Abstract
Background and objectives: T-cadherin (T-cad) is one of the adiponectin receptors abundantly expressed in the heart and blood vessels. Experimental studies show that T-cad sequesters adiponectin in cardiovascular tissues and is critical for adiponectin-mediated cardio-protection. However, there are no data connecting cardiac T-cad levels with human chronic heart failure (HF). The aim of this study was to assess whether myocardial T-cad concentration is associated with chronic HF severity and whether the T-cad levels in human heart tissue might predict outcomes in patients with non-ischemic dilated cardiomyopathy (NI-DCM). Materials and Methods: 29 patients with chronic NI-DCM and advanced HF were enrolled. Patients underwent regular laboratory investigations, echocardiography, coronary angiography, and right heart catheterization. TNF-α and IL6 in serum were detected by enzyme-linked immunosorbent assay (ELISA). Additionally, endomyocardial biopsies were obtained, and the levels of T-cad were assessed by ELISA and CD3, CD45Ro, CD68, and CD4- immunohistochemically. Mean pulmonary capillary wedge pressure (PCWP) was used as a marker of HF severity, subdividing patients into two groups: mean PCWP > 19 mmHg vs. mean PCWP < 19 mmHg. Patients were followed-up for 5 years. The study outcome was composite: left ventricular assist device implantation, heart transplantation, or death from cardiovascular causes. Results: T-cad shows an inverse correlation with the mean PCWP (rho = −0.397, p = 0.037). There is a tendency towards a lower T-cad concentration in patients with more severe HF, as indicated by the mean PCWP > 19 mmHg compared to those with mean PCWP ≤ 19 mmHg (p = 0.058). Cardiac T-cad levels correlate negatively with myocardial CD3 cell count (rho = −0.423, p = 0.028). Conclusions: Univariate Cox regression analysis did not prove T-cad to be an outcome predictor (HR = 1, p = 0.349). However, decreased T-cad levels in human myocardium can be an additional indicator of HF severity. T-cad in human myocardium has an anti-inflammatory role. More studies are needed to extend the role of T-cad in the outcome prediction of patients with NI-DCM.
Highlights
The current concept of heart failure (HF) pathogenesis includes a broad spectrum of structural, functional, electrophysiological, cellular, and molecular abnormalities [1]
The inclusion criteria were as follows: the exacerbation of HF symptoms, accompanied by echocardiographic evidence of dilated cardiomyopathy: (1) left ventricular end-diastolic diameter (LVEDD) > 117% (>2 SD of the predicted value of 112% corrected for age and body surface area) (2)
Out of 29 patients with non-ischemic dilated cardiomyopathy (NI-DCM) included in the study, 25 (86%) were ranked as NYHA III and IV classes, and all had increased B-type natriuretic protein (BNP) values (Table 1)
Summary
The current concept of heart failure (HF) pathogenesis includes a broad spectrum of structural, functional, electrophysiological, cellular, and molecular abnormalities [1]. Patients with advanced HF develop various additional derangements, including changes in adipokine levels, long-term systemic inflammation, and progressive catabolism [4,5]. One such adipokine, which has a critical signaling function in the heart, is adiponectin (APN). Its anti-inflammatory [10], hypertrophy [11] and fibrosis [12] reducing activity is considered to be important in cardio-protection. There are no data connecting cardiac T-cad levels with human chronic heart failure (HF). The aim of this study was to assess whether myocardial T-cad concentration is associated with chronic HF severity and whether the T-cad levels in human heart tissue might predict outcomes in patients with non-ischemic dilated cardiomyopathy (NI-DCM). Mean pulmonary capillary wedge pressure (PCWP) was used as a marker of HF severity, subdividing patients into two groups: mean PCWP > 19 mmHg vs. mean
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