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)

Angina pectoris is chest discomfort associated with myocardial ischemia. When coronary blood flow is inadequate to meet myocardial tissue demand, lactate accumulates, resulting in diastolic and systolic left ventricular dysfunction. This leads to ST-segment abnormalities and eventually to angina pectoris. Angina, most commonly a pressure-type sensation in the midanterior chest precipitated by exercise, stress, or cold, typically lasts 1-5 minutes and is alleviated by rest or nitroglycerin. Diagnostic studies to assess myocardial ischemia include treadmill exercise testing, Holter monitoring, and coronary angiography. Treadmill exercise testing has a relatively low accuracy for diagnosing coronary artery disease. This can be improved by combining exercise with thallium-201 imaging, two-dimensional echocardiography, or positron emission tomography (PET). Thallium-201 scintigraphy and exercise echocardiography have reported sensitivities of 70-85% and specificities of 50-60% when applied to low-risk, asymptomatic populations. PET scanning has a high predictive accuracy (sensitivity 90%, specificity 90-95%) and is more useful as a screening test; it can also assess the functional significance of coronary artery stenoses and differentiate viable myocardium from infarcted tissue. Holter monitoring is too insensitive and nonspecific to be used as a screening test for coronary artery disease; it can, however, assess the total ischemic burden in patients with known coronary artery disease and correlate symptoms and ST-segment abnormalities during episodes of pain at rest. Coronary angiography has been the gold standard for diagnosing coronary artery stenoses. Quantitative angiography has improved the assessment of coronary artery narrowing but is still limited in evaluating coronary blood flow. Doppler flow studies provide useful information regarding coronary flow reserve. Myocardial ischemia as a cause of chest pain is determined by evaluating the clinical characteristics consistent with angina, correlating electrocardiographic abnormalities with perfusion defects or wall motion abnormalities, and determining the extent and functional significance of coronary artery stenoses by coronary angiography.
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PMID:Excluding heart disease in the patient with chest pain. 159 64

Although careful history taking and physical examination seem to have been supplanted in some parts of modern medicine by expensive and high-tech laboratory tests, evaluation of chest pain is an exception. It still depends on careful attention to the basics of a directed line of history taking and physical examination. Careful correlation of the details elicited with the pathophysiology of myocardial ischemia leads the astute clinician through the maze of various causes of chest pain to the proper final diagnosis.
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PMID:Evaluation of chest pain. Back to the basics of history taking and physical examination. 160 48

Validation of the London School of Hygiene (Rose) Questionnaire with objective measures of myocardial ischemia is incomplete. Therefore, we compared the Rose Questionnaire with exercise thallium-201 myocardial scintigraphy in 147 male and 97 female patients with chest pain referred for clinical exercise testing. Of those with "Rose Questionnaire angina", 26% of the females and 73% of the males had positive thallium-201 scans. Negative results on both the Rose Questionnaire and thallium-201 scintigraphy were observed in 71% of the females and 47% of the males. The sensitivity of the Rose Questionnaire was similar in females (41%) and males (44%). The specificity was 77% in males, while in females it was significantly lower at 56%. The specificity values reflect the higher (p less than 0.05) prevalence of "false positive" Rose Questionnaire results in females (75%) compared with males (27%). In addition, males had a greater (p less than 0.05) number of "false negative" results (53%) than females (29%). The accuracy of the Rose Questionnaire for myocardial ischemia was 0.19 in females, 0.48 in males, and 0.29 overall when including both males and females. Our results indicate a generally poor relationship between Rose Questionnaire angina and thallium-201 scintigraphy, an objective measure of myocardial ischemia in patients with chest pain referred to clinical exercise testing. Further, there are gender-specific differences in this relationship between the questionnaire and exercise thallium-201 imaging.
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PMID:Comparison of "Rose Questionnaire Angina" to exercise thallium scintigraphy: different findings in males and females. 161 50

The objective of this study was to assess whether a 10-d treatment with oral theophylline improves the working capacity in patients with ischaemic heart disease, and to compare theophylline with conventional anti-anginal therapy. Twenty-four patients with stable effort-induced angina were included in the study. The patients received double-blind treatment in randomized order during 4 consecutive 10-d periods, separated by a 4-d wash-out period, with (a) metoprolol durules 200 mg once daily + theophylline durules 300 mg b.i.d., (b) theophylline + placebo, (c) metoprolol + placebo, and (d) placebo alone. At the end of each period a supine exercise stress test was performed. Maximal workload increased to 111 +/- 6 W during treatment with theophylline, compared to 106 +/- 6 W during placebo treatment (P = 0.01). Metoprolol increased the maximal workload to 117 +/- 6 W (P less than 0.001). The effects of metoprolol and theophylline were additive, and the working capacity increased to 123 +/- 7 W during combined therapy. Neither the degree of ST-depression nor the scoring of chest pain at maximal workload differed between the four treatment regimens. An improved working capacity was shown in patients with stable effort-induced angina pectoris during long-term theophylline treatment. The effect was additive to that of beta-blockade.
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PMID:Improved working capacity in patients with ischaemic heart disease during a 10-day treatment with oral theophylline. 164 Jan 92

Among the numerous variables measured by the electrocardiogram during exercise little attention has been paid to the "septal" Q wave. We examined changes of the "septal" Q wave amplitude during exercise in 43 patients with chest pain. Coronary arteriography showed significant changes in 23 patients and normal arteries in 20. The Q wave amplitude was measured in leads V4-V6 immediately before and at the peak of submaximal bicycle exercise. The amplitude of "septal" Q wave increased during exercise in 11 (55%) patients, and decreased or was not changed in 9 (45%) of the normal subjects (p greater than 0.05). However, the Q wave amplitude increased in 6 (26%) patients, and decreased or was not changed in 17 (74%) patients with ischaemic heart disease (p less than 0.05). Thus, the sensitivity of Q wave analysis in the detection of coronary disease was 74% (p less than 0.05), but specificity was only 55% (p greater than 0.05).
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PMID:[The importance of changes in the septal Q wave induced by exercise in the detection of ischemic heart disease]. 164

In the Thrombolysis in Myocardial Infarction (TIMI) Phase II trial, patients received intravenous recombinant tissue-type plasminogen activator (rt-PA) and were randomized to either a conservative or an invasive strategy. Within this study, the effects of immediate versus deferred beta-blocker therapy were also assessed in patients eligible for beta-blocker therapy, a group of 1,434 patients of which 720 were randomized to the immediate intravenous group and 714 to the deferred group. In the immediate intravenous group, within 2 hours of initiating rt-PA metoprolol was given (5 mg intravenously at 2-minute intervals over 6 minutes, for a total intravenous dose of 15 mg, followed by 50 mg orally every 12 hours in the first 24 hours and 100 mg orally every 12 hours thereafter). The patients assigned to the deferred group received metoprolol, 50 mg orally twice on day 6, followed by 100 mg orally twice a day thereafter. The therapy was tolerated well in both groups and the primary end point, resting global ejection fraction at hospital discharge, averaged 50.5% and was virtually identical in the two groups. The regional ventricular function was also similar in the two groups. Overall, there was no difference in mortality between the immediate intravenous and deferred groups, but in the subgroup defined as low risk there were no deaths at 6 weeks among those receiving immediate beta-blocker therapy in contrast to seven deaths among those in whom beta-blocker therapy was deferred. These findings for a secondary end point in a subgroup were not considered sufficient to warrant a recommendation regarding clinical use. There was a lower incidence of reinfarction (2.7% versus 5.1%, p = 0.02) and recurrent chest pain (18.8% versus 24.1%, p less than 0.02) at 6 days in the immediate intravenous group. Thus, in appropriate postinfarction patients, beta-blockers are safe when given early after thrombolytic therapy and are associated with decreased myocardial ischemia and reinfarction in the first week but offer no benefit over late administration in improving ventricular function or reducing mortality.
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PMID:Immediate versus deferred beta-blockade following thrombolytic therapy in patients with acute myocardial infarction. Results of the Thrombolysis in Myocardial Infarction (TIMI) II-B Study. 167 47

Although the efficacy of long-term administration of antithrombotic agents in unstable angina has been established, short-term effects on myocardial ischemia are unknown. A retrospective analysis was performed in 47 patients undergoing three-channel continuous ST segment monitoring as part of a multicenter trial using esmolol in unstable angina, in which 20 patients received a continuous heparin infusion during the initial assessment of chest pain. Concomitant medications included calcium channel blockers, beta-adrenergic blockers, nitrates, and aspirin in the majority of patients. Clinical variables between the heparin and no heparin groups were similar, except for fewer males and fewer total artery occlusions in the heparin group. No significant differences in the incidence or duration of ischemia were found in a 36 +/- 16 hour monitoring period. Forty percent of the heparin group had 35 episodes of ischemia with a mean of 11 +/- 10 minutes per episode and a total ischemic time of 48 +/- 39 minutes per patient with ischemia. Forty-four percent of the no heparin group had 47 episodes of ischemia with a mean of 13 +/- 13 minutes per episode and a total ischemic time of 58 +/- 47 minutes per patient with ischemia. Multiple linear regression analysis to adjust for intergroup differences did not alter the results. Eighty-five percent of all episodes were asymptomatic. Clinical events, such as episodes of chest pain, emergency coronary arteriography, or coronary revascularization, were also similar between groups. Thus the short-term administration of heparin did not alter the incidence or duration of ischemia in patients with unstable angina.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Failure of adjuvant heparin to reduce myocardial ischemia in the early treatment of patients with unstable angina. 168 22

To evaluate the long-term prognosis of patients with acute chest pain, prospective clinical data and long-term follow-up data (mean 30.1 +/- 9.4 months) were collected for 1,956 patients who presented to the emergency department of an urban teaching hospital with this chief complaint. During follow-up of the 1,915 patients who were discharged alive from the emergency department or hospital, there were 113 (6%) cardiovascular deaths. No differences were detected in the post-discharge cardiovascular survival rates after 3 years of experience with patients who were discharged from the emergency department with a known prior diagnosis of angina or myocardial infarction (89%) and patients who had been admitted and found to have acute myocardial infarction (85%), angina (87%), or other cardiovascular diagnoses (87%). Patients who were discharged from either the hospital or the emergency department without cardiovascular diagnoses had an excellent prognosis. Multivariate Cox regression analysis identified 5 independent correlates of cardiovascular mortality after discharge: age, prior history of coronary disease, ischemic changes on the emergency department electrocardiogram, congestive heart failure and cardiogenic shock. These findings indicate that the postdischarge cardiovascular mortality of patients with chest pain who are discharged from the emergency department with a known history of coronary disease is similar to that of admitted patients with angina or myocardial infarction. These data suggest that the same types of prognostic evaluation strategies that have been developed for admitted patients with ischemic heart disease should also be considered when such patients present to the emergency department but are not admitted.
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PMID:Long-term survival of emergency department patients with acute chest pain. 173 49

To verify whether plasma beta-endorphin and bradykinin affects the pathophysiology of myocardial ischemia and the perception of cardiac pain, 35 patients with coronary artery disease were subjected to treadmill testing and 48-hour Holter ECG monitoring to measure their pain thresholds. Patients were divided into two groups during exercise testing: group 1 (N = 19) who had ST segment depression, and group 2 (N = 16), who had chest pain. Both groups were then compared with 12 age-matched control subjects. Pain thresholds were measured after Holter ECG monitoring, and blood samples were drawn before and immediately after exercise. No statistical differences were noted between groups 1 and 2 with regard to the severity of myocardial ischemia as assessed by ST segment depression or exercise tolerance time. The frequency of the episodes of silent myocardial ischemia in group 1 was found to be significantly (p less than 0.05) higher than that in group 2. The duration of the episodes of silent myocardial ischemia in group 1 was 41.9 minutes (range 3 to 343 minutes), which was significantly (p less than 0.05) longer than that in group 2 (11.5 minutes; range 0 to 74). The pain threshold in group 1 was a statistically (p less than 0.05) higher value than that in group 2. Although the resting plasma beta-endorphin level in group 1 was not statistically significantly different from values in either group 2 or the control group, during exercise the plasma beta-endorphin levels in both group 1 and the control group were significantly (p less than 0.05) elevated in comparison with their resting levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differences in plasma beta-endorphin and bradykinin levels between patients with painless or with painful myocardial ischemia. 173 63

Recently, the presence of vasospasm in small coronary arteries is speculated in animals and humans. A 40-year-old female patient complained of chest pain at rest. Left ventriculogram showed normal wall motions. Left and right coronary arteries were also normal. After methylergometrine maleate was selectively administered to a right coronary artery, she complained of chest pain, and ST-segment elevation was detected in leads II, III, and aVF of ECG. Right coronary arteriography was performed immediately, but no coronary stenosis was found. The next day, methylergometrine maleate was again administered intravenously and the patient complained of chest pain, but no ischemic changes were observed in ECG. Thallium-201 myocardial scintigraphy followed immediately. Apical perfusion defect was detected in stress image. In the delayed image, it showed complete redistribution. Three days later, catheterization and scintigraphy were performed at the same time. When methylergometrine maleate was administered to the left coronary artery, she complained of chest pain within a few minutes of the injection; however, ECG remained unchanged. 201Tl myocardial scintigraphy was performed immediately. In the stress image, it showed apical perfusion defect as shown in the intravenous methylergometrine maleate injection study. It also showed complete redistribution in the delayed image. Apical perfusion defect can be attributed to myocardial ischemia of left coronary artery, which are too small to be detected by conventional coronary arteriography. Vasospasm in small coronary arteries may be involved in this phenomenon.
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PMID:Angina pectoris due to possible vasospasm of small coronary arteries. 174 12


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