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)

From March 1986 through October 1987, elective diagnostic coronary angiography was performed in 1,542 consecutive patients. Among them, silent myocardial ischemia was investigated based on the histories in their medical questionnaires, the results of exercise stress tests and the presence of significant coronary artery stenosis. Exercise-induced silent myocardial ischemia was documented only in 3% in the non-infarction group, and in 2.1% of those with significant coronary stenosis. However, asymptomatic post-infarction patients comprised 33%. With regard to the extent of coronary artery disease in the non-infarction group, one-, two- and three-vessel disease accounted for 42%, 29% and 29%, respectively (NS). However, one-vessel disease was predominant among the asymptomatic post-infarction patients (p < 0.01). Among the non-infarction group, those with asymptomatic coronary stenosis had a relatively high incidence of diabetes mellitus (p < 0.01), but such a difference was not significant among the asymptomatic post-infarction patients. Among the post-infarction group, many of those who had chest pain during exercise showed redistribution on exercise thallium scintigraphy. Angioplasty was performed in most of the patients in the asymptomatic group, but its long-term effects are yet unknown.
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PMID:[Angiography of silent myocardial ischemia]. 184 31

Myocardial ischemia must be the first concern of every emergency physician in evaluating chest pain in the adult patient. Any suspicion of myocardial ischemia must be promptly evaluated and admitted. The American College of Emergency Physicians has recently published a standards document on the care of chest pain in the adult patient. The emergency physician must be familiar with this document. Once myocardial ischemia and other life-threatening causes are ruled out, one can consider that cervical disk disease may be the cause of chest pain. The authors present two cases of patients who presented to the Emergency Department with signs and symptoms consistent with cardiac ischemia. Both patients were found to have herniated cervical disks. Subsequent surgical repair completely relieved their symptoms. Evaluation of the literature reveals that this entity was well described from 1950 to the 1960s. Most recent discussions do not mention disk herniation as even an infrequent cause of chest pain. If there is no life-threatening disease present, one should consider cervical disk disease.
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PMID:Herniated cervical disk presenting as ischemic chest pain. 186 3

To evaluate the prognostic significance of scintigraphic silent myocardial ischemia (SMI) detected by stress thallium scan in patients with myocardial infarction (MI), we performed a retrospective investigation on cardiac events (CE) during a two-year follow-up period in 149 patients with MI within three months of onset (34 +/- 19 days). SMI was defined as asymptomatic redistribution (RD) in the infarcted area. The patients were divided into three groups based on results of stress thallium scan as follows: 50 patients with neither chest pain nor RD (Group A), 46 patients with SMI (Group B) and 53 symptomatic patients (Group C). In comparison of the incidence of CE, which included cardiac death, recurrent MI, chronic heart failure, angina pectoris, PTCA, CABG and severe ventricular arrhythmia (lown grade greater than or equal to 3) during two-year follow-up, Group C had significantly higher incidence of PTCA and CABG than Group B (p less than 0.01), but there was no significant difference of other CE between groups B and C except PTCA and CABG. In addition, Groups B and C had a significantly higher incidence of CE than Group A in cardiac event-free curves, but there was no significant difference for Groups B and C. We conclude that patients with SMI are associated with unfavorable prognosis as symptomatic patients and that these patients should undergo careful follow-up.
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PMID:[Prognostic significance of scintigraphic silent myocardial ischemia detected by stress thallium scan in patients with recent myocardial infarction]. 188 81

Unstable angina is a clinical syndrome of recurrent myocardial ischemia. In some cases, this reflects episodic platelet activation and coronary thrombosis. Thus, the biosynthesis of thromboxane A2, which is largely derived from activated platelets, is increased, often coincident with chest pain. The major role of platelets in unstable angina may influence the response to plasminogen activators. Platelets increase the resistance of thrombi to lysis, by inducing clot retraction and cross-linking and by releasing inhibitors. Thus, coronary thrombi in unstable angina may be resistant to lysis. Furthermore, both t-PA and streptokinase cause platelet activation and thrombin formation in vivo, possibly via plasmin. Plasmin can activate platelets and factor V directly. These prothrombotic effects of plasminogen activators may limit their activity in unstable angina. At the very least, their therapeutic efficacy may be highly dependent on the coadministration of potent antiplatelet agents and anticoagulants.
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PMID:Platelet activation in the pathogenesis of unstable angina: importance in determining the response to plasminogen activators. 189 67

A significant minority of patients with chest pain who undergo cardiac catheterization are found to have angiographically normal coronary arteries. Over the past 25 years, several studies have shown that a subset have demonstrable abnormalities in coronary flow and cardiac function; however, only a minority of these patients have convincing evidence for myocardial ischemia during stress, and alternative mechanisms have been explored to explain the frequent and debilitating symptoms of pain experienced by the majority of these patients undergoing study. Abnormal visceral nociception appears to be a fundamental abnormality in this population, whether or not demonstrable abnormalities in coronary flow or cardiac function can be demonstrated.
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PMID:Microvascular angina. Cardiovascular investigations regarding pathophysiology and management. 189 8

Rapid atrial pacing may reveal myocardial ischemia but the sensitivity for the diagnosis of coronary artery disease is not high enough for routine use. Therefore, the value of atrial pacing coupled with Thallium 201 scintigraphy was evaluated. Sixty-two patients (53 men and 9 women) referred for investigation of angina or chest pain were divided into two groups: a control group of 13 patients (9 men and 4 women, average age: 57.1 years) with insignificant coronary lesions (less than 50%) (N = 5) or normal coronary angiography (N = 8), and a group of 49 patients (44 men and 5 women, average age: 55.5 years) 27 of whom had a history of myocardial infarction (17 posterior, 10 anterior). Coronary angiography showed single vessel disease in 44.9% of cases, double vessel disease in 34.7% and triple vessel disease in 18.4% of cases, and 1 patient with left main stem disease. All 62 patients underwent the same study protocol which comprised: incremental atrial pacing (to the calculated maximal heart rate), Thallium 201 myocardial scintigraphy immediately after pacing and during the redistribution phase, and coronary angiography. The sensitivities of anginal pain (36.7%) and ECG changes during atrial pacing (57.1%) were too low for the diagnosis of myocardial ischemia. On the other hand, Thallium 201 scintigraphy with atrial pacing was more sensitive (87.8%) and specific (84.6%) for coronary artery disease. Stenosis of the left anterior descending artery was diagnosed with a sensitivity of 96.4% and that of the right coronary artery with a sensitivity of 90.9%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnosis of coronary artery disease by thallium 201 myocardial scintigraphy during atrial pacing]. 189 14

A case of severe myocardial ischaemia complicated by syncopal ventricular tachycardia during injection of Dipyridamole for stress Thallium myocardial scintigraphy in a coronary patient is reported. Myocardial ischaemia (chest pain, ECG changes) is classically rare (30% of cases) and usually benign during Dipyridamole injection, and either regress spontaneously or after administration of Theophylline. However, the possibility of serious complications such as this justifies the same criteria of strict surveillance as for classical exercise stress testing.
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PMID:[Severe ischemic ventricular arrhythmia during dipyridamole scintigraphy]. 189 21

The purpose of this study was to determine whether reperfusion of acute myocardial infarction (AMI) by recombinant tissue-type plasminogen activator (rt-PA) or percutaneous transluminal coronary angioplasty, or both, would improve left ventricular (LV) function when it is measured several months later at rest or maximal bicycle exercise, or both. Radionuclide angiography was performed in 44 patients 5 months (range 6 weeks to 9 months) after AMI to assess function, and tomographic myocardial thallium-201 imaging was performed at maximal exercise and delayed rest to determine whether there was any evidence of myocardial ischemia. As expected, no patient had chest pain or redistribution of a thallium defect during the exercise test, because patients had undergone angioplasty (n = 28) or coronary bypass graft surgery (n = 5) where clinically indicated for revascularization. The LV ejection fraction was plotted as a function of the time elapsed between the onset of chest pain and the time when coronary angiography confirmed patency of the infarct-related artery (achieved in 91% of 44 patients by rt-PA [n = 31] or percutaneous transluminal coronary angioplasty [n = 9] ). Functional responses differed markedly between patients with anterior (n = 20) versus inferior (n = 24) wall AMI. LV ejection fraction during exercise correlated with time to reperfusion in patients with an anterior wall AMI (r = -0.58; standard error of the estimate = 11.9%; p less than 0.02) but not in patients with an inferior AMI (r = 0.10; standard error of the estimate = 13.1%; difference not significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of time required for reperfusion (thrombolysis or angioplasty, or both) and location of acute myocardial infarction on left ventricular functional reserve capacity several months later. 190 37

To evaluate whether endogenous opioids (EO) play a role in the perception of anginal pain, a randomized double blind clinical trial, using naloxone (N) and placebo (P) and measuring beta-endorphin (beta-ep) plasma levels, was performed. We studied 10 patients with angiographically assessed coronary artery disease (CAD) and stable exercise-induced myocardial ischemia (established by 2 preliminary bicycle ergometric tests) of whom 5 symptomatic (SYM) and 5 asymptomatic (ASYM) and 5 subjects without CAD as a control group (CON). On a third exercise test the beta-ep plasma level (fmol/ml) was measured at rest (SYM 5.4 +/- 2.3 vs ASYM 7.2 +/- 2.3 vs CON 6.8 +/- 2.6, NS), at peak exercise (SYM 4.4 +/- 1.8 vs ASYM 8.0 +/- 4.2 and vs CON 6.2 +/- 2.7, NS) and during recovery (SYM 7.5 +/- 4.2 vs ASYM 7.2 +/- 3.0 vs CON 6.7 +/- 2.5, NS). On 2 subsequent tests patients received N (0.2 mg/kg) or P intravenously and chest pain was evaluated on an analogue scale (score from 1 to 10). After N compared to P we observed: an increased perception of chest pain in SYM (6.8 +/- 1.5 vs 4.2 +/- 1.0; p less than 0.01) without significant changes of the ischemic threshold (total work, heart rate-blood pressure product, ST segment changes, 2D-echocardiographic wall motion abnormalities); no modifications in ASYM and CON.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of endogenous opioids on nociceptive threshold in patients with exercise-induced myocardial ischemia. 191 14

Intravenous infusion of adenosine in patients with ischaemic heart disease (IHD) has been shown to induce chest pain and ST-depression. The aim of this study was to determine whether such myocardial ischaemia could be due to an increase in myocardial work. Thus patients with stable angina pectoris (n = 8) were randomly allocated to exercise or adenosine infusion, with a 1-h rest period before the second test. The maximal tolerable work load was 120 +/- 13 W, where all patients but one experienced typical angina pectoris. ECG revealed ST-depressions in all patients. The maximal tolerable dose of adenosine was 108 +/- 6 micrograms kg-1 min-1. All patients experienced chest pain typical of habitual angina pectoris, and all but one developed ST-depressions. During exercise there was a gradual and marked increase in the rate pressure product (RPP), in parallel with the development of ST-depression. By contrast, during infusion of adenosine there was only a minor increase in RPP (P = 0.0001). In conclusion, infusion of adenosine provokes signs and symptoms of myocardial ischaemia in patients with IHD with only a minor increase in cardiac work compared to exercise. These results are consistent with the hypothesis of a myocardial steal.
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PMID:Adenosine provokes myocardial ischaemia in patients with ischaemic heart disease without increasing cardiac work. 191 25


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