Background-In idiopathic dilated cardiomyopathy, there are scarce data on the influence of late gadolinium enhancement (LGE) assessed by cardiovascular magnetic resonance on left ventricular (LV) remodeling. Methods and Results-Fifty-eight consecutive patients with idiopathic dilated cardiomyopathy underwent baseline clinical, biohumoral, and instrumental workup. Medical therapy was optimized after study enrollment. Cardiovascular magnetic resonance was used to assess ventricular volumes, function, and LGE extent at baseline and 24-month follow-up. LV reverse remodeling (RR) was defined as an increase in LV ejection fraction ≥10 U, combined with a decrease in LV end-diastolic volume ≥10% at follow-up. ΔLGE extent was the difference in LGE extent between follow-up and baseline. LV-RR was observed in 22 patients (38%). Multivariate regression analysis showed that the absence of LGE at baseline cardiovascular magnetic resonance was a strong predictor of LV-RR (odds ratio, 10.857 [95% confidence interval, 1.844-63.911]; P=0.008) after correction for age, heart rate, New York Heart Association class, LV volumes, and LV and right ventricular ejection fractions. All patients with baseline LGE (n=26; 45%) demonstrated LGE at follow-up, and no patient without baseline LGE developed LGE at follow-up. In LGE-positive patients, there was an increase in LGE extent over time (P=0.034), which was inversely related to LV ejection fraction variation (Spearman ρ, −0.440; P=0.041). Five patients showed an increase in LGE extent >75th percentile of ΔLGE extent, and among these none experienced LV-RR and 4 had a decrease in LV ejection fraction ≥10 U at follow-up. Conclusions-In patients with idiopathic dilated cardiomyopathy, the absence of LGE at baseline is a strong independent predictor of LV-RR at 2-year follow-up, irrespective of the initial clinical status and the severity of ventricular dilatation and dysfunction. The increase in LGE extent during follow-up was associated with progressive LV dysfunction. (Circ Cardiovasc Imaging. 2013;6:790-799.)

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Background: Overt thyroid dysfunction, hypothyroidism in particular, may lead to coronary artery disease (CAD). Whether more subtle anomalies of thyroid hormone metabolism influence the progression of CAD remains a matter of speculation. Hypothesis: The occurrence of CAD and long-term prognosis in patients without a history of either primary thyroid disease, myocardial infarction, or chronic heart failure is related to serum levels of biologically active free triiodothyronine (fT3). Methods: The cohort consisted of 1047 clinically and biochemically euthyroid patients (median age 65.6 y and 69% male) who underwent coronary angiography in our institute for suspected CAD. Results: Lower fT3 levels were predictive of both single-vessel (p = 0.012) and multivessel (p = 0.009) CAD. Through a multivariate logistic regression analysis, fT3 was still linked to the presence of CAD (hazard ratio [HR]: 0.48, 95% confidence interval [CI]: 0.34-0.68, p < 0.001). After a mean follow-up of 31 months, the survival rate was 95% and total mortality (log-rank 6.75, p = 0.009), as well as cardiac mortality (log-rank 8.26, p = 0.004), was greater among patients with low T3 (fT3<2.10 pg/mL) syndrome. At subsequent multivariate Cox regression analysis, the association between low T3 syndrome and survival was maintained (total mortality HR: 1.80, 95% CI: 1.05-3.10, p = 0.034; cardiac mortality HR: 2.58, 95% CI: 1.13-5.93, p = 0.025). Conclusions:In this selected population, fT3 levels were inversely correlated to the presence of CAD and low T3 syndrome conferred an adverse prognosis, even after adjusting for traditional coronary risk factors.