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)

Midmyocardial and subendocardial pH monitoring was used as an indirect method for continuous evaluation of regional canine myocardial ischemia. Left ventricular midmyocardial pH (pHm) at 4 mm. depth was monitored in 10 dogs, under resting conditions, by means of a 5 mm. Beckman pH probe. pHm was 6.96 +/- 0.03, recorded at myocardial temperatures of 35 to 37 degrees C. Ischemia was then produced by snare occlusion of the proximal left main coronary artery for 2 minutes. pHm decreased to 6.87 +/- 0.03 (p less than 0.01) at 1 minute and 6.80 +/- 0.04 (p less than 0.005) in 2 minutes. When flow was restored, pHm returned toward normal within 2 minutes (pH 6.86 +/- 0.03) and at 5 minutes had returned to control values (pH 6.93 +/- 0.03). In another 5 dogs under similar conditions, pHm at 4 mm. and subendocardial pH (pHe at 8 mm.) were measured. Baseline pHm (6.97 +/- 0.01) and pHe (6.84 +/- 0.02) levels were significantly different (p less than 0.0005). After 2 minutes of ischemia, pHm was 6.82 +/- 0.03, whereas pHe decreased to 6.78 +/- 0.04 (p less than 0.1). Five minutes after snare release, pHe remained at 6.73 +/- 0.07; pHm (6.93 +/- 0.03) returned to control values. Both pHm (6.93 +/- 0.02) and pHe (6.84 +/- 0.09) levels were normal 15 minutes after release of the snare. The midmyocardium and subendocardium have different pH levels which can be monitored. Ischemia produces different pH patterns in these layers. pHm returns to control values within 5 minutes after 2 minutes of ischemia, whereas pHe remains depressed for at least 5 minutes. pH monitoring provides an accurate and simple method for on-line evaluation of endocardial ischemia.
J Thorac Cardiovasc Surg 1976 Jul
PMID:Monitoring of midmyocardial and subendocardial pH in normal and ischemic ventricles. 0 26

Lidocaine and tocainide had no effect on ventricular conduction of extrasystoles with coupling intervals longer than 500 msec in isolated blood-perfused dog hearts, but caused interval-related increases in conduction time of extrasystoles in the range of 250--400 msec, here called mid-range extrasystoles (MRE). Quinidine, procainamide, disopyramide, and methyl lidocaine increased conduction times of extrasystoles at all coupling intervals, and no additional slowing of MRE was observed. The slowing of MRE specific to lidocaine and tocainide was confirmed in the intact dog heart. During acute myocardial ischemia in the intact dog heart, conduction was slowed and additional slowing of MRE was found. Lidocaine and tocainide caused further slowing of conduction of MRE. This unique effect of lidocaine and tocainide on the conduction of MRE may be important in the suppression of reentrant arrhythmias. However, lidocaine and tocainide were also found to be arrhythmogenic when extrasystoles were introduced, after acute coronary occlusion, in those animals in which such occlusion alone did not allow demonstration of arrhythmias due to extrasystoles.
J Cardiovasc Pharmacol
PMID:A specific effect of lidocaine and tocainide on ventricular conduction of mid-range extrasystoles. 9

The association of a left coronary artery-main pulmonary artery fistula and an anomalous right coronary artery originating from the main pulmonary artery is the subject of this report. This unique combination of congenital cardiac anomalies establishes a double coronary steal from the left coronary artery, which hemodynamically represents the sole source of myocardial perfusion. The left coronary artery-main pulmonary artery fistula was closed and the coexisting anomalous right coronary artery reimplanted into the anterior aspect of the ascencing aorta. A dual coronary supply was therefore established and thus eliminated the potential threat of total myocardial ischemia should the left coronary artery become critically compromised. Patency of both the left coronary artery and the transplanted right coronary artery was documented 1 year postoperatively by aortic root angiography.
J Thorac Cardiovasc Surg 1975 Jul
PMID:Surgical correction of congenital left coronary artery-main pulmonary artery fistula in association with anomalous right coronary artery. 12 68

The data regarding the effect of physical of physical conditioning on the progression of myocardial is chemia, although suggestive of a favorable influence, are in no way definitive. Efforts to alter the physical activity habits of our population should not supersede efforts directed to alter the major risk factors. The emphasis in the prevention of coronary atherosclerotic heart disease for the general public should be on the well established cardinal risk factors, that is, hypercholesterolemia, hypertension, and cigarette smoking. The National Postinfarction Rehabilitation Study, when completed, may demonstrate how physical conditioning influences the progression of myocardial ischemia. However, "moderate activity is a part of a balanced satisfying living and is the safe and sane hygienic prescription of the thoughtful physician for his patients, the high risk and the healthy alike.
Cardiovasc Clin 1977
PMID:Does exercise conditioning delay progression of myocardial ischemia in coronary atherosclerotic heart disease? 13 6

Echocardiography is a valuable technique for the diagnosis and serial follow-up of patients with impaired cardiac function. It is subject to certain limitations due to the assumptions inherent in deriving ventricular volume from a one-dimensional measurement and must be interpreted with caution in cases of suspected regional abnormalities of contraction. Given these caveats, echocardiography is valuable in the quantitative assessment of cardiac size and the level of compensation in patients with primary myocardial disease, valvular heart disease, and left ventricular hypertrophy. It can detect abnormal contraction in some patients with ischemic heart disease and provides an accurate method to serially follow changes produced as a result of drug or surgical therapy. Finally, two-dimensional techniques promise to provide a new perspective on the evaluation of patients with regional wall motion abnormalities.
Prog Cardiovasc Dis
PMID:The use of echocardiography for quantitative evaluation of left ventricular function. 15 Jun 20

Although corticosteroids have been shown to stabilize lysosomal membranes and prevent release of hydrolytic enzymes, the mechanism of membrane stabilization remains obscure. The few reports regarding the use of steroids in myocardial ischemia have been conflicting. This study was undertaken to determine if a pharmacologic dose of the glucocorticoid methylprednisolone would protect the heart during ischemic cardiac arrest. A randomized double-blind study was performed in 25 dogs. Biochemical and hemodynamic parameters were assessed during and after cardiopulmonary bypass and after 30 minutes of ischemic cardiac arrest. Animals were divided into two groups. Group I served as controls and consisted of dogs injected intravenously with the vehicle of methylprednisolone 18 hours and 1 hour prior to experiment. Group II comprised dogs injected with methylprednisolone, 30 mg. per kilogram, IV, at the same time periods. Blood pH, gases, and electrolytes were measured; aortic, left atrial, and left ventricular pressures were monitored; the first derivative of the left ventricular pressure (dp/dt max.) was also determined. Arterial and coronary sinus blood samples were assayed for lactate levels and activity of the lysosomal enzyme, beta-glucuronidase. Left ventricular muscle was assayed for the nucleotides cyclic adenosine 3',5' monophosphate (AMP) and cyclic guanosine 3',5' monophosphate (GMP). Following restoration of coronary flow, mean aortic and left ventricular systolic pressures and left ventricular contractility as determined by dp/dt max. and dp/dt max./IP were depressed in both groups as expected but were significantly higher in Group II than in Group I (p less than 0.05). An increase in levels of both cyclic nucleotides occurred in each group during ischemia, but this increase in cyclic GMP was significantly greater in Group I (p less than 0.05). beta-glucuronidase activity and myocardial potassium loss as determined in coronary sinus blood were both significantly greater in Group I than in Group II (p less than 0.05). Results of this study demonstrate that pretreatment with a pharmacologic dose of methylprednisolone significantly enhances cardiac recovery after ischemia. Lysosomal membrane stability and modulation of cyclic GMP levels may be critical determinants in the mechanism of cardiac ischemia.
J Thorac Cardiovasc Surg 1975 Dec
PMID:Protective effect of methylprednisolone on the heart during ischemic arrest. 17 23

Although the internal mammary artery bypass seems an ideal coronary bypass vessel, it has not usually been possible to use this vessel to bypass distal lesions in the right coronary circulation. In this experiment, the right internal mammary artery was utilized in retrograde fashion to evaluate this anatomically more suitable vessel as a bypass graft to the occluded right coronary artery in the dog. Reversal of acute myocardial ischemia was demonstrated by mapping epicardial ST-segment elevation and measuring surface pH. Preliminary long-term experiments have also demonstrated patency and perfusion of the distal right coronary artery by this method.
J Thorac Cardiovasc Surg 1975 Jul
PMID:Revascularization of the right coronary artery by retrograde perfusion of the mammary artery. An experimental study. 23 91

The natural history of patients with ischemic heart disease and depressed left ventricular function is dismal, and medical therapy has failed to alter its course. To assess the results of aorta-coronary bypass grafting in patients with coronary artery disease and decreased left ventricular ejection fraction (LVEF less than or equal to 0.3), we compared 70 medically treated patients to 46 patients having aorta-coronary bypass grafting. The duration of follow-up was 6 to 72 months (mean 19 months). All patients had angina pectoris. Congestive heart failure was present in 56 percent (39/70) of the medical and 43 percent (20/46) of the surgical group. The medical group had a mean LVEF of 0.20 and a mean left ventricular end-diastolic pressure (LVEDP) of 29 mm. Hg. The surgical group had a mean LVEF of 0.21 and a mean LVEDP of 24 mm. Hg. Three vessel disease was found in 60 percent (42/70) of the medical group and 83 percent (38/46) of the surgical group. The operative mortality rate in the surgical group was 4 percent (2/46). There were four late deaths. The 2 year actuarial survival rate for medical and surgical groups was 47 percent and 83 percent, respectively. Significant improvement in angina pectoris and/or congestive heart failure was found in 16 percent (11/70) of medically treated patients and 95 percent (38/40) of the surgically treated patients. Aorta-coronary bypass grafting can be performed in patients with poor left ventricular function with a low operative mortality rate, relief of angina pectoris, and improvement in symptoms of congestive heart failure.
J Thorac Cardiovasc Surg 1977 Jul
PMID:Ischemic cardiomyopathy: medical versus surgical treatment. 30 91

Myocardial ischemia causes a series of anatomic and physiologic abnormalities that can be detected and quantified by assessment of myocardial perfusion, mechanical function, electrophysiology, and metabolism. These methods of assessment vary widely in sensitivity, specificity, relevance, cost, and ease of application. Although occasionally the appropriate choice of diagnostic procedures is clinically difficult, the demonstrated potential of coronary artery bypass surgery to reverse both acute and chronic myocardial ischemia makes the detection of ischemia an important effort in the care of patients with coronary artery disease.
Cardiovasc Clin 1977
PMID:Detection of myocardial ischemia. 33 74

Little is known of the clinical significance of myocardial bridges, which may be recognized angiographically as systolic coronary artery narrowing (SCAN). A retrospective review of a 1 year's experience (313 consecutive coronary arteriograms) revealed 5 patients with SCAN, an incidence of 1.6%. SCAN involved the proximal and/or middle segments of the left anterior descending coronary artery in all patients. It is of particular note that the administration of nitroglycerin noticeably accentuated the SCAN phenomenon in each of 3 patients to whom it was administered. Four of the 5 patients had left ventricular hypertrophy due to hypertrophic cardiomyopathy (2), aortic stenosis (1), and hypertension (1). All 5 patients with the SCAN phenomenon had anginal chest pains, and critical obstructive coronary atherosclerosis was observed in only 2 cases. The other 3 patients showed, otherwise normal coronary arteriograms. Thus, myocardial bridges appear to be angiographically manifest predominantly in patients with cardiac hypertrophy. Nitroglycerin, which accentuates SCAN, might be useful as a provocative test to enhance the angiographic recognition of this phenomenon. The possible role of myocardial bridges in the production of myocardial ischemia warrants further investigation.
Cathet Cardiovasc Diagn 1977
PMID:Myocardial bridges in man: clinical correlations and angiographic accentuation with nitroglycerin. 40 19


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