Ventricular septal defect (VSD) is a severe complication of myocardial infarction (MI) with a high mortality rate. We report a case of a large post-MI VSD treated with percutaneous venoarterial extracorporeal membrane oxygenation (VA-ECMO) to restore hemodynamic stability and to avoid surgery in the acute setting. VSD closure with endoventricular patch and implantation of biventricular assist device (BiVAD) was arranged sixteen days after MI. Because of no signs of myocardial recovery, implantation of durable left ventricular assist device (LVAD) as a bridge to transplant was provided, leaving right ventricular assist device (RVAD) to right ventricle recovery. RVAD was explanted 18 days after durable LVAD placement and the patient was discharged home two months after MI. The use of durable LVAD is a unique solution that can be applied in selected patients with MI-VSD and heart failure.
Cardiovascular diseases (CVD) are the most common cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). C1q TNF-related protein 3 (CTRP3) is a novel adipokine that reduces inflammation and acts cardioprotectively. The aim of our study was to analyze serum levels and gene expression of CTRP3 in subcutaneous and epicardial adipose tissue in patients with CVD and T2DM undergoing elective cardiac surgery.
38 patients with coronary artery disease (CAD) without T2DM (CAD group), 21 subjects with CAD and T2DM (T2DM group) and 18 patients with a valvular defect without CAD or T2DM (nonCAD group) were included into the study. Peripheral blood, subcutaneous (SAT) and epicardial adipose tissue (EAT) were examined at the start and end of elective cardiac surgery. mRNA expression was determined using qRT-PCR. 21 healthy subjects served as controls for serum CTRP3 (C group).
Baseline anthropometric and biochemical parameters were comparable in all groups except of higher fasting blood glucose (6.0±1.2 vs. 5.5±0.2 vs. 6.0±0.9 vs. 8.5±0.4 mmol/l for CAD vs. nonCAD vs. C vs. T2DM, p<0.001) and HbA1C (34.2±1.6 vs. 39.1±0.9 vs. 38.7±6.4 vs. 53.1±1.9 mmol/mol, p<0.001) in T2DM group. Compared to controls, all 3 CVD groups showed lower systemic CTRP3 concentrations (65.6±2.2 vs. 69.3±4.7 vs. 64.8±3.5 vs. 90.8±3.7 ng/ml for CAD vs. nonCAD vs. T2DM vs. C, p<0.001). In EAT, we found reduced mRNA expression of CTRP3 in T2DM compared to nonCAD group (0.61±0.27 vs. 6.61±2.33, p=0.005) and a similar, albeit non-significant trend in CAD group (1.55±0.32, p=0.132). Cardiac surgery resulted in a significant decrease in serum CTRP3 in all patients without affecting mRNA expression in EAT or SAT.
To conclude, decreased serum levels of CTRP3 in patients with CVD together with reduced mRNA expression in EAT in T2DM subjects with CAD indicate a possible role of CTRP3 in the pathogenesis of cardiovascular complications of type 2 diabetes mellitus.
Disclosure
H. Kratochvilova: None. B. Kasperova: None. Z. Lacinova: None. I. Lankova: None. J. Trnovska: None. I. Netuka: None. P. Ivak: None. J. Mahrík: None. D. Hlavácek: None. M. Mraz: None. M. Haluzik: Advisory Panel; Self; Lilly Diabetes, Sanofi. Consultant; Self; Ethicon US, LLC. Speaker’s Bureau; Self; AstraZeneca, Mundipharma International, Novartis AG, Novo Nordisk A/S.
Funding
Institute for Clinical and Experimental Medicine (00023001); RVOVFN64165; Ministry of Health of the Czech Republic (NV19-02-00118)
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