Pathophysiology Of Heart Disease Research Articles

Phospholamban-mediated stimulation of Ca2+ uptake in sarcoplasmic reticulum from normal and failing hearts.

Studies in animal models have suggested that alterations affecting phospholamban-mediated stimulation of Ca2+ uptake by sarcoplasmic reticulum are involved in the pathophysiology of heart disease. A monoclonal antibody that binds to phospholamban and stimulates Ca2+ uptake was used to characterize phospholamban-mediated effects in human cardiac sarcoplasmic reticulum and to compare these effects in tissue from normal and failing hearts. Stimulation of Ca2+ uptake by anti-phospholamban monoclonal antibody simulated the effect of phosphorylation of phospholamban by cAMP-dependent protein kinase. Binding of anti-phospholamban antibody reduced the K0.5 of the Ca2(+)-transporting ATPase from 0.53 microM [( Ca2+]) to 0.29 microM [( Ca2+]), without affecting Vmax or nHill. At 0.2 microM Ca2+, stimulation was 1.93-fold in sarcoplasmic reticulum prepared from normal human left ventricular myocardium and 1.94-fold in sarcoplasmic reticulum prepared from the left ventricular myocardium of patients with heart failure resulting from idiopathic dilated cardiomyopathy. Stimulation of Ca2+ uptake in canine cardiac sarcoplasmic reticulum under identical conditions was 1.89-fold. Phospholamban-mediated stimulation of Ca2+ uptake in human cardiac sarcoplasmic reticulum is thus comparable in magnitude to that observed in other species and results from an increase in the apparent affinity of the Ca2(+)-transporting ATPase for Ca2+. The pathogenesis of heart failure in idiopathic dilated cardiomyopathy does not, however, appear to involve intrinsic alterations of this mechanism.

Oxygen radicals in the pathophysiology of heart disease: Edited by Pawan K. Singal: Kluwer Academic Publishers, Boston (1988) 348 pages, $75.00 ISBN: 0‐898‐98383‐757

Clinical CardiologyVolume 12, Issue 3 p. 174-174 Book ReviewFree Access Oxygen radicals in the pathophysiology of heart disease: Edited by Pawan K. Singal: Kluwer Academic Publishers, Boston (1988) 348 pages, $75.00 ISBN: 0-898-98383-757 Peter A. Ward, Peter A. Ward Ann Arbor, MichiganSearch for more papers by this author Peter A. Ward, Peter A. Ward Ann Arbor, MichiganSearch for more papers by this author First published: March 1989 https://doi.org/10.1002/clc.4960120314AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume12, Issue3March 1989Pages 174-174 RelatedInformation

Oxygen radicals in the pathophysiology of heart disease

Oxygen radicals in the pathophysiology of heart disease

Biochemical approaches to the pathophysiology of heart disease with reference to cardiac myosin isozymes

Biochemical approaches to the pathophysiology of heart disease with reference to cardiac myosin isozymes

Assessment of myocardial perfusion during cold stress using thallium-201 scintigraphy in diabetic patients with abnormal changes in left ventricular function during cold stress.

Eleven type-I (insulin-dependent) diabetic patients with abnormal changes in left ventricular function in response to cold stress (CS) were investigated to try and determine the cause of these abnormal responses. Resting M-mode echocardiography demonstrated that all 11 patients had normal left ventricular dimensions and wall motion, thereby excluding overt cardiomyopathy. Thallium-201 scintigraphy was used to assess myocardial perfusion during CS and eight patients were found to have perfusion defects during stress which persisted in four. It is possible that CS unmasks evidence of myocardial ischemia but it is also possible that the abnormal responses to CS reflect altered vasomotor reactivity in the diabetic patient, producing coronary spasm. Left ventricular function may be influenced by many factors in diabetes and an abnormal CS test may not necessarily indicate structural disease. Such tests, however, may help in the further understanding of the pathophysiology of heart disease in diabetes.

The Anesthetic Evaluation and Management of the Surgical Patient with Heart Disease

Successful management of a patient with heart disease requires an understanding not only of the pharmacology of anesthesia but also of the pathophysiology of heart disease. Both of these factors as well as the choice and conduct of anesthesia by the anesthesiologist are thoroughly explored in this article.

Quantitative contrast angiography for assessment of ventricular performance in heart disease

Contrast angiography provides much information about ventricular and valvular size and function. This review describes the calculation of left ventricular chamber volume and wall thickness and the derivation of ejection fraction, cardiac output, mass and wall tension and stress. In patients with valvular regurgitation, valve orifice area can be calculated by using the angiographic output and regurgitant flow determined by comparing the angiographic output with the cardiac output measured using Fick or indicator-dilution techniques. By analyzing ventricular volume in conjunction with pressure, it is possible to assess pressure-volume work, compliance and contractility. Regional wall motion can be measured from the change in ventricular contour with time. When applied clinically, these methods and measurements have been used to determine the hemodynamic characteristics of the compensated and decompensated left ventricle in valvular and coronary heart disease. The information derived from quantifying information in angiographic images contributes to patient diagnosis, assessment of prognosis and evaluation of therapy, and has added to our knowledge concerning the pathophysiology of heart disease.

Anaesthesia for cardiac patients having non-cardiac operations

It is difficult to pick out a sensitive marker for the effectiveness with which patients with heart disease have been managed for non-cardiac operations. Reinfarction rates have frequently been cited for this purpose over the past 20 years and it is interesting and perplexing that, until very recently, we have been unable to show significant decreases in reinfarction rates in patients who have had a myocardial infarction within six months of surgery. It has been our opinion for a number of years that, in general, patients with heart disease are well managed in the intraoperative phase of their hospital stay. The successful management of patients during this period is based on the fact that the majority of anaesthetists now appear to have a good understanding of the pathophysiology of heart disease and are becoming more aggressive in the monitoring and treatment of abnormal haemodynamics when they occur. The ultimate extent to which morbidity and mortality can be reduced in patients with heart disease for non-cardiac surgery will not be known until patients at high risk receive the same intensive postoperative care that patients who undergo heart surgery enjoy. It is the fact that patients are haemodynamically stable and do not have myocardial ischaemia throughout the peri-operative period that is important, rather than the way in which it is achieved.

Heart Disease

This book is a new addition to the list of encyclopedic cardiovascular texts. It is different from most in that two authors have collaborated to write all but three of the 40 chapters. In the preface, the authors state that "every modern physician and surgeon interested in cardiovascular disease must now have a firm grounding in circulatory physiology." Their aim is to provide a clinical text for the practicing physician, with a simultaneous emphasis on the physiological bases of cardiovascular diseases. To achieve this goal, each chapter was first written by the clinical author (Silber) and then reviewed and revised with the physiologist author (the late Dr Katz, one of the most distinguished cardiac physiologists). This approach seems to have worked well. The first 11 chapters, on the physiology and pathophysiology of heart disease, are clearly the best in the book. The chapters on cellular electrophysiology and cardiac arrhythmias are