glycogen and Aortic-Valve-Insufficiency

Geriatric cardiology requires special knowledge and experience. It is not possible to extrapolate directly experience obtained with young patients to old people. Because of the multiple illnesses, many serious, in the elderly cardiac patients, it is imperative for the cardiologist to be, first of all, a master internist at all times. Old patients with their multiple illnesses are also sensitive to drugs, including digitalis and diuretics. There is a need to train more physicians in geriatric cardiology in order to offer the old patient the best of care since so many old people are living today. There is also a need to learn the effects of the aging process itself on the human heart. Such studies should command priorities in financial and other forms of support.

Topics: Age Factors; Aging; Aortic Valve Insufficiency; Aortic Valve Stenosis; Cardiac Output; Dyspnea; Edema; Electrocardiography; Female; Glycogen; Heart; Heart Diseases; Heart Function Tests; Histocytochemistry; Humans; Hypertension; Hypotension, Orthostatic; Male; Microscopy, Electron; Myocardium; Radiography; Rheumatic Heart Disease; Thyroid Diseases; Vectorcardiography

Differentiation of foetal cardiomyocytes is accompanied by sequential actin isoform expression, i.e. down-regulation of the 'embryonic' alpha smooth muscle actin, followed by an up-regulation of alpha skeletal actin (alphaSKA) and a final predominant expression of alpha cardiac actin (alphaCA). Our objective was to detect whether re-expression of alphaSKA occurred during cardiomyocyte dedifferentiation, a phenomenon that has been observed in different pathologies characterized by myocardial dysfunction. Immunohistochemistry of alphaCA, alphaSKA and cardiotin was performed on left ventricle biopsies from human patients after coronary bypass surgery. Furthermore, actin isoform expression was investigated in left ventricle samples of rabbit hearts suffering from pressure- and volume-overload and in adult rabbit ventricular cardiomyocytes during dedifferentiation in vitro. Atrial goat samples up to 16 weeks of sustained atrial fibrillation (AF) were studied ultrastructurally and were immunostained for alphaCA and alphaSKA. Up-regulation of alphaSKA was observed in human ventricular cardiomyocytes showing down-regulation of alphaCA and cardiotin. A patchy re-expression pattern of alphaSKA was observed in rabbit left ventricular tissue subjected to pressure- and volume-overload. Dedifferentiating cardiomyocytes in vitro revealed a degradation of the contractile apparatus and local re-expression of alphaSKA. Comparable alphaSKA staining patterns were found in several areas of atrial goat tissue during 16 weeks of AF together with a progressive glycogen accumulation at the same time intervals. The expression of alphaSKA in adult dedifferentiating cardiomyocytes, in combination with PAS-positive glycogen and decreased cardiotin expression, offers an additional tool in the evaluation of myocardial dysfunction and indicates major changes in the contractile properties of these cells.

Topics: Actinin; Actins; Animals; Aortic Valve Insufficiency; Atrial Fibrillation; Biomarkers; Cell Dedifferentiation; Cells, Cultured; Coronary Artery Disease; Down-Regulation; Female; Glycogen; Goats; Humans; Myocardial Stunning; Myocytes, Cardiac; Protein Isoforms; Rabbits; Up-Regulation

Degenerated cardiac muscle cells were present in hypertrophied ventricular muscle obtained at operation from 12 (38%) of 32 patients with asymmetric septal hypertrophy (hypertrophic cardiomyopathy) or aortic valvular disease. Degenerated cells demonstrated a wide variety of ultrastructural alterations. Mildly altered cells were normal-sized or hypertrophied and showed focal changes, including preferential loss of thick (myosin) filaments, streaming and clumping of Z band material, and proliferation of the tubules of sarcoplasmic reticulum. Moderately and severely degenerated cells were normal-sized or atrophic and showed additional changes, including extensive myofibrillar lysis and loss of T tubules. The appearance of the most severely degenerated cells usually reflected the cytoplasmic organelle (sarcoplasmic reticulum, glycogen, or mitochondria) which underwent proliferation and filled the myofibril-free areas of these cells. Moderately and severely degenerated cells were present in areas of fibrosis, had thickened basement membranes, and had lost their intercellular connections. These observations suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with chronic ventricular hypertrophy.

Topics: Adolescent; Adult; Aortic Stenosis, Subvalvular; Aortic Valve Insufficiency; Aortic Valve Stenosis; Cardiomegaly; Cell Membrane; Child; Female; Glycogen; Golgi Apparatus; Heart Septum; Heart Ventricles; Humans; Lipofuscin; Male; Middle Aged; Mitochondria, Muscle; Myocardium; Myofibrils; Ribosomes; Sarcolemma; Sarcoplasmic Reticulum

Light and electron microscopic observations were made on left ventricular myocardium removed at operation from 16 patients with chronic aortic valve disease. In all 16 patients most cardiac muscle cells were hypertrophid, and surrounded by small amounts of fibrous tissue. In two of the six patients with pure aortic regurgitation and in four of the five patients with combined aortic stenosis and regurgitation, cardiac muscle cells with evidence of degeneration were present in addition to hypertrophied, nondegenerated cells. Degenerated cardiac muscle cells were not observed in the six patients with predominant aortic stenosis. Cardiac muscle cells with mild degeneration showed focal myofibrillar lysis, with preferential loss of thick myofilaments, and focal proliferation of tubules of sarcoplasmic reticulum. More severely degenerated muscle cells showed a marked decrease in the numbers of myofibrils and T tubules and proliferation of sarcoplasmic reticulum or mitochondria, or both. Severly degenerated cells usually were present in areas of marked fibrosis, often were atrophic, had thickened basement membranes and had lost their intercellular connections. These findings suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with chronic aortic valve disease.

Topics: Adolescent; Adult; Aortic Valve Insufficiency; Aortic Valve Stenosis; Basement Membrane; Cell Nucleus; Child; Cytoplasmic Granules; Endoplasmic Reticulum; Female; Glycogen; Histocytochemistry; Humans; Male; Microscopy, Electron; Microtubules; Middle Aged; Mitochondria, Muscle; Myocardium; Myofibrils; Pigments, Biological; Sarcolemma; Sarcoplasmic Reticulum

Topics: Aortic Valve Insufficiency; Cardiomegaly; Cardiomyopathy, Hypertrophic; Glycogen; Histocytochemistry; Humans; Myocardium

Topics: Adult; Aortic Valve Insufficiency; Aortic Valve Stenosis; Biopsy; Cardiomyopathies; Cell Membrane; Cytoplasmic Granules; Desmosomes; Endocardium; Endoplasmic Reticulum; Female; Glycogen; Golgi Apparatus; Heart Valve Diseases; Heart Ventricles; Humans; Male; Microscopy, Electron; Mitochondria; Mitral Valve Insufficiency; Myocardium; Myofibrils; Sarcoplasmic Reticulum; Temperature

Topics: Adaptation, Physiological; Adenine Nucleotides; Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphatases; Adenosine Triphosphate; Animals; Aortic Valve Insufficiency; Biopsy; Cardiomegaly; Glycogen; Heart Failure; Heart Ventricles; Lactates; Muscle Proteins; Myocardium; Phosphocreatine; Rabbits