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

The total number of outpatient visits to 10 hospital emergency rooms declined 64 per cent and emergency admissions 35 per cent immediately after the February 1978 blizzard in Rhode Island; both quickly returned to normal levels. Three days after the storm, admissions for myocardial infarction increased markedly. Total mortality and ischemic heart disease deaths showed a considerable increase for the five-day period following the blizzard. The physical and psychological stress of the blizzard probably precipitated cardiac deaths in susceptible individuals.
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PMID:Blizzard morbidity and mortality: Rhode Island, 1978. 48 59

Twelve different approaches to laboratory diagnosis of angina pectoris are reviewed here. They employ no fewer than seven different means of intentionally provoking a disparity between myocardial requirement and supply: dynamic exercise, hypoxia, prandial stress, raised systemic vascular resistance, paced tachycardia, mental stress, and exposure to normal environment. Of these, only dynamic exercise and the diverse combinations of stresses in the normal environment are capable of altering the heart's oxygen requirement-supply ratio threefold or more, accounting for the successful results from tests using these means of stress. The reviewed tests use three different means of detecting myocardial ischemia provoked by stress: electrocardiography to indicate impaired ventricular repolarization, indirect graphic records sensitive to impairment of mechanical ventricular function, and detection of insufficient myocardial perfusion patterns by radioactive tracer. The latter approach is particularly appealing because it directly reflects the pathophysiologic anomaly of interest. It should be remembered, however, that the basic differences in these methods of detecting ischemia make them complementary to each other and encourage their use in combination for improved diagnostic sensitivity.
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PMID:Interesting approaches to the diagnosis of angina pectoris. 63 19

Information obtained during the past decade suggests that the onset of myocardial infarction and sudden cardiac death is frequently triggered by daily activities. The importance of physical or mental stress in triggering coronary thrombosis is supported by finding that (1) the frequencies of the onset of myocardial infarction, sudden cardiac death, and stroke show marked circadian variations, with similar increases in the period from 6 AM to noon; (2) the frequency of transient myocardial ischemia shows a similar increase in the morning, and episodes are often preceded by mental or physical triggers; (3) a ruptured atherosclerotic plaque, often nonobstructive by itself, lies at the base of most coronary thrombi; (4) a number of physiologic processes that could lead to plaque rupture, a hypercoagulable state, or coronary vasoconstriction, are accentuated in the morning; and (5) aspirin and beta-adrenergic blocking agents that affect certain of these processes have been shown to prevent disease onset. The hypothesis presented is that occlusive coronary thrombosis occurs when (1) an atherosclerotic plaque becomes vulnerable to rupture; (2) mental or physical stress causes the plaque to rupture; and (3) increases in coagulability or vasoconstriction, triggered by daily activities, contribute to complete occlusion of the coronary artery lumen. Recognition of the circadian variation--and the possibility of frequent triggering--of the onset of acute disease suggests the need for pharmacologic protection of patients during the vulnerable periods and provides clues to the mechanism of disease onset, the investigation of which may lead to improved methods of prevention.
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PMID:Triggering and hourly variation of onset of arterial thrombosis. 134 90

Episodes of ST depression are closely related to transient decreases in regional myocardial perfusion during physical or mental stress. At the onset of these events, there is transient constriction of atherosclerotic stenoses, with an increase in myocardial demand as reflected by increases in heart rate and blood pressure. Recent research has shown that normal epicardial coronary arteries respond to these provocations and to increasing blood flow with progressive vasodilation. In contrast, atherosclerotic vessels lose this ability to dilate and may show paradoxical constriction. This abnormal constriction parallels the response of the arteries to acetylcholine, which can be used to assess the ability of the coronary endothelium to regulate vasodilation. The loss of endothelium-dependent vasodilation appears to be an important functional manifestation of coronary atherosclerosis and a potential triggering mechanism for transient ischemia. Dysfunctional endothelium may also result in a procoagulant surface, with cell adherence and local thrombus formation. Restoration of normal endothelial function is likely to emerge as an important therapeutic objective in the management of myocardial ischemia and coronary atherosclerosis.
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PMID:New insights into the management of myocardial ischemia. 144 5

Platelet function can be assessed by various techniques in vitro or in vivo, but methodological problems in the field are considerable. By use of the conventional in vitro technique (Born aggregometry), it has been shown that sympathoadrenal activation in vivo (e.g., mental stress, epinephrine infusions, exercise, and surgical stress) may result in either enhanced or reduced platelet aggregability in vitro. In vivo measures of platelet function (platelet counts, size distribution, and aggregability, as reflected by filtragometry ex vivo) more consistently indicate platelet activation during stress. Platelet-specific proteins in plasma are less readily affected by stress. Elevations of circulating epinephrine do not seem to explain proaggregatory effects of stress. Aggregatory responses to epinephrine may be enhanced by propranolol in vitro, because of unopposed alpha 2-stimulation (beta 2-stimulation attenuates aggregation). Other in vitro effects of beta-blockade seem to be related to nonspecific effects at very high concentrations. Studies of the effects of beta-blockade in vivo have yielded conflicting data. Some studies suggest that beta 2-blockade may reduce platelet cAMP and enhance aggregability in vitro; other studies show that propranolol attenuates platelet aggregability, particularly in patients with ischemic heart disease. There is, however, a need for well-conducted studies assessing platelet function in vivo during beta-blockade to evaluate whether platelet responses contribute to favorable effects of beta-blockade in unstable angina, for example, or after myocardial infarction. Methodological developments are needed to better understand platelet function in vivo in humans. Available data suggest that stress enhances and beta-blockade reduces platelet function. This may influence thrombus formation in the short term and atherosclerosis in the long term.
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PMID:Effects of stress and beta-blockade on platelet function. 168 10

In patients with coronary artery disease, radionuclide investigations have documented a high incidence of mental stress-induced myocardial ischemia in the absence of significant electrocardiographic changes and/or angina. To investigate the causes of the low electrocardiographic sensitivity, we recorded body surface maps during mental arithmetic in 22 normal volunteers and 37 postinfarction patients with residual exercise ischemia. Myocardial perfusion was studied with thallium-201 or technetium-99 (SESTAMIBI) planar scans. In 14 patients, body surface maps were also recorded during atrial pacing at the heart rate values achieved during mental stress. While taking the body surface maps, the area from J point to 80 msec after this point (ST-80) was analyzed by integral maps, difference maps, and departure maps (the difference between each patient's difference map and the mean difference map for normal subjects). The body surface mapping criteria for ischemia were a new negative area on the integral maps, a negative potential of more than 2 SD from mean normal values on the difference maps, and a negative departure index of more than 2. Scintigraphy showed asymptomatic myocardial hypoperfusion in 33 patients. Eight patients had significant ST segment depression. The ST-80 integral and difference maps identified 17 ischemic patients. Twenty-four patients presented abnormal departure maps. One patient presented ST depression and abnormal body surface maps without reversible tracer defect. In 14 of 14 patients, atrial pacing did not reproduce the body surface map abnormalities. The analyses of the other electrocardiographic variables showed that in patients with mental stress-induced perfusion defects, only changes of T apex-T offset (aT-eT) interval in Frank leads and changes of maximum negative potential value of aT-eT integral maps significantly differed from those of normal subjects. Our results confirm the low electrocardiographic sensitivity for detecting mental stress-induced myocardial hypoperfusion in postinfarction patients. ST analysis in the body surface map increases the information content of the electrocardiographic signal. T wave analysis appears to offer fewer diagnostic advantages.
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PMID:Electrocardiographic markers of ischemia during mental stress testing in postinfarction patients. Role of body surface mapping. 182 36

In asymptomatic patients the importance of silent ischemic ST-T wave changes on Holter monitoring is known to be a significant predictive variable for one-year mortality of postmyocardial infarction patients. This case report represents the uses of ambulatory ECG to detect ischemic ST changes in patients who have had recent strokes. The cases reported here of silent myocardiac ischemia in stroke patients reflect previous reports in which 70% of the ischemic episodes in patients with symptomatic coronary artery disease are not associated with angina and in which approximately 10% to 15% of acute myocardial infarctions are silent. We now believe that the incidence of "silent" ischemia may be precipitated in poststroke patients during their rehabilitation program. This belief is supported by two main factors. First, a high level of personally relevant mental stress exists which activates the sympathoadrenal system, which may lead to myocardial ischemia. Second, some stroke patients become aphasic and are unable to communicate adequately even if they experience angina symptoms. We have found that poststroke, most patients could not undergo exercise treadmill testing secondary to a variety of factors: inability to coordinate limbs, poor endurance, inability to follow directions, and/or lack of attention. We now propose that 24-hour monitoring for ST-T wave changes poststroke should be considered as part of a vigorous investigation for myocardial ischemia during the rehabilitation of these patients because they have an increased risk of cardiac morbidity.
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PMID:Silent myocardial ischemia during rehabilitation for cerebrovascular disease. 198 25

To assess the prevalence of mental stress-induced myocardial ischemia and investigate the pathogenetic mechanisms by which emotional stress may induce myocardial ischemia, we studied 372 patients with angina pectoris who underwent mental arithmetic and exercise stress testings. Hyperventilation tests were also performed in 176 patients, and 340 patients underwent coronary arteriography. Sixty-one patients showed significant ST segment abnormalities during mental arithmetic and exercise stress testings (group 1). Two hundred eleven patients had negative responses to mental stress but positive exercise tests (group 2), whereas both tests were negative in 100 patients (group 3). Mental stress induced significant increases in heart rate and systolic blood pressure in the three groups of patients; however, group 1 patients had higher increases in rate-pressure product (mm Hg x beats/min) than group 2 and group 3 patients (14,909 +/- 3,894 versus 12,985 +/- 2,900 versus 12,724 +/- 4,400 mm Hg x beats/min, p less than 0.01). Group 1 patients had shorter exercise durations than group 2 or group 3 (4.06 +/- 1.55 versus 7.65 +/- 3.07 versus 13.9 +/- 5.31 minutes, p less than 0.01), although rate-pressure products at peak exercise were similar in groups 1 and 2 (20,277 +/- 6,058 versus 20,768 +/- 3,864, p = NS) and significantly higher in group 3 (26,221 +/- 7,100/mm Hg x beats/min, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mental stress as a provocative test in patients with various clinical syndromes of coronary heart disease. 200 19

Recent research examining the effects of mental stress on left ventricular wall motion and/or ejection fraction has used four techniques to measure contractile function: radionuclide ventriculography, a stationary nuclear probe, two-dimensional echocardiography, and an ambulatory radionuclide left ventricular function monitor. This research has consistently revealed that mental stress-induced myocardial ischemia occurs frequently during laboratory stress testing, particularly among patients with exercise-induced ischemia. This ischemia is usually silent, occurs at low heart rate elevations but with significant blood pressure increases compared with exercise-induced ischemia, and is frequently not detected when electrocardiographic markers are used alone. Exploration of factors underlying differences between mental stress- and exercise-induced ischemia has provided a means for studying the complex pathophysiology of myocardial ischemia.
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PMID:Ventricular responses to mental stress testing in patients with coronary artery disease. Pathophysiological implications. 200 21

We tested the hypothesis that psychological stress testing in the clinical laboratory provokes changes in the sympathetic and vagal activities regulating heart rate that can be assessed noninvasively using spectral analysis of RR variability. To account for the effects on respiration produced by talking, this study was performed with two different procedures: the I.K.T. (i.e., a computer-controlled mental task that is performed in silence and does not entail human confrontation) and a stressful interview. Finally, we assessed whether ischemic heart disease modifies the spectral changes induced by psychological stress by comparing a group of healthy subjects (age, 38 +/- 2 years) with a group of patients (age, 52 +/- 3 years) recovering from 1-month-old myocardial infarctions. The findings indicate that psychological stress induced marked changes in the sympathovagal balance, which moved toward sympathetic predominance. The low-frequency component of RR variability, a marker of sympathetic activity, increased from 58 +/- 5 normalized units (NU) to 68 +/- 3 NU with the I.K.T. and to 76 +/- 3 NU with the interview. This increase was absent in the group of post-myocardial infarction patients. However, arterial pressure increased significantly in both groups of subjects. The possibility of age playing an important role in determining the differences observed was disproved by the findings of a marked increase in low frequency with mental stimuli in an additional group of borderline hypertensive subjects with ages (55 +/- 2 years) comparable to those of post-myocardial infarction patients.
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PMID:Sympathovagal interaction during mental stress. A study using spectral analysis of heart rate variability in healthy control subjects and patients with a prior myocardial infarction. 200 29


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