Lower levels of triiodothyronine are associated with poor hemodynamic profile and all-cause mortality in heart failure.

Background: We aimed to assess the association of triiodothyronine (T3) hormone with invasive hemodynamic parameters and all-cause mortality in heart failure with reduced ejection fraction (HFrEF). Results: About 483 HFrEF patients were enrolled. Patients with the lowest T3 tertile had advanced New York Heart Association (NYHA) classes, had higher uric acid, brain natriuretic peptide. T3 level had a positive correlation with cardiac index (CI) and a negative correlation with pulmonary vascular resistance and pulmonary capillary wedge pressure. Adjusted with NYHA III-IV classes, uric acid, aspartate aminotransferase and CI, T3 level was found to be an independent predictor of all-cause mortality. In Kaplan-Meier analysis, the lowest T3 tertile had the lowest survival function. Conclusion: Free T3 is positively correlated with CI and negatively correlated with pulmonary vascular resistance and pulmonary capillary wedge pressure in patients with HFrEF. Lower levels of T3 seems to be a poor prognostic factor in this particular patient population.

The other side of the medallion in heart failure: Reverse metabolic syndrome.

BACKGROUND AND AIMS: Lower levels of cardiovascular risk factors are associated with an increase in mortality in H.F. To explain this paradox, the term reverse metabolic syndrome (RMetS) has recently been proposed. We suggest defining these patients with lower levels of three risk factors can be combined under the heading "RMetS." We aimed to investigate the effect of MetS and RMetS on hemodynamic parameters and prognosis in patients with H.F. and reduced ejection fraction (HFrEF). METHODS AND RESULTS: We included 304 patients who were performed right heart catheterization and followed up for a median of 16 (0-48) months. We first grouped patients according to the presence of MetS or not, then we added the RMetS category and stratified patients into three groups as MetS, RMetS, and metabolic healthy. Compared with not MetS group, Pulmonary arterial pressures and VO2 were higher in MetS group. In the second step, LVEF, CI, VO2I, O2 delivery, and LVSWI were lowest in RMetS, pulmonary artery pressures were higher in MetS group. In multivariate Cox regression analysis, being in RMetS group was associated with 2.4 times and 1.8 times increased risk for composite end point (CEP) and all-cause mortality, respectively. In Kaplan Meier analysis, RMetS had the highest all-cause mortality and CEP. CONCLUSIONS: We determined that RMetS patients had the worst prognosis with unfavorable hemodynamic profile. Hence, a better understanding of the pathophysiology of RMetS may help refine the treatment targets of CV risk factors, may yield new interventions targeting catabolic syndrome.