Remodeling of the heart (membrane proteins and collagen) in hypertensive cardiopathy.
The basis for impaired left ventricular function of hearts in moderate to severe stages of hypertrophy and congestive heart failure remains uncertain. At the cellular level, the mechanisms governing the movements of calcium in the myocardium are actually depressed and might at least in part account for the slowing of the maximum shortening velocity and the impaired relaxation. These alterations of membrane proteins seem particularly important in species where the slowing of Vmax cannot be a consequence of the myosin heavy chain shift. They lead to an unstable equilibrium of calcium homeostasis and to calcium overload in heart failure. On the other hand, the enhanced density and remodeling of collagen in the hypertrophied heart, which would depend on elevation in circulating aldosterone, impair myocardial stiffness with diastolic dysfunction and lead to altered pumping capacity of the heart. Disturbances of calcium metabolism and matrix collagen remodeling enhance early afterdepolarizations and arrhythmias.
Sainte Beuve
C
C
INSERM, U127, Hopital Lariboisière, Paris, France.
Leclercq
C
C
Rannou
F
F
Oliviero
P
P
Mansier
P
P
Chevalier
B
B
Swynghedauw
B
B
Charlemagne
D
D
D000818:Animals; D002118:Calcium / Q000378:metabolism; D006332:Cardiomegaly / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D003094:Collagen / Q000378:metabolism*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D008565:Membrane Proteins / Q000378:metabolism*
D008565:Membrane Proteins; D003094:Collagen; D002118:Calcium