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The present study aimed to investigate the success rate, methods and associated complications of left ventricular lead (LVL) extraction and venous pathway reimplantation in patients with cardiac resynchronization therapy device/defibrillator (CRT/CRTD). A retrospective analysis was performed in the patients who underwent CRT/CRTD extraction and reimplantation at our hospital from January 2012 to October 2018. The methods, patient complications and success rate of extraction and reimplantation of LVL were analyzed. A total of 54 patients underwent CRT/CRTD removal (pacemaker infection, n=51; LVL dysfunction, n=3; CRT/CRTD, 34/20). A total of 54 LVLs were removed (3 active electrodes and 51 passive electrodes). The average implantation duration of the LVL was 53.5 months (range, 1–204 months), whereas the success rate of the LVL extraction was 100% (94% completely removed and 6% clinically removed. A total of 6 patients (11%) were treated only by manual traction, whereas the remaining patients had their LVL successfully removed using extraction tools. In the peri-operative period, one fatality occurred (2%). The highest complication rate of the lead extraction was 2% and no minor complications were observed. A total of 36 patients were reimplanted on the right side, which was successful in 31 cases (success rate, 86.1%), whereas 3 cases were successfully reimplanted on the left side. The total success rate of LVL reimplantation was 87.2%. The procedure of the LVL removal and reimplantation exhibited a high success rate and a lower incidence of complications compared with that in patients with cardiac devices. [ABSTRACT FROM AUTHOR]

Diabetic cardiomyopathy (DCM) is characterized by structural and functional changes in the myocardium. Several studies have revealed that myocardial apoptosis and fibrosis occur during DCM. Studies have also indicated that oxidative stress may be a major factor associated with the development of DCM. Protein kinase C (PKC)β2 has been demonstrated to be activated in diabetic rats, and overexpression of PKCβ2 in the myocardium may result in cardiac hypertrophy and fibrosis. The P66shc adaptor protein, which is mediated by PKCβ, serves an important role in apoptosis during oxidative stress. The aim of the present study was to investigate whether the PKCβ2/P66shc oxidative stress pathway is associated with DCM, and to investigate the role and mechanisms of carvedilol in preserving cardiac function. Experimental diabetic rat models were induced by streptozotocin treatment accompanied by high energy intake. Carvedilol was orally administrated at a dose of 1 or 10 mg/kg/day. Cardiac function was evaluated by serum N-terminal pro-B-type natriuretic peptide level and cardiac ultrasound. Myocardial inflammation, oxidative stress, apoptosis and fibrosis were assessed by histopathological and echocardiographic analyses and tests for oxidative markers. Associated proteins and factors were examined by immunohistochemical and western blot analyses. Rats in the diabetes mellitus group exhibited significantly decreased systolic cardiac function along with elevated expression levels of phosphorylated (p)-PKCβ2, phos-P66shc, caspase-3, malondialdehyde, collagen type I, tumor necrosis factor-α and interleukin-1β, which were accompanied by disorder in metabolic processes. Treatment with carvedilol reversed these changes. Thus, the present results suggest that the PKCβ2/P66shc signaling pathway may be associated with diabetic cardiomyopathy; furthermore, carvedilol, as a novel β-receptor blocker, may protect the myocardium from injury by suppressing the myocardial inflammatory response, fibrosis, P66shc-mediated oxidative stress and subsequent apoptosis in myocardial tissue. Consequently, carvedilol may have potential as a therapy for the treatment of DCM. [ABSTRACT FROM AUTHOR]