Description
Springer Cellular and Molecular Alterations in the Failing Human Heart 1st Editon 2011 Softbound by Hansjörg Just, Gerd Hasenfuss, Christian Holubarsch, N.R. Alpert
The myocardium in heart failure: Cellular and subcellular alterations in the failing human myocardium. H. Just Medizinische Universitatsklinik Freiburg i. Br., Innere Medizin III - Kardiologie, FRG The syndrome of heart failure continues to be a major challenge to clinicians and scientists. Incidence and mortality of the disease are high, the patient is disabled, and is permanently threatened by the high morbidity and mortality. The clinician faces a syndrome of complex pathophysiology. Multiple causes or underlying disorders of the heart have to be differentiated from heart failure itself, which often results in exceedingly difficult diagnoses. Likewise, prognostication meets with difficulties due to problems in separating influences of the underlying disease and the heart failure syndrome itself. In chronic refractory failure annual mortality may exceed 50%. If aortic stenosis or ischemic cardiomyopathy with main stem lesions are present, this percentage may be even higher. The situation becomes particularly threatening to the patient when the reduction in cardiac performance goes along with complex ventricular arrhythmias. Therapy has remained difficult and of limited effectiveness. Major progress was achieved with the introduction of diuretic substances. Of similar importance was the introduction of va so dilating drugs into the treatment of heart failure. The principle of vasodilation has greatly improved our understanding of the disease, and has brought about a major improvement of symptoms, increase of exercise capacity, and reduc tion of mortality. This is especially true for the introduction of the angiotensin converting enzyme inhibitors. Sarcolemma and phosphodiesterases.- Receptor systems in the nonfailing human heart.- Changes in the receptor-G protein-adenylyl cyclase system in heart failure from various types of heart muscle disease.- Quantification of Gia-proteins in the failing and nonfailing human myocardium.- Regulation and possible functional implications of G-protein mRNA expression in nonfailing and failing ventricular myocardium.- Phosphodiesterase inhibition and positive inotropy in failing human myocardium.- Cardiovascular cyclic nucleotide phosphodiesterases and their role in regulating cardiovascular function.- Na, K-ATPase expression in normal and failing human left ventricle.- Excitation-contraction coupling and contractile proteins.- Structural and functional diversity of human ventricular myosin.- Contractile protein function in failing and nonfailing human myocardium.- Troponin T isoform expression in the normal and failing human left ventricle: A correlation with myofibrillar ATPase activity.- Effects of different expression and posttranslational modifications of myosin light chains on contractility of skinned human cardiac fibers.- Responsiveness of the myofilaments to Ca2+ in human heart failure: Implications for Ca2+ and force regulation.- The regulation of the human ? myosin heavy-chain gene.- Mutations in cardiac myosin heavy-chain genes cause familial hypertrophic cardiomyopathy.- The membrane proteins of the overloaded and senescent heart.- Contraction frequency dependence of twitch and diastolic tension in human dilated cardiomyopathy.- Alterations of the force-frequency relationship in the failing human heart depend on the underlying cardiac disease.- Pathophysiology of cardiac hypertrophy and failure of human working myocardium: Abnormalities in calcium handling.- Ca2+-currents and intracellular [Ca2+]I,-transients in single ventricular myocytes isolated from terminally failing human myocardium.- Dynamic calcium requirements for activation of human ventricular muscle calculated from tension-independent heat.- The calcium-release channel from cardiac sarcoplasmic reticulum: Function in the failing and acutely ischaemic heart.- Immune-mediated modulation of sarcoplasmic reticulum function in human dilated cardiomyopathy.- Calcium uptake by sarcoplasmic reticulum and its modulation by cAMP-dependent phosphorylation in normal and failing human myocardium.- Contractile proteins and sarcoplasmic reticulum calcium-ATPase gene expression in the hypertrophied and failing heart.- Extracellular matr.- Factors associated with reactive and reparative fibrosis of the myocardium.- The extracellular matrix in the failing human heart.- Mitochondrial function.- Dysfunction of the ADP/ATP carrier as a causative factor for the disturbance of the myocardial energy metabolism in dilated cardiomyopathy.- Adenine nucleotide metabolism and contractile dysfunction in heart failure — Biochemical aspects, animal experiments, and human studies.- Achievements of the Symposium.- Cellular and molecular alterations in the failing human heart.