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)

1). In 1001 patients with acute myocardial infarction 403 cases were found (40.2%) showing possible relapse. A study was made of 125 cases (12.5%) with positive diagnosis of acute myocardial infarction relapse, and among them, 12 were found to be occurring for the third time. Is possible for the real frequency of the iterative infarction to be even higher, because many cases were dismissed (27.7%) for lacking of conclusive electrocardiographic data pointing to myocardial transmural infarction. 2). Investigations were conducted about the evolutive condition of the danger factors in the coronary profile as well in the male as in the female group. Besides, a comparative study was made about symptoms, complications, morbidity and mortality. Clinical, enzimatic and electrocardiographic proofs were found, in every case, of a new myocardial transmural necrosis which was in evolution, with waves of injury and ischemia. Thirty eight deaths were registered in hospitals (30.4%) and in 25 of these, a necropsic study was conducted. 3). This illness is more frequent among men than among women, in a 3.5 to 1 proportion. The recurrent myocardial necrosis tends to be more frequently present during the first year following the first episode. In women, the first myocardial infarction as well as the iterative infarction occur at an older age than in men. 4). The influence of personality and stress is a very important factor of danger in the iterative infarction. Familiar antecedents of ischemic cardiopathy constitute a danger factor in patients presenting a single episode of myocardial infarction; nevertheless they don't seem to have a determining influence in this group of relapsing infarction. Although this study confirms with statistics that smoking has a decisive influence in the first myocardial infarction, neither frequency nor mortality of the relapsing infarction are in any way modified by the diminishing or suppression of the smoking habit.
Arch Inst Cardiol Mex
PMID:[Myocardial reinfarction in male and female]. 69 61

A coronary angiography was taken to 80 patients whose twelve leads exercise ECG had been found positive. This group included 38 patients with old myocardial infarction and 42 with coronary insuficiency. When looking for a relation between: 1. The amount of positivity in the exercise ECG and the number on injured vessels, and 2. the ischemia located in the effort test and the blocked vessels shown by the angiography. We found a reasonable relation between the exercise ECG and the severity of the injuries. This co-relation is of 100% between the old infarction area and the severe or total obstruction of the corresponding vessel. It was observed then, that a close relation exists between the ischemia area and the obstructive injuries. In a second group of 15 patients we failed to find atero sclerotic injuries in the corresponding vessel, but observed some vascular anomalies which explained the ischemia. The effort test with twelve leads exercise ECG makes easier the localization of obstructions, single or multiple, on the area supposedly affected.
Arch Inst Cardiol Mex
PMID:[Correlation between findings of exertion ECG with 12 derivations and coronoriography]. 69 70

25 anesthetized mongrel dogs underwent a left thoracotomy. Creatine kinase (CK) activity was measured in serial blood samples drawn simultaneously from the aorta and a coronary vein. The distribution of myocardial perfusion was determined by a continuous infusion of krypton-81m (half-life 13 sec) into the aortic sinuses. Heart rate and arterial blood pressure were also measured throughout the procedure. In 20 dogs regional myocardial ischemia was produced by ligation of a major branch of the left anterior descending coronary artery. Five of these dogs received 1 microgram.kg-1 nifedipine i.v. and a further 5 received 13 microgram.kg-1. Thoracotomy alone produced a slight rise in plasma CK activity but the arteriovenous difference (AV) across the segment of the heart remained positive over 5 h. Myocardial ischemia in the untreated dogs caused a considerable increase in CK activity and the AV difference became negative at 90 min. Treatment with the lower dose of nifedipine considerably reduced the plasma CK activity and the AV difference did not become negative until 3 h. Regional myocardial perfusion showed a significant improvement. Conversely, the higher dose of nifedipine produced a marked increase in the area of ischemia and an acceleration of CK release from the heart. This was associated with a decrease in arterial pressure and an increase in heart rate. These results show that nifedipine can be beneficial in experimental myocardial infarction but care must be taken to avoid hypotension and increases in heart rate.
Eur J Cardiol 1978 Jul
PMID:Effects of nifedipine on creatine kinase release during myocardial ischemia in dogs. 69 37

The majority of deaths from coronary heart disease (CHD) occur before the victims receive medical attention. Chronic ventricular ectopic activity (VEA) is a well-established predictor of coronary mortality as well as sudden death. Evidence that chronic VEA is independently and causally related to sudden death, however, remains equivocal. Only more advanced grades of chronic VEA appear to be significant. Arrhythmias are clearly more common in patients with advanced coronary obstruction, and therefore prone to new ischemic events and their associated electrical disturbances. Autopsy studies are limited in their ability to identify an acute myocardial infarction in patients who die suddenly, but experience with the mobile coronary care units has reemphasized the role of acute ischemia. The prospective, randomized trial, including reliable assessment of VEA, offers the only definitive means of identifying the contribution of chronic VEA to the incidence of sudden death from CHD.
Eur J Cardiol 1978 Jul
PMID:Chronic ventricular ectopic activity and sudden death. 69 44

Epicardial ECG signs have been studied in 26 anesthetized and thoracotomized dogs in an attempt to follow the progress of tissue damage during regional myocardial ischemia. Epicardial ECG's were recorded before and during 15 min, 1 and 5 h of severe left anterior descending coronary artery narrowing. Epicardial ST segment elevation followed a complicated natural history. An analysis of variance showed the significant effects of respiration, heart rate and changes in time during myocardial ischemia. Regional epicardial R waves showed a transient increase in amplitude following coronary narrowing. There was no loss of electrically active myocardium following 15 min of ischemia. Irreversible loss of R waves were noted at between 30 and 45 min and progressed to full development within 5 h following coronary artery narrowing. The loss of electrically active myocardium (R loss plus Q waves) at 5 h was closely related to the myocardial depletion of creatine kinase activity (mu/mg DNA-1) at 24 h in each dog. The early manifestation of myocardial ischemia (ST segment elevation at 17 min) was closely related in the later evidence of cell death (R loss plus Q waves) in each dog. These relationships were less precise when the results were combined and this showed the variability between dogs in heart size and infarct size. The study suggested that the individual complete natural history of these ECG signs must be studied before they can be used to assess the extent and progress of myocardial ischemia and cell death.
Eur J Cardiol 1978 Sep
PMID:Electrocardiographic signs in experimental myocardial ischemia and infarction. 69 50

Intending to find out which is the prevalence of mitral valvular prolapse in cases of ischemic cardiopathy with "normal" coronariography, a review was made of the coronary-ventriculographic studies at the I.N.C. archives, which showed as clinical diagnosis that of ischemic cardiopathy with "normal" coronaries. In the present studies we record 47 cases showing chest angina and/or electrocardiographic changes in rest or effort tests, compatible with myocardic ischemia and coronariography undoubtedly normal. We found 30 cases (63.8%) showing strong evidence of mitral prolapse in the left cineventriculography taken in right-front oblique position.
Arch Inst Cardiol Mex
PMID:[Prolapse of the mitral valve]. 70 34

During ischemia, myocardial adenosine triphosphate is degraded to adenosine, inosine and hypoxanthine. These nucleosides are released into coronary venous blood and may provide an index of ischemia; adenosine may also participate in the autoregulation of coronary flow. In dogs, the temporal relations between reactive hyperemic flow and nucleoside concentrations in regional venous blood were correlated after brief occlusions of a segmental coronary artery. Reactive hyperemia and adenosine release peaked together in 10 seconds, persisted for 10 to 30 seconds and then decreased in a pattern consistent with the hypothesis that they are related. During initial reflow after 45 seconds of ischemia, mean concentrations of adenosine, inosine and hypoxanthine increased, respectively, to 52, 67 and 114 nmol/100 ml plasma; after 5 minutes of ischemia, the respective levels increased to 58, 1,570 and 1,134 nmol and fell quickly. In nine patients there was a similar release of nucleosides into coronary sinus blood during reperfusion after 59 to 80 minutes of ischemic arrest during cardiac surgery. With initial reflow, adenosine, inosine and hypoxanthine levels reached 65, 655 and 917 nmol/100 ml of blood, respectively. Inosine and hypoxanthine concentrations remained high for 5 to 10 minutes after cardiac beating resumed, often when production of lactate had decreased. The results indicate that postischemic release of nucleosides reaches significant levels in man as well as animals, is parallel with the duration of ischemia, is temporary and may be a useful supplement to measurement of lactate as an index of prior myocardial ischemia.
Am J Cardiol 1979 Jan
PMID:Release of nucleosides from canine and human hearts as an index of prior ischemia. 75 70

The antianginal effect of three drugs (isosorbide dinitrate-nifedipine-oxprenolol) and of two drug associations (isosorbide dinitrate-oxprenolol; nifedipine-oxprenolol) was studied in six patients, by means of a bicycle ergometer exercise test. The study was double blind; placebo was also included in the test. Treatments were administered according to the sequence of a 6 X 6 "balanced" latin-square design. After treatment with isosorbide dinitrate and nifedipine a significant delay in the appearance of angina and of signs of electrocardiographic positivity was observed while after treatment with oxprenolol a significant delay was noticed only in the time of appearance of electrocardiographic positivity. On the contrary, placebo did not determine significant changes in the studied parameters. The best results were achieved with the associations oxprenolol-isosorbide dinitrate and oxprenolol-nifedipine. With these treatments, angina appeared during the exercise test in only two patients while the others had to stop the test because of muscular exhaustion; electrocardiographic signs of ischemia did not appear in one patient. The favourable results of the associations oxprenolol-isosorbide dinitrate and oxprenolol-nifedipine can be explained by the pharmacologic effect of these drugs and by their complementary action.
G Ital Cardiol 1976
PMID:[Evaluation and comparison of five antianginal treatments by means of a bicycle ergometer exercise test (author's transl)]. 79 9

In 10 patients without and 20 patients with various degrees of angiographically proven CAD 93 pacing runs were studied. Changes of PAm, of ECG, and of anginal pain serving as parameters of myocardial ischemia were correlated to the rate-pressure-product. In patients without CAD no correlations could be ascertained. In each patient with CAD determination of ischemia was achieved reproducibly. Ischemia threshold is represented by a sharp increase of PAm. Ischemia threshold seems a parameter to be preferred as compared to pain threshold. The extent of CAD (angiographically estimated) correlates well with the pacing test especially when collaterals are taken into account. After NG no substantial improvement of ischemia can be detected: Ischemia threshold before and after NG was reached at same rate pressure in each case. We conclude the atrial pacing test to be an excellent test for the provocation of myocardial ischemia. The test is also useful for estimation of the extent of CAD.
Basic Res Cardiol
PMID:Pacing-induced myocardial ischemia in spite of nitroglycerin. Correlations regarding the extent of coronary artery disease. 80 82

To determine the effect of isosorbide dinitrate or ischemic myocardium, this agent was administered to dogs with well developed coronary collateral vessels 8 to 14 weeks after embolization and subsequent occlusion of the left anterior descending coronary artery. After thoracotomy the left coronary artery was cannulated and perfused with blood from the femoral artery. The distal left anterior descending artery was cannulated to monitor peripheral coronary pressure. Regional contractile force in the normal left circumflex and potentially ischemic left anterior descending regions was measured with isometric strain gauge arches sewn to the epicardium. Moderate decreases in coronary perfusion pressure averaging 27 mm Hg produced selective ischemia in the myocardium beyond the site of occlusion of the left anterior descending artery. Under these conditions the average increase in peripheral coronary pressure produced by intracoronary injection of isosorbide dinitrate was 9.0 mm Hg, whereas contractile force in the ischemic region increased by 30 percent. The contractile force was unchanged in the normal regions. Therefore, isosorbide dinitrate can dilate coronary collateral vessels and improve contractile force in ischemic areas. Intracoronary injection of nitroglycerin had similar effects. The durations of responses to isosorbide dinitrate and nitroglycerin were remarkably similar: 6.4 and 6.7 minutes, respectively. Although isosorbide dinitrate can directly dilate coronary collateral vessels, its effects are not longer lasting than those of nitroglycerin.
Am J Cardiol 1976 Feb
PMID:Comparative effects of nitroglycerin and isosorbide dinitrate on coronary collateral vessels and ischemic myocardium in dogs. 81 10


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