Cardiomyocyte–extracellular matrix interactions from excess collagen may alter microvascular, mechanical, and electrical function among the many changes that occur with the progression of heart failure with preserved ejection fraction (HFpEF). The purpose was to see if myocardial fibrosis (MF) is as common in those with HFpEF as it is in those at risk for HFpEF, and if it is associated with disease severity and outcomes in both groups. An observational cohort process was conducted in a cardiovascular magnetic resonance (CMR) centre serving an integrated health system from June 1, 2010, to September 17, 2015, with follow-up until December 14, 2015. Patients with an intact systolic function who were referred for CMR in a row were eligible. Patients with cardiac amyloidosis (n=19) were excluded using cardiovascular magnetic resonance. Extracellular volume (ECV) CMR values were used to assess myocardial fibrosis. Baseline BNP; subsequent hospitalization for heart failure or death were the outcomes. Out of the 1,174 patients recognized (537 [46%] female; median [interquartile range {IQR}] age, 56 [44-66] years), 250 patients were “at-risk” for HFpEF due to high brain-type natriuretic peptide (BNP) levels, 160 patients had HFpEF by verified clinical diagnosis, and 745 patients did not have HFpEF. In comparison to individuals without HFpEF, patients at risk for HFpEF or with HFpEF had a higher prevalence/extent of MF and a worse prognosis. The actual diagnosis of HFpEF was not related with significant differences in MF (median ECV, 28.2%; IQR, 26.2% -30.7% vs 28.3%; IQR, 25.5% -31.4%; P=.60) or prognosis (log-rank 0.8; P=.38) among individuals at risk for HFpEF or with HFpEF. 61 patients with those at risk of HFpEF had adverse events during a median of 1.9 years (19 hospitalizations for heart failure, 48 deaths, 6 with both). Whether grouped with patients at risk for HFpEF or not, ECV was associated with baseline log BNP (disease severity surrogate) in multivariable linear regression models and with outcomes in multivariable Cox regression models (eg, hazard ratio 1.75 per 5% increase in ECV, 95% CI, 1.25-2.45; P=.001 in the stepwise model). MF was also widespread among patients with or at risk for HFpEF, despite the several alterations that occurred during the apparent progression of HFpEF when increased BNP was prevalent. MF could theoretically occur before the clinical diagnosis of HFpEF. In any case, MF was linked to illness severity (BNP) and outcomes. Further research is needed to see if the cells and secretomes that mediate MF are therapeutic targets in HFpEF.

 

Link:jamanetwork.com/journals/jamacardiology/fullarticle/2646532?resultClick=1