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)

Evidence is mounting that three drugs that inhibit platelet function--aspirin, dipyridamole, and sulfinpyrazine--have an antithrombotic effect in humans. Particularly in men, aspirin is beneficial in controlling transient ischemic attacks and stroke, and there is evidence that it may be effective in preventing thrombotic and embolic complication of hip surgery. It abolishes symptoms in peripheral ischemia associated with thrombocytosis and spontaneous platelet aggregation and may prove effective in coronary artery disease. When combined with oral anticoagulants, aspirin is more effective than oral anticoagulants alone in preventing systemic embolism in patients with prosthetic heart valves. Dipyridamole in combination with oral anticoagulants reduces the incidence of systemic embolism after prosthetic heart valve replacement. Sulfinpyrazone reduces the incidence of sudden death in the first year after myocardial infarction, decreases the incidence of arteriovenous shunt thrombosis in patients undergoing chronic hemodialysis, and when combined with anticoagulants, may be effective in reducing the frequency of episodes in recurrent venous thrombosis.
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PMID:Antiplatelet drugs in thromboembolism. 38 46

Altered regional mechanical myocardial performance is an early, sensitive marker of myocardial ischemia, and can be estimated in man with reasonable accuracy. Identification, localization and quantification of abnormalities in mechanical performance can be used to predict the presence of coronary artery disease. Testing techniques that have little or no effect on diagnostic efficiency must be replaced with more sensitive indicators of ischemia. If experimental data are validated by findings in human subjects, accurate identification of regional wall motion changes during test conditions should prove to be a powerful marker of ischemia. To be of value, a diagnostic test must strongly increase the frequency of identification of subjects with a high probabilty for the presence of coronary artery disease in an otherwise low-prevalence population, and of those with known disease who are at the highest risk for complications including myocardial infarction or death.
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PMID:Mechanical function of the heart and its alteration during myocardial ischemia and infarction. Specific reference to coronary atherosclerosis. 38 87

Thirty patients with triple-vessel coronary artery disease proven by angiography, symptomatic angina and a positive ECG stress test were evaluated with thallium-201 (201TI) scintigraphy. Twenty patients also had aortocoronary saphenous vein bypass surgery; 15 of them had repeat noninvasive evaluation. Seventy percent of these patients showed ischemia by 201TI scintigraphy, of which one-half returned to normal after surgery. Postoperative reversion of the ECG stress test together with 201TI stress/reperfusion imaging correlated well with the completeness of surgical revascularization. We could not explain the prevalence (80%) of infarcts detected by 201TI in this group, of which 76% could be anatomically correlated to epicardial scars. The positivity of infarcts by 201TI exceeded that predicted by previous history of infarction, Q waves on resting ECG or ventriculographic akinesis. These observations suggest that 201TI scintigraphy is a useful noninvasive tool in the follow-up and understanding of patients with coronary heart disease. These conclusions also support the concept that 201TI stress imaging need not have the identical connotation as the ECG stress test.
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PMID:Thallium-201 myocardial scintigraphy in patients with triple-vessel disease and ischemic exercise stress tests. 42 10

The efficacy of single injection thallium-201 exercise stress and rest redistribution imaging in the evaluation of myocardiacl ischemia was compared with stress electrocardiography and coronary arteriography. Thallium-201 imaging was interpreted at two levels of sensitivity in order to define the circumstances under which it best serves as a screening modality for coronary arteriography. With the prevalence of coronary disease usually found in patients referred for coronary arteriography (75%), unprocessed thallium-201 imaging is as good as stress electrocardiography in identifying patients apt to show coronary artery abnormalities, but not much better than stress electrocardiography in delineating those patients unlikely to show coronary artery disease. In contrast, processed lesion enhanced images showing normal results virtually eliminate the possibility of significant arteriographic findings. With this screening technique, many patients may be spared unnecessary coronary arteriography.
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PMID:Single injection thallium-201 stress and redistribution myocardial perfusion imaging: comparison with stress electrocardiography and coronary arteriography. 42 86

Doppler ankle blood pressures were performed inere obtained in 100 consecutive patients with peripheral arterial insufficiency after treadmill exercise. A twelve lead electrocardiogram was monitored during and after exercise. Despite a restricted ability to exercise because of peripheral vascular insufficiency, forty-six patients had ventricular dysrhythmia or ischemia, or both, usually without associated symptoms. Electrocardiographic monitoring during treadmill exercise proved a useful predictor of postoperative complications. Thirty-two vascular operations were performed in patients with no electrocardiographic evidence of ischemia. No patient had a postoperative myocardial infarction or died. Sixteen vascular procedures were performed in patients with ischemic responses on exercise electrocardiography. Six patients had postoperative myocardial infarctions, two of which were fatal. Electrocardiographic monitoring during treadmill exercise for peripheral vascular insufficiency in recommended (1) to assess the severity of coronary artery disease and the likehood of postoperative complications, and (2) as a precautionary measure to identify potentially dangerous dysrhthmias or ischemia during exercise before the development of clinical symptoms.
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PMID:Assessment of operative risk with electrocardiographic exercise testing in patients with peripheral vascular disease. 42 97

Sixteen patients with significant two and three vessel coronary artery disease but without clinical congestive heart failure were studied during rapid atrial pacing before and after infusion of 0.015 mg/kg of ouabain. Seven patients with a decreased (less than 50 percent) ejection fraction and nine patients with a normal ejection fraction had a significant (P less than 0.05) increase in resting arterial systolic pressure after the administration of ouabain. However, resting values for coronary sinus flow, coronary vascular resistance, myocardial oxygen consumption and myocardial lactate extraction did not change significantly in either group. During pacing, patients with a decreased ejection fraction demonstrated more ischemia than patients with a normal ejection fraction; however, the administration of ouabain did not significantly alter pacing-related changes in coronary sinus flow, myocardial oxygen consumption, myocardial lactate extraction, ischemic electrocardiographic changes or onset of chest pain in either group. The administration of ouabain has a negligible effect on coronary hemodynamics, myocardial metabolism or clinical signs of ischemia in patients with coronary artery disease with normal or abnormal left ventricular function.
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PMID:Lack of ouabain effect on pacing-induced myocardial ischemia in patients with coronary artery disease. 43 84

The effects of the beta-adernergic blocking drug acebutolol were studied in 23 patients with angina pectoris and angiographically documented coronary artery disease. Patients were evaluated clinically, by graded treadmill testing and by 24-hour Holter monitoring in the control state, after 2 weeks treatment with placebo, and after 2 weeks treatment with 600 mg. and then 1,200 mg. of acebutolol. Acebutolol (in a daily dose of 600 mg.) was an effective antianginal drug: the number of clinical attacks of angina pectoris (p less than 0.001) and the consumption of sublingual nitrate decreased (p less than 0.01), there was a significant increase in the treadmill effort tolerance as measured by the time to appearance of ischemic ECG changes (p less than 0.001) and the total work performed (p less than 0.001), and there was also a significant decrease in ischemic ST segment depression on 24-hour Holter monitoring. Treatment with 1,200 mg. acebutolol was associated with a further decrease in heart rate and a further improvement in effort tolerance on treadmill testing (p less than 0.05). On the large dose of the drug, however, there was no further clinical improvement, and no further improvement on 24-hour ECG monitoring; several patients complained of weakness and fatigue. Graded treadmill testing was an excellent objective method for assessing physical effort tolerance and its improvement after treatment with the beta-blocking drug. Twenty-four-hour Holter monitoring was a useful and complementary test, especially in patients who stopped exercising on the treadmill because of fatigue or weakness, and especially for assessing the efficacy of beta-blockade in controlling emotionally induced tachycardia and ischemia in the patient's own daily environment.
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PMID:Evaluation of the beta-blocking drug acebutolol in angina pectoris. 49 6

We describe a patient who presented with acute massive pulmonary edema, clinically and on chest roentgenogram. Two hours later the patient became hypotensive and was found to have a low pulmonary capillary wedge pressure (PCWP). The blood pressure returned to normal after administration of fluids. Acute pulmonary edema develops if PCWP rises higher than 25 to 30 mm Hg. In our patient, the elevated PCWP fell to low normal within two hours, when chest roentgenogram and clinical examination still suggested severe pulmonary edema. A phase lag existed between lowering of the pulmonary capillary wedge pressure and clearing of fluid from the alveolar and interstitial spaces in the lungs. At least three different pathogenetic mechanisms in patients with coronary artery disease can produce this phase lag. Transient global ischemia of the left ventricle was thought to be the responsible mechanism in our patient.
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PMID:Cardiac-pulmonary edema and low pulmonary capillary wedge pressure. 50 73

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P less than 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P less than 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P less than 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.
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PMID:Right ventricular diastolic pressure in coronary artery disease. 50 30

Left ventricular ejection fraction (LVEF) determined by first pass radionuclide (Nucl.) and biplane contrast angiocardiography (Angio.) was compared in 62 patients with suspected coronary artery disease under resting conditions and in 32/62 patients during bicycle ergometry at identical work load. At rest both methods correlated with r = 0.81 with similar heart rates in both determinations. The mean value of LVEF (Nucl.) was lower than the mean value of LVEF (Angio.), at 50 +/- 2 (SE) % and 58 +/- 2% respectively (p less than 0.001). During exercise a significant correlation between the two methods was again found (r = 0.76). This time no difference was detected between the mean values for LVEF (50 +/- 3% [Nucl.] vs 48 +/- 2% [Angio.], n.s.), which may be explained by the higher heart rates during the invasive study (123 +/- 5/min [Angio.] vs. 108 +/- 4/min [Nucl.], p less than 0.001), resulting in a higher degree of ischemia and hence a lower LVEF. The interobserver variability did not differ between the two methods.
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PMID:[Radionuclide determination of the left ventricular ejection fraction under stress: comparison with angiocardiography]. 53 55


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