This review highlights the pathophysiological roles of local peptides and circulating RAAS hormones in driving post-MI cardiac fibrosis and adverse remodelling.
May guide dual systemic-local RAAS targeting post-MI; leaves open clinical translation pending prospective trials.
Following myocardial infarction (MI), extensive fibrosis appears at and remote to the MI and is associated with diastolic dysfunction. Both circulating and tissue hormones contribute to the adverse structural remodelling of the myocardium and thereby influence the progressive nature of heart failure. In this review, factors contributing to the appearance of fibrous tissue will be considered, with special emphasis on the role of peptides produced within the diseased myocardium and on the circulating hormones of the renin-angiotensin-aldosterone system.
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Sun et al. (1998) studied this question.
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