Myocardial fibrosis is the common pathophysiologic denominator between myocardial remodeling and the failing heart. Experimental evidence points toward a prominent role of CD4+ T helper (Th) lymphocytes, particularly Th17 and Th22 cells, as key players in myocardial remodeling, hence their involvement in humans remains unclear.
Quantitative tissue characterization by cardiac magnetic resonance imaging supports noninvasive detection of diffuse myocardial interstitial remodeling by measurement of rates of T1 relaxation