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)

Altogether 359 paired bicycle ergometries coupled with administration of single doses of antianginal drugs were carried out in 62 men suffering from angina pectoris of effort, functional classes II and III. A study was made of the indicator characterizing the time that elapsed since the onset of a typical angina pectoris attack till the appearance of the signs of ischemia on the ECG. Administration of effective single doses of antianginal drugs raised the time elapsed since the pain onset till the appearance of the ST segment greater than or equal to 1.0 mm fall during the exercise. Administration of ineffective doses of nitrates, calcium antagonists and placebo entailed a decline of that indicator, a rise of the number of cases where the segment ST greater than or equal to 1.0 mm fall was recordable before the onset of painful sensations. Administration of propranolol in ineffective single doses failed to provoke a decrease of the time elapsed since the typical pain onset till the appearance of the ST segment greater than or equal to 1.0 mm fall. Intake of ineffective single doses of nitrates, calcium antagonists and placebo may deprive certain patients of early signalization and appearance of the ECG signs of myocardial ischemia.
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PMID:[The effect of single doses of antianginal preparations on the correlation of the time of the onset of typical pain and the electrocardiographic signs of myocardial ischemia in patients with stenocardia of effort]. 194 22

Of 255 consecutive patients with acute myocardial infarction, 111 were eligible for attempted late thrombolysis. They were randomly assigned to either thrombolytic and antithrombotic treatment (treatment group) or routine treatment (control group). Patients in the treatment group received streptokinase initiated late (mean 32 hours; range 12 to 49) after the onset of symptoms, followed by heparin infusion for at least 5 days and warfarin and dipyridamole for at least 3 months. Patients were examined clinically and by bicycle ergometry on discharge from the hospital and after 3 and 12 months. The two groups did not differ with respect to deaths or reinfarctions. There was a trend toward a lower incidence of angina pectoris in the treatment group. Exercise tolerance in this group was significantly higher than in the control group (at 3 months 124 +/- 39 W vs 107 +/- 41 W; p less than 0.05). The difference was entirely accounted for by patients with no previous history of infarction or angina pectoris (at 3 months 142 +/- 37 W vs 112 +/- 45 W; p = 0.01). ECG signs of myocardial ischemia, silent or symptomatic, occurred at significantly lower levels of exercise among patients in the control group compared with patients in the treatment group. The results support the notion that thrombolytic therapy given as late as 12 to 49 hours after the onset of symptoms may reduce the incidence of residual ischemia during the postinfarction period.
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PMID:Late streptokinase infusion and antithrombotic treatment in myocardial infarction reduce subsequent myocardial ischemia. 200 Jul 39

We report the case of a patient with ventricular tachyarrhythmia, which occurred after atropine was given intravenously for diagnostic purposes. The arrhythmia was accompanied with precordial pain and nitroglycerin promptly reduced both events. On the ECG an elevated ST segment in leads I, aVL, V4, V5, V6 was observed for few hours after the end of the arrhythmia, followed by a pattern of myocardial ischemia. Serum enzymes were repeatedly normal. Spontaneous anginal attacks, usually accompanied with ECG signs of myocardial ischemia and 2nd degree AV block, were often observed by means of 24 hours ECG monitoring (Holter) in the following weeks, in spite of appropriate treatment. Either myocardial ischemia, induced by the increased heart rate following atropine administration, or direct electrophysiologic effects of the drug upon the ventricle muscle (possibly in association with ischemia) could have caused the ventricular arrhythmia.
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PMID:[Hyperkinetic ventricular arrhythmia induced by atropine administration]. 688 46

The purpose of this study was to determine the response of plasma levels of endothelin-1 (ET-1) to dynamic exercise in patients with coronary artery disease and chronic stable angina pectoris and positive exercise tolerance test, before and after treatment with the calcium antagonist nisoldipine (20 mg/day buccally for 7 days). Plasma ET-1 levels and hemodynamic parameters (blood pressure and heart rate) were determined at rest, at peak exercise and recovery. All patients had a positive electrically and clinically stress test and all of the eight patients did not developed ECG signs of myocardial ischemia after nisoldipine administration. Before nisoldipine treatment the plasma ET-1 levels did not increase significantly during exercise. After nisoldipine treatment the plasma ET-1 levels were significantly lower at rest and during exercise compared with those revealed before calcium antagonist treatment. In conclusion our results suggest that in patients with chronic stable angina pectoris the treatment with calcium antagonist nisoldipine reduced ischemia and plasma ET-1 levels.
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PMID:Plasma endothelin-1 concentrations in patients with coronary artery disease during stress test before and after nisoldipine administration. 874 13