The purpose of this study was to determine if biochemical, functional, and ultrastructural abnormalities persist in nonnecrotic postischemic myocardium salvaged by coronary reperfusion. Anesthetized dogs were subjected to 15 min of occlusion of the left anterior descending (LAD) coronary artery followed by 3 days of reperfusion. Biopsies were obtained for measurement of adenosine 5'-triphosphate (ATP) and creatine phosphate (CP) nmol/mg protein), and regional function was evaluated using sonomicrometry. Myocardial ATP concentration after 15 min of occlusion was 37 +/- 1 nmol/mg cardiac protein in nonischemic subendocardium and 19 +/- 2 nmol/mg in ischemic subendocardium. After the hearts underwent 90 min and 72 h of reperfusion, ATP remained significantly depressed in reperfused subendocardium with values of 25 +/- 5 and 29 +/- 2 nmol/mg, respectively (P less than 0.05 and P less than 0.01 compared with the nonischemic zone in which ATP remained normal). CP levels fell during ischemia but returned to normal by 90 min of reperfusion. Percent systolic shortening of myocardial segments fell from +18 +/- 1% (active shortening) to -13 +/- 2% (passive lengthening) during ischemia and was still significantly depressed at +11 +/- 1% (P less than 0.05 vs. preocclusion) at 72 h of reperfusion. Histological examination showed no necrosis, but ultrastructural abnormalities were present. Therefore brief periods of myocardial ischemia are not associated with necrosis but result in functional, biochemical, and ultrastructural abnormalities, which are present for at lest 3 days after coronary reperfusion.
SUMMARY We determined the prevalence of mitral valve prolapse (MVP) in presumably healthy young men by studying 107 male house officers and medical students with cardiac auscultation in the supine, sitting and standing positions. Echocardiograms were performed at rest in the supine position before and after amyl nitrite inhalation and were obtainable in 101 subjects. Eleven of the 101 subjects had abnormal findings on auscultation: four had an isolated click and seven had a click and late systolic murmur. Correlation of the independent auscultatory and echocardiographic data in the 101 subjects showed that all seven of the subjects with a click and a murmur had echocardiographic evidence of prolapse. None of the 90 subjects with normal auscultation or the four with an isolated click had an abnormal echocardiogram. All seven subjects with MVP had thoracic skeletal abnormalities, but only one was symptomatic. These data suggest that the prevalence of MVP in healthy young males is similar to the reported 6-10% prevalence in healthy young females.THE MITRAL VALVE PROLAPSE SYNDROME was described clinically by Barlow et al." 2 as a midsystolic click and/or late systolic murmur. The clinical spectrum of mitral valve prolapse ranges from normal mitral anatomy and function to severe distortion of leaflet and chordal anatomy with severe mitral regurgitation.Multiple etiological factors contribute to mitral valve prolapse, as indicated by its association with Marfan's syndrome, thoracic skeletal deformities, connective tissue disorders, rheumatic heart disease, decreased left ventricular dimensions as seen in secundum atrial septal defect and aging, hypercontractile states of the ventricle, and coronary artery disease with papillary muscle dysfunction.3-5 Mitral prolapse also occurs in the absence of these related disorders and may be either sporadic or familial.A prevalence figure for mitral valve prolapse in the general population has been difficult to determine, since prevalence depends, in part, on the age, sex, and associated disease processes in the study population. The prevalence figures reported include 1.4% of black South African school children,2 5% in routine autopsies of patients over 40 years of age,6' 7 and 6-10% of presumably normal young women studied by echocardiography.8-10 In this study we assessed the prevalence of mitral valve prolapse in a group of young healthy adult males. MethodsThe study population comprised 107 male house staff and medical students of the Emory University School of Medicine stationed at the Atlanta Veteran's Administration HoQspital over a 3-month period.From Emory University School of Medicine, Department Echocardiograms were done at rest and after amyl nitrite inhalation and were interpreted by two echocardiographers who were unaware of the auscultatory findings. Results AuscultationEleven subjects had a midsystolic click that moved toward the first heart sound after standing. In four of these 11, there was no accompanying systolic murmur.
Three patients presented with severe congestive cardiomyopathy of unknown cause. All three had a profound depression of serum phosphorus levels resulting from the chronic ingestion of large quantities of a phosphorus-binding antacid. Results of physical examination and echocardiograms were consistent with cardiomegaly and severe myocardial dysfunction, and chest films showed enlargement of the cardiac silhouette with interstitial pulmonary edema. Serum phosphorus was restored to normal levels, and within 2 to 5 weeks the results of physical examination and echocardiogram of each patient returned to normal. We conclude that these patients had reversible hypophosphatemic cardiomyopathy and show the importance of inorganic phosphorus in myocardial metabolism and function. Serum phosphorus measurements should be a part of the routine evaluation of patients with congestive cardiomyopathy because, at least in some patients, hypophosphatemia appears to be a reversible cause of this disorder.
The purpose of this study was to determine whether or not the biochemical, functional, and ultrastructural abnormalities produced by brief temporary coronary occlusions (unassociated with necrosis) ever resolve and, if so, when they do. Anesthetized open-chest dogs were subjected to 15 min ofcoronary artery occlusion followed by 72 hr, 7 days, or 14 days of reperfusion. Serial in vivo myocardial biopsies were performed for measurement of ATP and for ultrastructural analysis. Regional function was evaluated by sonomicrometry. Mean (±SEM) my-
SUMMARY The purposes of this investigation were (1) to develop an in vivo method of determining the myocardium at risk after experimental coronary occlusion; (2) to define the spatial geometry of the salvageable ischemic border zone; and (3) to assess the ability of flurbiprofen, an antiinflammatory agent, to protect ischemic myocardium from necrosis. Twenty-two open-chest dogs underwent left anterior descending coronary artery occlusion and were randomized to treated (flurbiprofen 1 mg/kg i.v. at 30 minutes and 4 hours after occlusion; n = 11) or control (saline; n = 11) groups. Six hours after occlusion, methylene blue, 3 mI/kg, was injected into the left atrium, and immediately thereafter the hearts were removed and sliced transversely. Areas not perfused by methylene blue (area at risk [Ar]) were traced, planimetered, and compared to the area of necrosis (An) after incubation in triphenyltetrazolium chloride. The Ar for the two groups were similar (control 28.2 + 2.6%; treated 25.2 2.3% of total left ventricle; NS). In control dogs, An/Ar was 96.2 ± 0.7%, with similar values for the epicardium and endocardium. In treated dogs, An/Ar was 66.9 ± 8.9% (p < 0.001), with greater epicardial than endocardial salvage. Topographic superimposition of the An on the Ar showed that salvage occurred both on the epicardial and lateral aspects of the infarct.We conclude that (1) the in vivo methylene blue method of assessing myocardium at risk is useful in standardizing experimental infarct size; (2) flurbiprofen, administered 30 minutes and 4 hours after occlusion, is a potent agent for reducing infarct size; and (3) salvage of myocardium occurs both at the lateral and epicardial borders of the infarct in dogs treated with flurbiprofen.NUMEROUS INTERVENTIONS have been shown in experimental animal studies to preserve myocardium otherwise destined to become necrotic as a result of reduced blood flow.'-" An important omission in many previous studies has been the estimation of the quantity of myocardium that would have been expected to become necrotic without the intervention being tested. The ability to salvage ischemic myocardium has been ascribed to numerous agents, based on a statistically smaller mean infarct size in treated animals compared with the control group. However, the marked variability even in the results of experiments in untreated animals makes this criterion less than adequate. More
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.