Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-six patients with chronic stable angina were studied before and after coronary artery bypass grafting (CABG) to assess the prevalence and prognostic implications of asymptomatic myocardial ischemia obtained by ambulatory monitoring. Ambulatory monitoring performed during medical therapy before CABG detected 66 episodes of transient ischemia, 54 (82%) being asymptomatic. All patients were asymptomatic or with minimal symptoms 3 months after CABG. Additional ambulatory monitoring was performed for 36 hours. There were 39 episodes of silent ischemia detected in the 12 patients of group 1, whereas no episodes of ST-segment shift occurred in the 24 patients of group 2. Coronary artery bypass grafting reduced the frequency of transient ischemia by 41% (p less than 0.05) compared with medical therapy, whereas the number of ischemic episodes in group 1 increased from 23 during medical therapy to 39 episodes after CABG (41%, p less than 0.05). During a follow-up of 9 months, 8 cardiac events occurred: 6 in group 1 comprising sudden death (1), revascularization (2), and angina (3) and 2 in group 2, including revascularization (1) and angina (1) (p = 0.005). Kaplan-Meier analysis demonstrated that asymptomatic myocardial ischemia was correlated with a significant cumulative probability of cardiac events (p less than 0.025) and multivariate analysis of 11 variables showed that silent ischemia was the most powerful predictor of cardiac events (p less than 0.005). Silent ischemia was a forerunner for angina pectoris in some patients, whereas angina did not occur during the follow-up period in others. This study does not reveal whether or not these patients are at higher risk for cardiac events during long-term follow-up.
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PMID:Asymptomatic myocardial ischemia as a predictor of cardiac events after coronary artery bypass grafting for stable angina pectoris. 325 31

The results of current investigation suggest that a former clinical standby, namely, the presence or absence of angina, is no longer the principal prognostic factor for determining a patient's risk of cardiac events, including myocardial infarction. In a retrospective analysis, patients with chronic stable angina were compared on the basis of presence or absence of angina during ischemia detected by thallium imaging. Patients were similar in terms of risk factors, clinical characteristics and catheterization data. At 30 months of follow-up, the myocardial infarction rate was 22% in the silent group compared with 4% in the group with angina. Transient asymptomatic ischemia has prognostic value independent of other variables such as exercise stress testing or cardiac catheterization data. Future prognostic studies should be careful to include patient populations with similar characteristics; they also will need to provide protracted follow-up and utilize sensitive and reproducible diagnostic techniques.
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PMID:Prognosis in stable angina pectoris and silent myocardial ischemia. 328 19

Despite the widespread use of the exercise stress test in diagnosing asymptomatic myocardial ischemia, exercise radionuclide imaging remains useful for detecting silent ischemia in numerous patient populations, including those who are totally asymptomatic, those who have chronic stable angina, those who have recovered from an episode of unstable angina or an uncomplicated myocardial infarction, and those who have undergone angioplasty or received thrombolytic therapy. Studies show that thallium scintigraphy is more sensitive than exercise electrocardiography in detecting ischemia, i.e., in part, because perfusion defects occur more frequently than ST depression and before angina in the ischemic cascade. Thallium-201 scintigraphy can be performed to differentiate a true- from a false-positive exercise electrocardiographic test in patients with exercise-induced ST depression and no angina. The development of technetium-labeled isonitriles may improve the accuracy of myocardial perfusion imaging.
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PMID:Myocardial perfusion imaging for detection of silent myocardial ischemia. 328 20

Ambulatory electrocardiographic (ECG) monitoring of patients with chronic stable angina has demonstrated frequent and prolonged episodes of ischemic ST segment depression, but its clinical use requires an understanding of the components and extent of variability. Therefore, variations in the frequency and duration of episodes of ST segment depression were evaluated with ambulatory ECG recording at daily, weekly, and monthly intervals in 42 patients with chronic stable angina and known coronary artery disease. Data were analyzed with a nested analysis of variance design that yields estimates of variance components. From the estimates of variance components, power calculations and minimum significant percent reductions in frequency and duration of ischemia were derived. During 4,656 hours of ambulatory ECG monitoring, 1,262 episodes of ischemic ST segment depression were detected. The frequency of episodes was 6.3 +/- 0.45/24 hr (mean +/- SEM), and the duration of episodes was 18.3 +/- 2.8/24 hr. Because of variability over time, the ability to detect significant changes was dependent upon the number of subjects, length of monitoring period, and intervals between monitoring periods. In a clinical trial, for example, a sample size of 25 patients monitored for 48 hours with 1 week between control and test conditions would require a 65% reduction in frequency, whereas a sample size of 50 patients monitored under similar conditions would require a 46% reduction in frequency, to attribute the change with 90% power to a therapeutic intervention rather than to a spontaneous variation. When monitoring a single patient for 48 hours with 1 week or 1 month between control and repeat monitoring sessions, episodes of ischemic ST depression must be eliminated to detect significant therapeutic changes in ischemic activity at the 95% confidence level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Variability of transient myocardial ischemia in ambulatory patients with coronary artery disease. 338 11

Measures of the severity of angina pectoris, coronary anatomy, and left ventricular function are widely used to assess prognosis and determine management in patients with ischemic heart disease. However, recent evidence suggests that myocardial ischemia, with or without angina, is also a reliable prognostic sign. Studies using ambulatory ST-segment monitoring of patients with chronic stable angina out of the hospital have shown that the majority of episodes of transient myocardial ischemia are silent and surprisingly prolonged. Most episodes occur without the increase in heart rate noted during physical exertion. Characteristic abnormalities of regional myocardial perfusion have been observed using positron tomography during both painful and painless episodes of ischemia. Among these abnormalities is an absolute reduction in the perfusion to the poststenotic ischemic segment of myocardium. Episodes of ischemia can be induced in the hospital by a number of ordinary daily activities, including mental stress, cold, and cigarette smoking, and they often resemble episodes recorded from patients out of the hospital. These observations suggest that both an increased myocardial demand and a reduction in coronary blood flow may be important in the genesis of ischemia out of the hospital. If prospective studies confirm that myocardial ischemia is damaging, even in the absence of angina, investigation and treatment policies may need to be reevaluated. Results of ongoing clinical studies will show whether control of the total ischemic burden can prevent myocardial damage and improve the prognosis.
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PMID:Character and causes of transient myocardial ischemia during daily life. Implications for treatment of patients with coronary disease. 348 93

Myocardial uptake of the glucose analog F-18-2-fluoro-2-deoxy-D-glucose (FDG) was assessed by positron emission tomography in 6 normal volunteers, 7 patients with chronic stable angina and 22 patients with unstable angina at rest in fasting conditions. Regional myocardial perfusion was assessed by rubidium-82. The study was repeated a few days later after intravenous infusion of isosorbide dinitrate. FDG uptake was similar in control subjects and patients with stable angina (0.023 +/- 0.032 vs 0.012 +/- 0.008 mol/ml/min, p less than 0.42) but was about 4-fold higher on the average in patients with unstable angina (0.084 +/- 0.047, p less than 0.01). The severity of coronary obstructions in stable and unstable angina patients was similar. The increased uptake involved the whole heart, including areas not distal to critically stenosed vessels; it was not associated with reduced myocardial perfusion and was not related to a recent episode of transient ischemia as assessed by symptoms and by Holter monitoring. After continuous infusion of nitrates, FDG uptake was consistently and significantly reduced toward normal levels both in areas perfused by critically stenosed coronary arteries and by noncritically stenosed vessels.
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PMID:Beneficial effect of nitrates on myocardial glucose utilization in unstable angina pectoris. 350 Jun 29

Pathological and clinical studies have suggested that platelets have a role in the pathogenesis of unstable angina and myocardial infarction. However, the relation of platelet activation to episodic ischemia in patients with unstable angina is unknown. We assessed the biosynthesis of thromboxane and prostacyclin as indexes of platelet activation in patients with stable and unstable coronary disease by physicochemical analysis of metabolites in plasma and urine. Prostacyclin biosynthesis was markedly elevated in patients with acute myocardial infarction and correlated with plasma creatine kinase (r = 0.795; P less than 0.001). The largest rise in thromboxane synthesis was observed in patients with unstable angina, in whom 84 percent of the episodes of chest pain were associated with phasic increases in the excretion of thromboxane and prostacyclin metabolites. However, 50 percent of such increases were not associated with chest pain, possibly reflecting silent myocardial ischemia. These data indicate that platelet activation occurs during spontaneous ischemia in patients with unstable angina. The increment in prostacyclin biosynthesis during such episodes may be a compensatory response of vascular endothelium that limits the degree or effects of platelet activation. If so, biochemically selective inhibition of the synthesis or action of thromboxane A2 would be desirable in the treatment of unstable angina. In contrast, thromboxane inhibitors or antagonists would not be expected to be effective in patients with chronic stable angina, in whom there was no increase in the formation of thromboxane A2.
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PMID:Platelet activation in unstable coronary disease. 353 59

Ambulatory electrocardiographic (ECG) monitoring of ischemia in patients with coronary artery disease (CAD) provides a new technique for the assessment of ischemic activity and the evaluation of therapies outside of the hospital. Numerous studies have demonstrated that the majority of patients with CAD have episodes of symptomatic and asymptomatic ST segment depression during routine daily activities. Rubidium-82 positron-emission tomographic studies have provided evidence for decreased myocardial perfusion during these episodes of ST segment depression. The prognostic importance of asymptomatic ischemia has been shown in patients with unstable angina to be a marker for early unfavorable cardiac events. Preliminary results suggest a poorer outcome for those patients with chronic stable angina who show episodes of ischemia as well. Ambulatory monitoring studies suggest that total ischemic activity may be underestimated by conventional testing. Whether all ischemic activity detected by ambulatory monitoring requires treatment awaits further study.
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PMID:Characteristics and significance of ischemia detected by ambulatory electrocardiographic monitoring. 355 18

In 50 patients with chronic stable angina and in 10 asymptomatic young male volunteers, the behavior of S-wave amplitude was studied during episodes of ischemic ST-segment depression, both induced by exercise testing and occurring during ambulatory electrocardiographic monitoring. With exercise, all patients showed diagnostic ST-segment depression (0.16 +/- 0.05 mV) which, in 49, was associated with an increase in S-wave amplitude. No consistent changes in R-wave amplitude were observed. S-wave amplitude also increased in all control subjects during exercise, but the sum of R and S wave remained constant, while it increased in 42 patients. In the 10 study patients undergoing Holter monitoring we identified 170 episodes of ischemic ST-segment depression, of which 169 were associated with increased S-wave amplitude. Isolated increases in S-wave amplitude without ST-segment changes occurred in 3 of 4 normal subjects. Dipyridamole echocardiography revealed regional wall motion abnormalities in 12 of 21 patients; the changes were invariably associated with increased S-wave amplitude but not necessarily with diagnostic ST-segment depression. An increase in S-wave amplitude is almost invariably associated with subendocardial ischemia, sometimes in the absence of ST-segment changes; this sign could represent a sensitive (although less specific) additional marker of myocardial ischemia.
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PMID:Increase in S-wave amplitude during ischemic ST-segment depression in stable angina pectoris. 359 82

Circadian periodicity was examined in 68 patients with chronic stable angina and in 9 patients with Prinzmetal angina. The frequency and duration of transient ischemic episodes were determined from analysis of 1 or more 24-hour Holter recordings by the compact analog technique. Ninety percent of the episodes in both syndromes were silent; 80% of the episodes of Prinzmetal angina were associated with ST-segment elevation and all episodes of chronic stable angina had ST-segment depression. Ischemic episodes were shorter (3 +/- 2 vs 18 +/- 23 minutes, p less than 0.0005) but more frequent (21 +/- 18 vs 6 +/- 4 per 24 hours, p less than 0.0001) in patients with Prinzmetal angina than in those with chronic stable angina. In patients with chronic stable angina, both silent and painful episodes had a peak occurrence in the morning and early afternoon hours (between 8 AM and 3 PM); the fewest episodes were between 1 AM and 5 AM. This distribution was not random by chi-square test (p less than 0.001). Cosinor analysis of ischemic episodes periodicity showed the acrophase at 1 PM, which was not different from that (3 PM) of the circadian rhythmicity for heart rate. In case of Prinzmetal angina, the acrophase of heart rate changes was at 5 PM, but a clear periodicity in the distribution of the ischemic episodes was not found. These differences in the circadian periodicity may reflect differences in the mechanism of ischemia in chronic stable angina and in Prinzmetal angina and are likely to be of therapeutic significance.
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PMID:Circadian variation in occurrence of transient overt and silent myocardial ischemia in chronic stable angina and comparison with Prinzmetal angina in men. 363 Sep 31


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