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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:[Prolapse of the mitral valve]. 70 34

The effects of atrial pacing (A.P.) on the myocardial balance of inorganic phosphate (Pi) were studied in 11 patients with coronary atherosclerosis and pacing-induced angina (Group C) and in 5 normal subjects (Group N). During A.P. in group C 64% of patients had myocardial loss of Pi, statistically significant (p less than 0,025) always with concomitant reduced myocardial extraction or production of lactate, but only 70% of patients with reduced myocardial extraction or production of lactate had myocardial loss of Pi. In only 1 p. of group N myocardial loss of Pi with normal lactate extraction was observed. These data show that during pacing-induced ischemia there is a negative myocardial balance of Pi, that can be used as a metabolic indicator of ischemia, but less reliable than lactate reduced extraction or production.
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PMID:[Liberation of inorganic phosphates in the coronary sinus as an indicator of human myocardial ischemia]. 75 26

We measured aortic and coronary sinus dopamine (DA), epinephrine (E), and norepinephrine (NE) in eight patients with cardiac ischemia (I) and eight control subjects (C). Samples were taken at rest (73 +/- 3 beats/min in C and 68 +/- 3 beats/min in I) and during coronary sinus pacing to peak rates (144 +/- 4 beats/min in C and 136 +/- 6 beats/min in I). Arterial NE was higher in the ischemic patients at rest (254 +/- 25 pg/ml in C and 324 +/- 21 in I; p less than 0.05). There were no differences in arterial E and DA. Neither pacing nor angina affected peripheral catecholamine concentrations. Resting myocardial NE flux was similar for both groups. With pacing, coronary sinus flow and net myocardial NE release increased significantly in both groups. The maximum relative increase in net myocardial NE release was less in the ischemic patients than in the controls (575 +/- 145% in C and 255 +/- 40% in I; p less than 0.05). Thus, angina induced by pacing does not augment peripheral sympathetic activity. Furthermore, pacing-induced angina appears to be associated with a decrease in cardiac sympathetic tone compared with that found in paced controls.
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PMID:Catecholamines in coronary sinus and peripheral plasma during pacing-induced angina in man. 75 22

The coronary venous efflux of lactate, inosine and hypoxanthine during pacing-induced angina has been compared with myocardial extraction of the catabolites during exercise-induced angina. Inosine and hypoxanthine were analyzed by enzyme assay after separation by column chromatography. Myocardial lactate extraction at rest (15 +/- 9%, mean +/- SD) was converted to production levels (-34 +/- 26%) during pacing-induced angina (p less than 0.0005) and increased (24 +/- 13%) during exercise (p less than 0.05). The arterial values at rest (850 +/- 330 mumol/1) were unchanged during pacing and increased five-fold during exercise (4380 +/- 1860 mumol/1). The mean myocardial inosine extraction at rest (33 +/- 10%) was transformed to release values (-41 +/- 30%) during pacing (p less than 0.0005) as well as during exercise (-20 +/- 27%) (p less than 0.0005). The hypoxanthine extraction at rest (25 +/- 11%) decreased during pacing (-7.8 +/- 29%) (p less than 0.0025) and exercise (10 +/- 25%) (NS). The slight increase of arterial inosine and hypoxanthine values was not significant. Myocardially produced lactate, a sensitive marker of pacing-induced ischemia, was obscured by elevated arterial concentrations during exercise. However, inosine significantly correlated with lactate during pacing, and was useful in detecting ischemic myocardial energy deficiency during exercise-induced angina.
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PMID:Myocardial release of lactate, inosine and hypoxanthine during atrial pacing and exercise-induced angina. 75 23

Unstable angina is a syndrome which comprises a spectrum of symptomatic manifestations of coronary artery disease which lies between stable angina pectoris and acute myocardial infarction. Patients fall into three groups: angina of recent onset (4 weeks), angina of changing pattern, and angina occurring at rest (longer than 15 minutes). The syndrome may presage acute myocardial infarction or sudden death, or may itself be the manifestation of a myocardial infarction. The pathophysiology may involve primary cardiac events or extracardiac precipitating factors, and does not appear to be the consequence of a particular anatomic pattern of coronary artery disease. Pain may occur as a result of regional reduction of coronary flow to pressure-dependent areas of myocardium during states of increased myocardial oxygen demand. Persisting ischemia leads to infarction via a series of events which may include myocardial edema formation, increased beta-sympathetic tone, and others which have been experimentally modified by interventions designed to limit infarct size. Although the incidence of acute myocardial infarction and death was high in early studies, in recent reports acute infarction occurs in under 15.5 per cent and death in under 2 per cent. Patients at high risk are those pain persists with bed rest, and those with preceding stable angina pectoris or myocardial infarction. Prognostic differences among Groups 1, 2, and 3 may exist but cannot be assessed from available studies. Studies of the management of unstable angina have generally been uncontrolled. Hospitalization, bed rest, and short- and long-acting nitrates are generally employed in Groups 2 and 3 patients and the marked reduction in myocardial infarction rates from early to recent studies tends to support these approaches. Anticoagulants are less used now than formerly. Propranolol can produce a significant reduction of myocardial oxygen consumption and may redirect coronary flow to ischemic areas. The drug has effectively controlled pain in several studies and is now widely used to manage unstable angina. Aortocoronary bypass surgery has been extensively employed but there is only one preliminary report of a controlled study available. The role of surgery is not yet defined. The optimal approach to therapy may eventually involve the use of medical therapy, including beta-blockade to stabilize patients, with delayed semielective coronary angiography and surgery in those who respond. Emergency angiography and surgery might then be reserved for the high-risk group of patients whose pain persists during optimal medical therapy.
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PMID:Unstable angina pectoris. 78 21

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.
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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.
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PMID:Pacing-induced myocardial ischemia in spite of nitroglycerin. Correlations regarding the extent of coronary artery disease. 80 82

An experimental model of angina pectoris has been developed in order to study the hemodynamic, metabolic and electrophysiological alterations of the heart assumed to occur in the human disease and to analyze the influence of nitroglycerin and dipyridamole on the above changes. In anesthetized and thoractomized dogs, the left anterior descending coronary artery was autoperfused from the subclavian artery. Coronary blood flow was reduced until the epicardial monopolar electrocardiogram recorded from the myocardial segment supplied by the constricted coronary artery was just short of ischemic changes. O2 consumption and lactate uptake of the same segment were determined from the arteriovenous difference by sampling venous blood draining this area. Increasing heart rate by 50 to 70 beats/min by electrical pacing of the right atrium evoked a reversible and reporducible elevation of the ST segment and T wave of the electrocardiogram. Blood flow to the area perfused by the constricted coronary artery as well as the O2 uptake of the same area failed to increase on pacing. A concomitant decrease of lactate uptake, sometimes becoming even negative, was indicative of ischemia of that area. These changes could be reduced or prevented by a 10-minute infusion of a total dose of 20 mug/kg of nitroglycerin but not by 60 mug/kg of dipyridamole. Since the changes are fully reversible and readily reproducible, and the response also appears to show parallelisms with those observed in the human patient during an acute angina pectoris attack, use of this model for the assay of antianginal drugs seems to be warranted.
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PMID:Nitroglycerin and dipyridamole on cardiac metabolism and dynamics in a new experimental model of angina pectoris. 81 80

Myocardial 201Tl uptake and regional blood flow by the microsphere technique were determined in anesthetized dogs undergoing either 20 min of coronary occlusion and 100 min of reperfusion (N = 10) or 120 min of occlusion (N = 4). In both groups, 201Tl was injected intravenously after 10 min of occlusion. In transiently occluded dogs, regional flow at the time of 201Tl administration was reduced to 8 +/- 3% of normal flow in endocardial layers of the central ischemic zone. After 100 min of reperfusion, flow values were not significantly different from normal. 201Tl activity after reperfusion rose to 56 +/- 5% of normal, demonstrating that redistribution of the radionuclide occurred during the reflow period. In animals with persistent occlusion, there was a significant relationship between 201Tl uptake and flow (r = 0.95) and no evidence of redistribution of 201Tl during the two hour occlusion period. In another five dogs receiving 201Tl, serial gamma camera images obtained during reperfusion showed increasing uptake of the tracer in apical defects which returned to normal by 4 hours of reflow. Thirteen patients with stable angina received 2 mCi of 201Tl intravenously at peak exercise, and multiple gamma camera images obtained serially. All demonstrated zones of diminished 201Tl uptake 10 min after exercise. Defects which partially or completely disappeared within 1-6 hours postexercise corresponded to areas supplied by coronary arteries with significant stenoses. Persistent defects were present in regions of old myocardial infarction. Six additional patients with acute myocardial infarction demonstrated 201Tl myocardial defects which showed no significant change over 6 hours. Thus, redistribution of 201Tl into ischemic myocardium was demonstrated during transient coronary occlusion in dogs and after exercise stress in man. Sequential imaging after a single dose of 201Tl at the time of exercise may provide a means for distinguishing between transient perfusion abnormalities or ischemia and myocardial infarction of scar.
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PMID:Differentiation of transiently ischemic from infarcted myocardium by serial imaging after a single dose of thallium-201. 83 45

Alternans of the elevated ST segment (STEA) was found in 8 of 21 patients (38%) with Prinzmetal's variant angina. In addition to STEA, all eight patients had varying cardiac arrhythmias: multiple premature ventricular depolarizations in eight, ventricular tachycardia in five, and ventricular fibrillation in three. There was no consistent temporal relationship between the occurrence of STEA and the cardiac arrhythmias. Alternans occurred during periods when no arrhythmias were present. All eight patients underwent coronary angiography. Spontaneous coronary artery spasm was documented angiographically in three patients including two who had minimal or no coronary atherosclerotic disease. Six patients had severe, fixed, occlusive coronary artery disease. Possible mechanisms for STEA include: 1) failure of regions of myocardium to depolarize on alternate beats due to variation in conduction and refractoriness between ischemic and nonischemic zones of myocardium, and 2) electrical alternans of the transmembrane action potential during phase 2 and 3 (repolarization) caused by changes in the rate and extent of electrolyte transfer across cell membranes during ischemia. It is postulated that STEA is an electrocardiographic sign in the surface ECG of a dysequilibrium of refractory periods during ischemia and reflects an unstable electrical state of the myocardium.
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PMID:Alternans of the ST segment in Prinzmetal's angina. 83 98


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