Thoracoscopic stapler-closure of left atrial appendage and epicardial clamp-isolation of pulmonary veins in a patient with non-valvular atrial fibrillation and short bowel: a case report.

BACKGROUND: Thromboembolic occlusion of the superior mesenteric artery (SMA) is a serious event in patients with atrial fibrillation (AF). Extensive bowel resection is frequently required, and the resulting short bowel syndrome hampers the intake of anticoagulant or anti-arrhythmic medication. CASE SUMMARY: We report the case of thoracoscopic surgery consisting of stapler-closure of the left atrial appendage and bilateral epicardial clamp-isolation of the pulmonary veins performed in a 66-year-old male patient with symptomatic persistent non-valvular AF who became unable to take in anticoagulants or anti-arrhythmic drugs because of thromboembolic SMA occlusion and subsequent total resection of the small intestine. The patient has been free from thromboembolic or arrhythmic symptoms during 6 months of follow-up despite taking no anticoagulant or anti-arrhythmic drugs. Electrocardiographic monitoring demonstrated a stable sinus rhythm for 48 h at postoperative Months 3 and 6. Echocardiography manifested an improvement of the left ventricular ejection fraction from a preoperative value of 44-69% at postoperative Month 6. DISCUSSION: The present technique may contribute to treating patients with symptomatic non-valvular AF and a complication similar to that of the present case.

Increased connective tissue growth factor relative to brain natriuretic peptide as a determinant of myocardial fibrosis.

Excessive fibrosis contributes to an increase in left ventricular stiffness. The goal of the present study was to investigate the role of connective tissue growth factor (CCN2/CTGF), a profibrotic cytokine of the CCN (Cyr61, CTGF, and Nov) family, and its functional interactions with brain natriuretic peptide (BNP), an antifibrotic peptide, in the development of myocardial fibrosis and diastolic heart failure. Histological examination on endomyocardial biopsy samples from patients without systolic dysfunction revealed that the abundance of CTGF-immunopositive cardiac myocytes was correlated with the excessive interstitial fibrosis and a clinical history of acute pulmonary congestion. In a rat pressure overload cardiac hypertrophy model, CTGF mRNA levels and BNP mRNA were increased in proportion to one another in the myocardium. Interestingly, relative abundance of mRNA for CTGF compared with BNP was positively correlated with diastolic dysfunction, myocardial fibrosis area, and procollagen type 1 mRNA expression. Investigation with conditioned medium and subsequent neutralization experiments using primary cultured cells demonstrated that CTGF secreted by cardiac myocytes induced collagen production in cardiac fibroblasts. Further, G protein-coupled receptor ligands induced expression of the CTGF and BNP genes in cardiac myocytes, whereas aldosterone and transforming growth factor-beta preferentially induced expression of the CTGF gene. Finally, exogenous BNP prevented the production of CTGF in cardiac myocytes. These data suggest that a disproportionate increase in CTGF relative to BNP in cardiac myocytes plays a central role in the induction of excessive myocardial fibrosis and diastolic heart failure.