[Physiopathology of cardiac insufficiency. Biological factors of adaptation and disadaptation of the heart to chronic mechanical overload].
The advent of molecular biology techniques has profoundly changed pathophysiological concepts of myocardial hypertrophy and overload-induced heart failure. Heart failure is a consequence of the limits and imperfection of biological adaptation to mechanical overload. Factors including fibrosis, senescence, ischemia, inflammation, catabolism and hormonal response may contribute to myocardial dysfunction. In humans changes in the genes coding for myosin are observed only in the atrial myocardium, in association with diastolic left ventricular function. In most animal species, alteration in proteins involved in intracellular calcium movement and autonomic nervous dysfunction are responsible for both reduction of Vmax and arrhythmias associated with myocardial hypertrophy. Moreover, myocardial fibrosis is a major determinant of enhanced left ventricular stiffness and arrhythmogenicity.
Swynghedauw
B
B
Unité 127-INSERM (IFR Circulation), Université Diderot, Hôpital Lariboisière, Paris.
D000222:Adaptation, Physiological; D009202:Cardiomyopathies / Q000378:metabolism; D003285:Contractile Proteins / Q000378:metabolism; D003971:Diastole; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D008565:Membrane Proteins / Q000378:metabolism; D013314:Stress, Mechanical; D016277:Ventricular Function, Left
D003285:Contractile Proteins; D008565:Membrane Proteins
Physiopathologie de l'insuffisance cardiaque. Facteurs biologiques d'adaptation et de désadaptation du coeur à une surcharge mécanique chronique.