Diastolic Relaxation of the Heart: Basic Research and Current Applications for Clinical Cardiology

by William Grossman, Beverly H. Lorell

Overview

viewed as rolling downhili from an uphill or This book represents an edited compilation of the scientific presentations given at an Interna- high-energy state. This transition results from tional Symposium on the Physiology of Diastole the opening of membrane pores that allow in Health and Disease, September 11 to 14, calcium to rush into the cytosol, triggering 1986, in Cambridge, Massachusetts. Numerous excitation-contraction coupling. If the energy studies have documented the importance of available to sarcoplasmic reticular and sarcolem- diastolic dysfunction in clinical heart disease. In mal calcium pumps was insufficient to remove recent years clinicians have become increasingly this calcium from the cytosol and res tore the aware that many patients with congestive heart 1O, OOO-fold calcium gradient, characteristic of failure have completely normal myocardial con- the "resting" myocyte, we would live for one tractile function. In these patients, inotropic glorious systole and die in cardiac rigor. The agents provide no clinical benefit and may in well-known phenomenon of rigor mortis re- fact exacerbate clinical manifestations of heart minds us that for skeletal muscles as weIl relaxation is the high-energy state and per- failure. These patients, who may be regarded as having diastolic heart failure, represent a major manent contraction is the inevitable downhili therapeutic challenge today. It has also become state for muscle that can no longer produce increasingly apparent that a variety of patho- adenosine triphosphate.

Product Details

ISBN-13:	9781461568346
Publisher:	Springer US
Publication date:	05/18/2012
Edition description:	1988
Pages:	320
Product dimensions:	7.01(w) x 10.00(h) x 0.03(d)

Table of Contents

I: Cell Biology of Diastole.- 1. Cellular Mechanisms of Relaxation: Lessons From Frogs, Birds, and Mammals.- 2. Sarcoplasmic Reticular Control of Cardiac Contraction and Relaxation.- 3. Calcium and Cardiac Relaxation.- 4. Variable Calcium Sensitivity of the Mammalian Cardiac Contractile System.- 5. Is Ischemic Contracture Preceded by a Rise in Free Calcium?.- 6. The Effect of Regional Myocardial Heterogeneity on the Economy of Isometric Relaxation.- 7. Functional Sequelae of Diastolic Sarcoplasmic Reticulum Ca2+ Release in the Myocardium.- II: Physiologic Modifiers of Relaxation in Experimental Models.- 8. Hypoxia and Relaxation.- 9. Ischemic/Hypoxic and Reperfusion/Reoxygenation Contractures: Mechanisms.- 10. Load Dependence of Relaxation.- 11. The Effects of Cardiac Hypertrophy on Intracellular Ca2+ Handling.- III: Evaluation of Relaxation and Compliance in the Intact Heart.- 12. Diastolic Myocardial Mechanics and the Regulation of Cardiac Performance.- 13. Evaluation of Time Course of Left Ventricular Isovolumic Relaxation in Man.- 14. Loading Conditions and Left Ventricular Relaxation.- 15. Influence of Pressure and Volume Overload on Diastolic Compliance.- 16. Influence of the Pericardium on Diastolic Compliance.- 17. Implications of Pericardial Pressure for the Evaluation of Diastolic Dysfunction.- 18. Comparative Effects of Ischemia and Hypoxia on Ventricular Relaxation in Isolated Perfused Hearts.- 19. Effects of Hypoxia on Relaxation of the Hypertrophied Ventricle.- 20. Relaxation and Diastolic Distensibility of the Regionally Ischemic Left Ventricle.- IV: Clinical Disorders of Diastolic Relaxation and Compliance.- 21. Altered Diastolic Distensibility During Angina Pectoris.- 22. Diastolic Function During Exercise-Induced Ischemia in Man.- 23. Left Ventricular Filling in Ischemic and Hypertrophic Heart Disease.- 24. Regional Diastolic Dysfunction in Coronary Artery Disease: Clinical and Therapeutic Implications.- 25. Ejection, Filling, and Diastasis During Transluminal Occlusion in Man: Consideration on Global and Regional Left Ventricular Function.- 26. Diastolic Ventricular Function in Primary and Secondary Hypertrophy: The Influence of Verapamil.- 27. Failure of Inactivation of Hypertrophied Myocardium: A Cause of Impaired Left Ventricular Filling in Hypertrophic Cardiomyopathy and Aortic Stenosis.