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.

Prognostic significance of myocardial energy expenditure and myocardial efficiency in patients with heart failure with reduced ejection fraction.

In heart failure with reduced ejection fraction (HFrEF) patients, myocardial blood flow (MBF), myocardial energy expenditure (MEE), myocardial efficiency has been poorly evaluated because of the necessity of invasive procedures in the determination of these parameters. Transthoracic echocardiography (TTE) can provide reliable data for MEE, MBF (via coronary sinus (CS) flows). Also, myocardial efficiency can be evaluated by the MEE to MBF ratio. We aim to assess MBF, MEE and energy efficiency and the prognostic value of these parameters in HFrEF. In this prospective study, a total of 80 patients with HFrEF due to either ischemic or non-ischemic etiology and 20 healthy control subjects were included. Median follow-up duration was 901 (27-1004) days. MBF was calculated via coronary sinus blood flow. MEE was measured from circumferential end-systolic stress, stroke volume and left ventricular ejection time. MEE to MBF ratio was determined as MEf. Primary composite end-point (CEP) was cardiovascular mortality, heart transplantation or mechanical circulatory support. MEE and MEf were lower and MBF per minute was higher in HF group compared to control subjects whereas MBF per 100 g left ventricular mass was not different. MEE and MEf have significantly negative correlation with troponin I, BNP, uric acid and positive correlation with epicardial fat thickness. In Cox regression analysis, per one calorie decrease of MEE was associated 4.3 times increased risk [HR 4.396 (95% CI 1.230-15.716)] and per one percent decrease of MEf was associated 3.3 times increased risk of CEP [HR 3.343 (95% CI 1.025-10.905)]. Our study demonstrated that while MEE and MEf diminished in HFrEF, MBF preserved with the symptomatic progression of HF. MEE and MEf were found to be associated with important prognostic markers and independent predictors of CEP in HFrEF. Evaluation of MEE, MBF and MEf with echocardiography may provide an additional data regarding prognostic assessment of HFrEF population.