significantly from 0.70 +/- 0.14 to 0.92 +/- 0.21 ml x min(-1) x g(-1) (P < 0.01). Mental stress caused significant increases (P < 0.01) in serum epinephrine (26 +/- 16 vs. 42 +/- 17 pg/ml), norepinephrine (272 +/- 139 vs. 322 +/- 136 pg/ml), and cardiac work [rate-pressure product (RPP) 8,011 +/- 1,884 vs. 10,416 +/- 2,711]. Stress-induced changes in cardiac work were correlated with changes in MBF (r = 0.72; P < 0.01). Multiple-regression analysis revealed stress-induced changes in the RPP as the only significant (P = 0.0001) predictor for the magnitude of mental stress-induced increases in MBF in healthy individuals. Data from this group of healthy individuals should prove useful to investigate coronary vasomotion in individuals at risk for or with documented coronary artery disease.
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PMID:Regulation of myocardial blood flow response to mental stress in healthy individuals. 1066 65


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