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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

This study was performed to test the existing notion that an increased muscle sympathetic nerve discharge is part of the underlying mechanism for the chronic pain syndrome of primary fibromyalgia. Muscle sympathetic nerve activity was recorded in the peroneal nerve in eight patients with primary fibromyalgia and eight age-matched controls. No difference in baseline sympathetic activity was observed between patients and controls. Furthermore, patients did not show exaggerated sympathetic nerve responses to static handgrip or jaw muscle contractions, postcontraction ischemia or mental stress. Thus the results do not indicate muscle sympathetic nerve overactivity in primary fibromyalgic patients.
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PMID:Do patients with primary fibromyalgia have an altered muscle sympathetic nerve activity? 159 59

To explore the effect of beta-adrenergic blockade on low heart rate-related (mental stress) ischemia, 19 patients with coronary artery disease were randomized into a double-blind crossover trial of metoprolol, 100 mg twice daily, and underwent serial mental stress/bicycle exercise studies. Mental stress-induced wall motion abnormalities occurred at a lower heart rate than exercise-induced wall motion abnormalities during placebo administration (81 +/- 16 vs. 123 +/- 20 beats/min, p less than 0.05). Metoprolol reduced the mean magnitude of exercise-induced wall motion abnormalities (2.8 +/- 2.0 vs. 1.6 +/- 2.4, p = 0.003); improvement was related to the magnitude of hemodynamic beta-blockade effect. Metoprolol did not significantly reduce the mean magnitude of mental stress-induced wall motion abnormalities (3.0 +/- 2.2 vs. 2.6 +/- 2.2), although individual responses predominantly either improved (50%) or worsened (29%). Unlike exercise, the magnitude of hemodynamic beta-blockade did not predict mental stress response and metoprolol did not block mental stress-induced blood pressure elevations. Patients with abolition of exercise-induced ischemia were more likely to have reduction of mental stress-induced ischemia. Patients whose ischemia worsened with metoprolol during mental stress had more easily inducible ischemia, as assessed by exercise-induced placebo wall motion abnormality, chest pain and prior myocardial infarction. Beta-blockade was associated with a lowering of ischemia-related hemodynamic thresholds compared with placebo. These results suggest that beta-blockade has a variable effect on low heart rate-related ischemia that may be due to a lack of effect on mental stress-induced blood pressure elevation in patients with easily induced ischemia or to effects on coronary vasomotor tone, or both.
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PMID:Effect of beta-blockade on low heart rate-related ischemia during mental stress. 167 34

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

PD--the electric potential difference across the gastric mucosa--is a variable used to describe the gastric mucosal integrity and function. A new, reliable, and easily applied method for gastric PD measurements corrected for the disturbing liquid junction potentials between gastric juice and the PD measuring probe is presented. PD is measured with the gastric lumen negative, and a numeric reduction in PD is used as an expression of an injured mucosal condition. A reduced gastric PD is found along with a reduced gastric mucosal blood flow after intravenous indomethacin in anesthetized dogs. Increasing the FFA/albumin ratios in mini-pigs causes vasoconstriction and PD reduction. Short hypoxia and selective gastric ischemia cause a reversible PD reduction and no morphologic changes in anesthetized dogs, but ischemia for 1 h causes more permanent changes in PD, pH, and morphology. This damage can be reduced by allopurinol pretreatment, possibly due to the inhibition of oxygen-derived free radical formation. Gastric PD and pH were measured in volunteers and duodenal ulcer patients during Stroop's color word conflict test, in which mental stress causes sympathetic activation. A PD reduction and a pH increase were found along with stress induction, thereby indicating an influence of mental stress on stomach mucosal function. It is concluded that gastric PD measurement may be useful in ulcer pathogenetic research, and a sufficient gastric mucosal blood flow is stressed as being important for the mucosal defense.
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PMID:Gastric potential difference measurements. The gastric mucosal integrity and function studied with a new method for measurement of the electric potential difference across the stomach wall. 192 6

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

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

The psychophysiological responses to two mental stress tests (mental arithmetic and an interactive concentration task) were assessed in 168 unmedicated, male, postinfarction patients 36-69 years old. Patients also completed a standard battery of psychological tests. Psychophysiological responses were generally unrelated to age and education. Comparison of patients scoring high (more than 75%) and low (less than 25%) relative to the normal population on psychological measures indicated that heart rate and blood pressure responses to mental stress tests were significantly greater in those reporting low than in those reporting high neuroticism. The study population was subsequently divided into high, medium, and low cardiovascular responders on the basis of rate-pressure product reactions to the two stress tests. The three cardiovascular response groups did not differ in age, interval between myocardial infarction and stress testing, ejection fraction, incidence of exercise-induced ischemia, or ischemic signs during Holter monitoring. However, the high cardiovascular responders were more likely to manifest possible or definite electrocardiographic signs of ischemia or significant arrhythmia during mental stress testing than were the medium or low cardiovascular responders (50% versus 19.6% and 7%, respectively). High cardiovascular responders also reported lower levels of trait anxiety, neuroticism, psychophysiological symptoms, and depression.
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PMID:Psychophysiological stress testing in postinfarction patients. Psychological correlates of cardiovascular arousal and abnormal cardiac responses. 200 27

Incidence and mechanisms of psychological stress-induced myocardial ischemia were investigated in a population of 63 patients using mental arithmetic. Fifty subjects (group 1) were selected as a consecutive population of ischemic patients with electrocardiographic documentation of ischemia at rest, on effort, or both. Mental arithmetic induced increases in heart rate, blood pressure, and rate-pressure product in all patients. Transient ischemic electrocardiographic changes occurred in 22 patients (44%; positive mental arithmetic), the majority of whom had both resting and exercise angina. In negative mental arithmetic tests, peak rate-pressure product was always lower than that achieved during exercise (mean +/- SD, 11.9 +/- 3 versus 21.3 +/- 5, p less than 0.01). Of the 22 patients with positive mental arithmetic tests, ischemia occurred in only six, at a rate-pressure product equal to or more than the one achieved during exercise (21.1 +/- 5 versus 19.4 +/- 4, p less than 0.01), suggesting an increase in myocardial O2 demand exceeding the limited increase in flow; in the remaining 16 patients, rate-pressure product values were significantly lower (14.8 +/- 3 versus 22.7 +/- 6, p less than 0.01), suggesting a primary reduction in coronary blood flow that is probably related to an increase in coronary tone. To assess the possible site of such a vasoconstriction, the effect of mental arithmetic on large coronary artery diameter was tested in 13 additional unselected patients (group 2) undergoing coronary angiography for a chest pain syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary dynamics and mental arithmetic stress in humans. 200 34


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