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)

Fifteen patients with frequent anginal chest pain underwent diagnostic cardiac catheterization. After coronary arteriography a specially designed cardiac catheter was seated in the aortic root, permitting the continuous infusion of krypton-81m into the right and left aortic sinuses. A gamma camera, areas of interest and a visual display unit were used to record images and the regional myocardial equilibrium of activity before, during and after a standarized atrial pacing test. The unique physical properties of krypton-81m allowed the continuous imaging and recording of moment to moment changes in regional myocardial perfusion. This investigation revealed that when the coronary arteriogram was normal or revealed lumonal stenosis of less than 50 percent, regional myocardial perfusion was uniform at rest and during stress. Two patients with a previous history of myocardial infarction had defects of regional perfusion at rest and during stress. Krypton scintigraphy demonstrated reversible regional defects in myocardial perfusion during stress in seven patients with greater than 70 percent stenosis of one or more coronary arteries. Alterations in regional myocardial perfusion occurred within 30 seconds of the start of atrial pacing in all the patients and preceded the onset of electrocardiographic signs of ischemia or chest pain.
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PMID:Krypton-81m in the physiologic assessment of coronary arterial stenosis in man. 42 Jan 4

Doppler ankle blood pressures were performed inere obtained in 100 consecutive patients with peripheral arterial insufficiency after treadmill exercise. A twelve lead electrocardiogram was monitored during and after exercise. Despite a restricted ability to exercise because of peripheral vascular insufficiency, forty-six patients had ventricular dysrhythmia or ischemia, or both, usually without associated symptoms. Electrocardiographic monitoring during treadmill exercise proved a useful predictor of postoperative complications. Thirty-two vascular operations were performed in patients with no electrocardiographic evidence of ischemia. No patient had a postoperative myocardial infarction or died. Sixteen vascular procedures were performed in patients with ischemic responses on exercise electrocardiography. Six patients had postoperative myocardial infarctions, two of which were fatal. Electrocardiographic monitoring during treadmill exercise for peripheral vascular insufficiency in recommended (1) to assess the severity of coronary artery disease and the likehood of postoperative complications, and (2) as a precautionary measure to identify potentially dangerous dysrhthmias or ischemia during exercise before the development of clinical symptoms.
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PMID:Assessment of operative risk with electrocardiographic exercise testing in patients with peripheral vascular disease. 42 97

A 65-year-old woman with an acute myocardial infarction, as judged by serial enzyme changes, developed transitory Q waves in leads V2 to V4 and leads 2, 3, and aVF during an attack of pain in the chest. These Q waves were not present 12 hours later. It is suggested that these changes represent a focal block in the septal fibers of the left bundle-branch system. This defect could underlie the transient right precordial Q waves seen in myocardial infarction or ischemia, as well as the fixed Q waves of many patients without septal infarction at autopsy.
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PMID:Transient focal septal block. 43 30

A total of 25 cases (12 men, 13 women) of complete left bundle branch block (LBBB) were found among 1,400 consecutive autopsy in the aged. Their ages ranged from 70 to 86 years (average 78.9). ECG was analyzed as for the occurrence of LBBB and myocardial infarction (MI). Pathological examinations included observations of the conduction system by serial sections. They were divided into group A with MI and group B without MI. Duration of LBBB was 1 to 3 days in 4 cases, more than 1 month in 7, and more than 1 year in 14. From the temporal sequence of LBBB and MI in group A, cases were classified into (1) MI preceding LBBB in 5, (2) both coexistent in 5, and (3) LBBB preceding MI in 1. There were 8 cases of normal electrical axis, 17 left axis deviation, 7 first degree A-V block, and 2 atrial fibrillation. Various heart diseases were underlying in 21 cases, including hypertension, MI, mitral and aortic regurgitation, and primary myocardial disease, and there were 4 cases with no cardiac diseases. Cause of death was cardiac in 12; MI, congestive heart failure, and sudden death. Heart weight was 410 Gm on the average (240 to 550 Gm). MI was found in 11, with stenotic index of 12/15, while it was 9/15 in group B. Lesions of the conduction system were slight to moderate (1.5 to 2.4) except left bundle branch, which showed marked changes in posterior (4.9) and anterior (4.8) fascicles. Site of interruption of the left bundle branch was the junction between the branching portion of the A-V bundle and the left bundle branch (Junctional type) in 17, and peripheral portion of the left bundle branch about 10 mm or more below the junction in 8 (Peripheral type). In conclusion, 2/3 of cases of LBBB belonged to the junctional type and most of them were not related to MI, but to the lesions caused by mechanical injuries at the septal summit. One third of the cases were as peripheral type, which was mainly related to the various types of lesions including septal ischemia (necrosis and fibrosis).
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PMID:A clinicopathological study on 25 cases of complete left bundle branch block. 44 51

The effectiveness of the calcium antagonist nifedipine in preserving postischemic myocardial function and structural integrity was experimentally demonstrated in isolated rabbit hearts, in conscious dogs subjected to myocardial infarction, in open chest anesthetized dogs with normothermic regional ischemia induced for 1 to 2 hours and in dogs undergoing hypothermic global ischemia for 2 hours followed by 2 hours of reperfusion. Nifedipine had a beneficial effect on postischemic myocardial stiffness and mitochondrial calcium accumulation, which were correlated. Administration of nifedipine at the onset of myocardial infarction increased blood flow to ischemic zones of myocardial infarction and resulted in less loss of creatine kinase. It reduced by two- to three-fold the volume of the ischemia-reperfusion injury induced by left anterior descending coronary arterial occlusion and release and preserved indexes of hemodynamic function. Nifedipine was found effective in protecting myocardial performance and structure after 2 hours of global ischemia during hypothermic cardiopulmonary bypass. It is suggested that this agent may be useful as an adjunct to cold cardioplegia in man for enhanced myocardial protection during cardiac surgery.
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PMID:Nifedipine: a myocardial protective agent. 49 88

Serial treadmill exercise testing (mean 5.5 tests/patient) was used to evaluate the prognosis of 200 males (mean age 53 years) without clinical heart failure or unstable angina pectoris 3 weeks after acute myocardial infarction (MI). Exercise-induced ischemic ST-segment depression greater than or equal to 0.2 mV 3 weeks after MI was significantly more prevalent in patients with subsequent cardiac arrest (100%) or coronary artery bypass graft surgery (64%) than in patients without subsequent events within 2 years of infarction (35%) (p less than 0.05). Exercise-induced ventricular arrhythmia on multiple tests 5-52 weeks after MI was more prevalent in patients with recurrent myocardial infarction (90%) than in patients without subsequent events (47%) (p less than 0.001). By contrast, exercise-induced ventricular arrhythmia on a single test at 3 weeks was a less powerful predictor of subsequent cardiac events. Exercise-induced ischemia 3 weeks after MI predicted early fatal events, while ventricular arrhythmia on serial testing predicted later nonfatal events.
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PMID:The prognostic significance of serial exercise testing after myocardial infarction. 49 48

Thrombotic complications of heparin administration were observed in eight patients during a two year period. At sites of subcutaneous heparin injection, six patients developed areas of the skin and subcutaneous necrosis. Systemic thrombotic events and thrombocytopenia were observed in two of these patients when they received intravenous heparin and in two other patients who did not have primary skin necrosis. The complications included peripheral ischemia in three patients (two requiring amputation), myocardial infarction in two, and a cerebral infarction in one. All patients were receiving heparin for at least six days before complications occurred. Seven patients received heparin of bovine origin. Heparin-induced in vitro platelet aggregation was present in all six of the eight patients tested. (It was marked in four of these patients). It is theorized that skin necrosis and the other thrombotic complications observed are the result of heparin-induced in vivo platelet aggregation followed by intravascular thrombosis. Heparin-induced skin necrosis is a rare but serious hazard encountered with prophylactic heparin regimens. If heparin-induced thrombosis is present, the further use of heparin is contraindicated in most instances.
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PMID:Thrombotic complications of heparin therapy: including six cases of heparin--induced skin necrosis. 50 70

Both crude and highly purified testicular hyaluronidase preparations have been shown to contain a component which increases the permeability of the microcirculation in rat skin. This permeability activity had an isoelectric point of 7.4 while hyaluronidase was 9.4. It also could be separated from hyaluronidase by acrylamide gel electrophoresis. The permeability factor was not inhibited by serum and may explain previous observations that hyaluronidase preparations decrease the ischemia and necrosis appropriate to experimental myocardial infarction in vivo.
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PMID:Permeability factor contaminating hyaluronidase preparations. 51 Dec 98

When exercise testing 159 patients with prior myocardial infarction, we identified 39 who were limited by fatigue. This group was all in sinus rhythm; none were taking drugs likely to impair the chronotropic response of the heart; none experienced chest pain or developed ischemic ECG changes. In 18 of this group, maximal heart rate achieved with exercise was 2SD or more below the age predicted value, and their heart rate response to exercise was reduced compared to that of the other 21 whose maximal exercise heart rates were within 2SD of age predicted values. A subgroup of 8 subjects with reduced exercise heart rates was studied before and after vagal blockade. In the 4 subjects whose infarction was inferior, the reduction in heart rate response was more profound and persisted after vagal blockade, suggesting either reduced pacemaker responsivness, due to ischemia or infarction, or autonomic imbalance as possible mechanisms. All 8 showed alinear increases in ventilation at higher power outputs and mean blood lactate postexercise was 7.5 mM/I without vagal blockade. Our findings suggest that a reduced heart rate response to exercise, already shown to imply added coronary risk, may be subdivided aetiologically and possibly prognostically. The use of a "Target Heart Rate" in such patients offers no safety margin, and maximal exercise capacity will be grossly over-estimated if extrapolated from the submaximal heart rate response. A cardiovascular limitation to exercise may be detected by an alinear increase in ventilation.
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PMID:Reduced heart rate response to exercise in ischemic heart disease: the fallacy of the target heart rate in exercise testing. 52 31

This investigation was undertaken in order to experimentally reassess the value of myocardial waviness and stretching as early histological indicators of acute myocardial infarction. Twenty three dogs were subjected to periods of ischemia, from 30 minutes to 4 hours; wavy fibers were present in 87% and 91% of the ischemic and non-ischemic samples respectively. It is concluded that myocardial fiber waviness lacks significance as an indicator or early myocardial infarction, whose diagnosis remains a major challenge.
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PMID:[Experimental reevaluation of myocardial ondulations in the early histological diagnosis of myocardial infarct]. 54


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