In experimental models, myocardial fibrosis is driven by mineralocorticoid excess and can be prevented or reversed with aldosterone receptor antagonists or ACE inhibitors.
Myocardial fibrosis is driven by mineralocorticoid excess rather than hemodynamic workload and can be prevented or reversed with aldosterone receptor antagonists or ACE inhibitors.
Left ventricular hypertrophy is a major risk factor associated with the appearance of adverse cardiovascular events. A distortion in myocardial structure, mediated by an abnormal accumulation of fibrillar collagen within the adventitia of intramyocardial coronary arteries and neighbouring interstitial spaces, alters the electrical and mechanical behaviour of the myocardium. The mechanisms responsible for the regulation of cardiac myocyte growth and collagen accumulation are therefore of considerable interest. Herein we review results of in vivo studies conducted in the authors' laboratory that addressed these issues in various experimental models. The findings indicate that in arterial hypertension myocardial hypertrophy is related to ventricular systolic pressure work. Myocardial fibrosis, on the other hand, is not related to haemodynamic workload, but rather the presence of mineralocorticoid excess relative to sodium intake and excretion. Accordingly, fibrosis can appear in both the hypertensive left and non-hypertensive right ventricles. Pharmacological probes, administered in variable doses, were used to further test and support this hypothesis. In both primary and secondary hyperaldosteronism, it was possible to prevent the pathological structural remodelling of the myocardium with an aldosterone receptor antagonist, while in unilateral renal ischaemia ACE inhibition was similarly cardioprotective. Other studies demonstrated that it was feasible to regress the fibrous tissue response and normalise diastolic stiffness. This concept of cardioreparation suggests that heart failure due to this type of structural remodelling may be reversible.
Weber et al. (2008) conducted a review in Myocardial hypertrophy and fibrosis. Aldosterone receptor antagonists and ACE inhibitors was evaluated. In experimental models, myocardial fibrosis is driven by mineralocorticoid excess and can be prevented or reversed with aldosterone receptor antagonists or ACE inhibitors.
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