Key Points
- To examine how structural abnormalities in the cardiac interstitium and activation of the renin-angiotensin-aldosterone system drive pathological left ventricular hypertrophy and myocardial dysfunction.
- Reviewed morphometric and morphological data from in vivo animal models of experimental hypertension.
- Assessed cardiac fibroblast activation and fibrillar collagen accumulation across ventricles under varying plasma concentrations of angiotensin II and aldosterone.
- Abnormal interstitial and perivascular fibrosis occurred in both the hypertensive, hypertrophied left ventricle and the normotensive, nonhypertrophied right ventricle, indicating systemic humoral regulation rather than purely local mechanical stress.
- Arterial hypertension combined with elevated circulating aldosterone stimulated cardiac fibroblast proliferation and collagen synthesis, leading to increased myocardial stiffness and ventricular dysfunction independent of myocyte hypertrophy.
Structured PICO
PPopulationAnimal models of experimental hypertension and left ventricular hypertrophy
IInterventionAlterations in plasma concentrations of angiotensin II and aldosterone
OOutcomeCardiac fibroblast growth and collagen synthesis (myocardial fibrosis)surrogate
Pathological left ventricular hypertrophy in hypertension is driven not only by myocyte hypertrophy but also by aldosterone-mediated interstitial fibrosis.