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)

A double-blind study including three different cardioselective beta-blockers, practolol, H 87/07 and metoprolol, was performed in 54 patients with acute myocardial infarction and chest pain shortly after onset of symptoms. Transmural infarctions were found in 42 patients while 12 patients had nontransmural infarctions. Chest pain and the product of heart rate and systolic blood pressure were significantly reduced in the beta-blocker groups whereas no changes were seen after saline. All patients with nontransmural infarctions and 14 out of 29 with transmural infarctions got pain relief lasting for at least 30 min. None of the patients developed signs of left ventricular backward failure, shock, or bradycardia. A decrease in ST segment elevation was observed in all the transmural infarctions after beta-blockade. No changes in ST segment elevation were found after analgesics when given after saline, but in some cases an increase was seen in this parameter when analgesics were given due to insufficient pain relief after beta-blockers or due to return of chest pain. It is suggested that pain relief by beta-blockers indicates decrease of myocardial ischemia.
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PMID:Double-blind study of the effect of cardioselective beta-blockade on chest pain in acute myocardial infarction. 0 98

In a cohort of 417 patients admitted consecutively to the Coronary Care Unit for acute myocardial ischemia (unstable angina pectoris in 121, acute myocardial infarction in 296 patients) 21 cases of non arrhythmogenic sudden death occurred within 24 hours after admission. 16 of these patients suffered from acute myocardial infarction and 5 from unstable angina pectoris. Cause of death was cardiac rupture in 12 and pump failure in 4 patients with acute myocardial infarction, whereas all patients with unstable angina pectoris died from pump failure. Patients with cardiac rupture within 24 hours after admission, had significantly higher systolic and diastolic blood pressure in comparison with the other groups and with patients dying from cardiac rupture on the third day, or later. All patients dying from pump failure with unstable angina pectoris and one of the patients dying from pump failure with acute myocardial infarction had beta blocker therapy. Beta blockers were given to 68 of the patients with unstable angina pectoris. Acute pump failure occurred in this group only. The risk of pump failure with beta receptor blocking drugs is indicated by angina decubitus, marked dyspnea during anginal attacks (even in patients free of signs of cardial insufficiency outside their attacks) and a lack of responsiveness to beta blocking therapy. In these patients rapid coronary angiography and bypass surgery seems to be the prefered method of management. Beta blockers should not be given to these patients or discontinued in cases which lack responsiveness.
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PMID:[Non arrhythmogenic sudden death as complication of coronary heart disease]. 4 54

In 8 patients affected with acute myocardial infarction verapamil was highly effective in controlling ventricular extrasystoles. Theoretically the drug ought not to be effective if the extrasystoles were related to fast cardiac fibers characterized by a rapid inward Na+ current. The result suggests that in acute myocardial ischemia ventricular extrasystoles are related to slow inward Ca++ currents.
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PMID:Effects of verapamil in ventricular premature beats of acute myocardial infarction. 7 83

In 24 patients with acute myocardial infarction intravenous nitroglycerin in 2 different dosages was administered and the effect on hemodynamics and extent of myocardial ischemia was investigated. According to the initial left ventricular filling pressure (LVFP) the patients were divided in Group I: LVFP below 20 mm Hg (13 patients) and in Group II: LVFP above 20 mm Hg (11 patients). Following an infusion of 3 mg of nitroglycerin in the first and 6 mg in the second hour, a significant decrease (P less than 0.0001) in the filling pressure (in Group I from 15 +/- 4 to 9 +/- 3 (+/-1 SD) and in Group II from 28 +/- 11 to 16 +/- 7 mm Hg) was observed. The mean arterial pressure decreased in both groups by an average of 9 mm Hg. The changes in the heart rate were minimal. The cardiac output decreased in Group I from 4.4 +/- 1.0 to 3.9 +/- 0.8 1/min (P less than 0.005) whereas in the group with left ventricular failure it increased significantly from a lowered initial value (3.4 +/- 1.0 to 4.0 +/- 1.1 1/min) (P less than 0.001). By using precordial mapping for estimation of ischemic injury in 12 patient sigma ST elevation decreased from 14.6 +/- 11.9 to 12.2 +/- 9.8 mV at a dose of 3 mg/h (P less than 0.03). The dose of 6 mg/h, however, was less effective on the extent of myocardial ischemia than 3 mg/h. Thus, the dosage of nitroglycerin may be critical in respect to infarct size, despite the beneficial hemodynamic effects of the drug.
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PMID:Effects of intravenous nitroglycerin on hemodynamics and ischemic injury in patients with acute myocardial infarction. 9 9

In 38 patients with acute myocardial infarction the effect of nitroglycerin on infarct size was studied. Patients were randomized into two groups. 16 patients received continuous nitroglycerin infusions of 0.6 to 6.0 mg/h (mean 2.3 mg/h) over a 48 h period, 22 patients received no specific therapy and served as control. Nitroglycerin was given in the mean 12 +/- 5 (+/- 1 SD) hours following onset of chest pain and 8 +/- 5 after the increase of CK values. Infarct size was determined according to the time activity curve of creatine kinase (CK) and of its myocardial isoenzyme (CK-MB). In all but one patient hemodynamic parameters (left ventricular filling pressure, blood pressure, cardiac index) were measured. The mean infarct size was 51 +/- 30 CK-g-equiv. in control patients, and 48 +/- 33 g in nitroglycerin treated patients. Infarct size as calculated from CK-MB values was 60 +/- 36 g (n=16) in control, and 52 +/- 41 g (n=11) in treated patients. At left ventricular filling pressure values (LVFP) below 20mm Hg infarct size amounted to 43 +/- 30 g (n=12) in control, and to 41 +/- 32 g (n=11) in the nitroglycerin group. At LVFP values above 20 mmHg infarct size was 61 +/- 29 g (n=10) in control as opposed to 64 +/- 32 g (n=5) in treated patients. There was no difference between infarct size as predicted during the first 7 h and the observed infarct size. - Despite the known beneficial effect of nitroglycerin on hemodynamics and on myocardial ischemia, infarct size seems not to be greatly reduced, however, intervention occurred fairly late (12 h). In early intervention beneficfial effects seem likely.
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PMID:[IX. Randomized study of the effect of nitroglycerin on CK and CK-MB infarct size. Preliminary report (author's transl)]. 10 61

The results of studying the excretion of testosterone and other androgens with the urine after a chorionic gonadotropin load in patients with ischemic heart disease and in persons who had suffered from acute myocardial infarction are discussed. In choriogonin load stimulating the gonads, there is noticeable variability in the excretion of testosterone and epitestosterone, androstenedione, and 7-keto-dehydroepiandrosterone in the urine. The data obtained are evidence of reduced functional reserves of the sex glands in some of the patients.
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PMID:[Effect of chorionic gonadotropin on the urinary excretion of testosterone and other androgens in healthy men and those with coronary arteriosclerosis]. 15 6

Several uncontrolled early studies established that corticosteroid administration to patients with ischemic heart disease and cardiogenic shock was relatively safe. Whether or not the glucocorticoids were of benefit or not remained unclear when mortality was used as an index of efficacy. Hemodynamically, glucocorticoids may decrease peripheral vascular resistance, increase cardiac output and coronary blood flow, but leave myocardial contractility unchanged. The mean arterial pressure may vary unpredictably. The increase in coronary blood flow may certainly be advantageous in treating patients with acute myocardial infarction. The decrease in infarct size recently reported, if confirmed in man, would also be desirable. However, there is a paucity of good data concerning the effects of corticosteroids in man postinfarction. In addition, through unproved mechanisms, the corticosteroids decrease the extent and severity of myocardial ischemic injury. While these fundamental actions may not result in improved mortality, ongoing studies suggest that minimization of ischemic injury may ultimately prove to be most rewarding in the prevention of cardiogenic shock.
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PMID:Glucocorticoid therapy for acute myocardial infarction. 17 21

Twenty-six patients suspected of having acute myocardial infarction (AMI) underwent myocardial scintigraphy sequentially with 201Tl and 99mTc-stannous pyrophosphate (99mTc-PPi). Of the 26 patients, 24 had AMI documented by enzyme and electrocardiographic changes. Nineteen had transmural and five had subendocardial myocardial infarctions. The remaining two patients had "unstable angina pectoris." The mean time from onset to imaging was 4 days. Of the 24 patients with AMI, 22 had positive 99mTc-PPi scintigrams. In 20 the area of acute myocardial damage appeared to be the same by 99mTc-PPi scintigram as by ECG; in two, the location could not be precisely determined. The two patients with negative 99mTc-PPi scintigrams at the time of combined myocardial imaging had had positive 99mTc-PPi images previously. In all 24 patients, the 201Tl images were abnormal in at least the location suggested by the electrocardiogram. In seven patients, the area of decreased 201Tl activity was grossly equal to the positive area on the 99mTc-PPi images; in 15, the 201Tl defect was definitely larger; and in two, the 201Tl defect appeared slightly smaller. Although the 99mTc-PPi and 201Tl myocardial images provide different information, both are valuable in determining the overall integrity of the myocardium in patients with ischemic heart disease.
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PMID:Acute myocardial infarction imaged with 99mTc-stannous pyrophosphate and 201Tl: a clinical evaluation. 18 30

150 patients, admitted to the coronary care unit with suspicion of acute myocardial infarction, received pyrophosphate labelled with 99mTc, 6-120 h after onset of symptoms, mean 24 h, and were examined in the anterior posterior position and in the left anterior oblique position with a mobile gamma camera. Scintigrams were obtained initially at the injection, and then every 15th min during 1h. The scintigrams were evaluated with regard to presence and localization of radionuclide uptake in myocardial area. In 98 patients with a clinical diagnosis of acute myocardial infarction, uptake was found in 95, with good correlation between ECG and scintigraphic localization. 2. patients with myocardial infarction, verified at autopsy, did not show any uptake and 1 patient, surviving the myocardial infarction, also showed negative result. 19 of 26 patients with unstable angina pectoris also exhibited an uptake in the myocardium. 25 of 26 patients with other diagnoses showed no uptake, while in 1 patient an uptake was recorded. It is concluded that with 99mTc-pyrophosphate scintigraphy it is possible to separate ischemic heart disease from other diseases in patients with chest pain.
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PMID:Myocardial scintigraphy with 99mTc-pyrophosphate in 150 coronary care unit patients. 18 27

Technetium-99m-stannous pyrophosphate (99mTc-PYP) accumulates in acutely infarcted myocardium and can be detected by scintiscanning. The clinical value of 99mTc-PYP scintiscanning was studied in 83 patients 6 hours to 21 days after the onset of acute chest pain. In 12 patients with normal electrocardiograms and serum enzyme values no uptake of 99mTc-PYP was detected on the scintigrams. Of 44 patients with electrocardiographic or enzyme evidence, or both, of acute myocardial infarction the scintigrams were positive in 31, "questionable" in 2 and negative in 11; no positive scan was obtained within 12 hours of the onset of pain, and the scans generally remained positive for up to 5 days. In 24 patients with evidence of prolonged myocardial ischemia the scans were positive in 2, questionable in 4 and negative in 18. The scans were negative in each of three patients with acute or constrictive pericarditis. Localization by electrocardiography and scintiscanning correlated nearly perfectly for transmural infarcts but subendocardial infarcts could not always be localized precisely by scintiscanning. The infarct area (total area of 99mTc-PYP uptake) correlated well with the peak serum value of creatine phosphokinase.
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PMID:Technetium pyrophosphate scanning in the detection of acute myocardial infarction: clinical experience. 18 87


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