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

The association of idiopathic hypertrophic subaortic stenosis (IHSS) with significant coronary atherosclerosis is little known, only 43 cases being available in the literature, 2 of which are personal ones. But the incidence of this association has certainly been underestimated. It is especially found from the sixth decade onwards, and at least 20% of patients with IHSS in and above the age group have stenosing lesions of the coronary artery. It is almost impossible to establish the presence of associated coronary abnormalities from the clinical features of from electrocardiogram. It does however seem worthwhile looking for this condition in IHSS when there is refractory chest pain, especially to beta-blockers, particularly if the patient is aged over 50 and has risk factors for ischaemic heart disease. It is also good to find IHSS associated with known coronary artery disease by using simple non-invasive techniques such as phonomechanocardiography and especially echo-cardiography; it is important not to miss the myocardial lesion and to treat concurrently if there is likely to be an indication for dealing with the coronary arteries surgically. The beta-blockers are the treatment of choice for both conditions, together with anticoagulents. If they fail, myectomy or myotomy together with aorto-coronary bypass graft should be considered.
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PMID:[Obstructive cardiomyopathy and associated coronary atherosclerosis. Review of the literature and report of 2 personal cases]. 10 92

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

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

The injury-vasospasm hypothesis of IHD was discussed in relation to coronary artery autoregulation and the anoxic-feedback mechanism. Observations in the recent literature, not usually attributed to spasm, were examined in light of this phenomenon. This includes reperfusion models of experimental AMI, the association of AMI with myocarditis, and findings in AMI and SCD as necrotic microlesions, prodromata, and epicardial arterial plaque rupture and hemorrhage. The disparity between the severity of coronary disease and the occurrence of the various types of IHD suggest that atherosclerosis itself does not precipitate attacks of chest pain. It was emphasized that plaque rupture due to spasm might help induce CAT. With exercise, the possible importance of the autoregulatory system was explored in the prevention and induction of AMI and SCD, and the improvement of AP. The role of spasm in IHD should be defined.
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PMID:The injury-vasospasm hypothesis of ischemic heart disease, revisited. 33 91

Coronary artery spasm is an important pathogenetic mechanism in some forms of myocardial ischemic disease. Factors that may be important in the genesis of spasm include the autonomic nervous system, prostaglandins, endoperoxides, thromboxanes, and the calcium availability to the contractile apparatus. Spasm results in myocardial ischemia with attendant chest pain and electrocardiographic and hemodynamic changes; it is the primary pathogenetic mechanism in Prinzmetal's variant angina and has been found in association with classic angina pectoris and acute myocardial infarction. Diagnosis of coronary artery spasm is firmly made only by coronary angiography. Treatment includes the use of both short- and long-acting nitrates and the slow-channel blocking agents such as verapamil, nifedipine, and perhexiline.
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PMID:Coronary artery spasm. 38 40

Oesophageal dysfunction (OD) is a common finding in patients discharged from a coronary care unit without definite diagnosis. Of 55 patients investigated with oesophageal manometry, acid perfusion test and exercise ECG, 32 had signs of OD and 19 signs of ischaemic heart disease (IHD). Symptoms such as heart burn, acid regurgitations, feeling of a lump in the throat, surfeitness after meals, chest pain at night, and relief of chest pain when lying with the head raised were significantly more common in patients with OD than in patients with normal oesophageal function. Chest pain was significantly more often provoked by effort, emotions or cold and more often relieved by nitroglycerine in patients with signs of IHD than in those without. These pain-provoking factors were, however, also common in patients with OD. A careful case history with specific inquiry directed at not only cardiac but also oesophageal symptoms is important in the differential diagnosis of chest pain.
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PMID:Oesophageal dysfunction in non-infarction coronary care unit patients. 43 65

The role of coronary artery spasm in the production of myocardial ischemia has recently become the focus of increased attention. This phenomenon is now well established as a causative mechanism underlying the resting chest pain attacks in Prinzmetal's variant angina. There is also evidence that coronary spasm may play a more significant role in the broad spectrum of ischemic heart disease than can be documented by current techniques. The autonomous nervous system constitutes a major element in the pathophysiology of spasm. Coronary arteriography, in spite of important limitations, remains the only technique for final documentation of this phenomenon, but radionuclide scintigraphy appears to be promising. Nitroglycerin is effective for the relief of the acute attack, while long acting nitrates and the calcium antagonists: nifedipine, perhexiline and verapamil are useful in the prevention of recurrences.
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PMID:Coronary artery spasm: its role in the pathogenesis of myocardial ischemia. 50 1

Sixty three male patients with billowing mitral leaflet syndrome (BML) and forty one age and sex match controls were studied with emphasis on the cineangiographic features of coronary arteries. In the BML group, the coronary arteries were considered normal in five and abnormal in fifty eight. In fifty eight with abnormal coronary arteries, twelve showed atherosclerotic occlusive lesions, fifteen showed combined occlusive lesions and nonocclusive abnormalities and thirty one showed nonocclusive abnormalities alone. The non-atherosclerotic abnormalities consisted of redundancy of the coronary arteries manifested by bizarre changes in configuration and motion. These abnormalities were present in only five patients in the Control Group. On the basis of our observations and corroborative evdience in the literature, a hypothesis is presented; the salient features of which are that: (1) the spectrum of BML may be considerably more complex than hitherto suspected, (2) a combination of BML and tortuous coronary arteries may form a distinct subset of this spectrum and (3) the increased tortuousity may result in impaired coronary perfusion causing myocardial ischemia thus offering a possible explanation for some of the symptoms - such as chest pain, arrhythmias and even sudden death seen in this syndrome.
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PMID:On the role of tortuous coronary arteries in billowing mitral leaflet syndrome. A hypothesis. 51 17


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