Artikel Jurnal PATOGENESIS HIPERTROFI VENTRIKEL KIRI

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Artikel Jurnal PATOGENESIS HIPERTROFI VENTRIKEL KIRI

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If the heart is facing a hemodynamic burden, it will compensate for the hemodynamic burden by: (1) using the Frank-Starling mechanism to increase contraction formation, (2) increasing the heart muscle mass to deal with extra load and (3) activating neurohormonal mechanism for increasing contractility. Hypertrophy due to hemodynamic load can be either adaptive (physiological) hypertension or maladaptive hypertrophy (pathology). Hypertrophy patterns that occur can be concentric or eccentric. Pathogenesis of pathological left ventricular hypertrophy due to primary stimulation of cardiac mechanical strain and / or neurohumoral factors that will be translated into cells as biochemical changes that activate the second (cytosolic) and third (nucleus) messengers that act on the cell nucleus, regulate transcription and so on determine gene expression that induces left ventricular hypertrophy. Pathological left ventricular hypertrophy can experience a transition to heart failure caused by diastolic dysfunction, systolic dysfunction or both.

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