Myocardial Fibrosis as a Key Determinant of Left Ventricular Remodeling in Idiopathic Dilated Cardiomyopathy

Abstract

Myocardial Fibrosis and LV Remodeling 791 Clinical Perspective on p 799 short-term follow-up (5 and 12 months, respectively), and the recovery of LV function was likely prompted by the resolu-tion of transient myocardial damage in a sizeable number of patients. Accordingly, it remains uncertain whether LGE is a predictor of LV-RR in patients with IDCM in response to OMT. In addition, at the moment, there are no data on the potential interplay between the changes in LGE over time and LV remodeling. Based on these premises, we conducted the current study with the following aims: (1) to assess whether LGE may be used to predict LV-RR at 2-year follow-up in patients with IDCM after optimization of medical therapy, and (2) to investigate the interaction between LGE variation and LV remodeling during follow-up. Methods Study Population Between May 2009 and July 2010, 112 consecutive patients with IDCM diagnosed in the preceding 12 months were prospectively evaluated at our institution (a tertiary referral hospital) for study enrollment. The diagnosis of IDCM was made according to World Health Organization criteria 12 and the evidence of an increased LV end-diastolic diameter indexed to body surface area at transthorac-ic echocardiography and a reduced LV ejection fraction based on published reference ranges. 13 Invasive coronary angiography was performed in all patients to exclude significant coronary artery ste-nosis. 14 Exclusion criteria included active myocarditis, peripartum cardiomyopathy, extracardiac systemic features of sarcoidosis, che-motherapy-induced cardiomyopathy, drug abuse or excessive alcohol consumption, tachycardia-induced cardiomyopathy, severe valvular disease, untreated hypertension, hypertrophic cardiomyopathy, car-diac amyloidosis, thyroid dysfunction, estimated glomerular filtration rate <30 mL/min, and contraindications to CMR. Active myocarditis was excluded by the absence of classical clinical feature and the in-crease in troponin I at study entry.