[Clinical aspects and treatment of tricuspid valve regurgitation]. / Klinik und Therapie der Trikuspidalklappeninsuffizienz.

Tricuspid regurgitation (TR) leading to right heart failure is prevalent and associated with increased mortality. The significant under-recognition of the disease resulted from insufficient medical therapies and the high associated risk of surgical therapy. Over the last decade there has been a rapid development of interventional treatment options so that the disease has increasingly become the focus of attention of specialists in internal medicine and interventional cardiologists. The etiology of TR is differentiated into primary TR, secondary atrial TR, secondary ventricular TR and TR associated with cardiac implantable electronic devices (CIED). The TR was identified as an independent predictor of mortality, independent of associated diseases such as atrial fibrillation, left-sided heart failure or pulmonary hypertension. Even patients with low to moderate TR have a significantly increased risk of mortality. Early diagnostics and estimation of the severity by echocardiography as well as timely referral to a tertiary heart valve center are decisive in order to evaluate possible treatment options before irreversible right ventricular damage and secondary organ dysfunction occur. For transcatheter edge-to-edge repair and transcatheter tricuspid valve replacement there is now first evidence from randomized controlled studies. While the understanding of TR is continuously improving, new tricuspid valve repair and replacement systems are in a state of steady progress. Whether the treatment has an effect on reduction of the mortality and stabilization of right ventricular failure with a reduction in hospitalization, will first be shown in future studies.

[Intensive care treatment of patients with left ventricular assist devices]. / Intensivbehandlung von Kranken mit Linksherzersatz.

Apart from heart transplantation, implantation of a left ventricular assist device (LVAD) is the only established surgical treatment for therapy-refractory terminal left heart failure, The specific intensive care unit (ICU) management of these patients depends on the reason for the ICU admission and requires understanding of the characteristic hemodynamics of non-pulsatile LVADs as well as of the inherent problems. Knowledge about the specific features in hemodynamic monitoring, understanding of pump characteristics, management of anticoagulation and hemostasis and the handling of problems, such as right heart failure, aortic valve insufficiency and infections is essential. The management of unconscious LVAD patients can be challenging. It requires a sophisticated transthoracic and transesophageal echocardiography (TTE/TEE) examination, targeted laboratory diagnostics and consideration of possible alternative diagnoses. Professional interdisciplinary cooperation and exchange of current knowledge is crucial.

Crucial role of rho-kinase in pressure overload-induced right ventricular hypertrophy and dysfunction in mice.

OBJECTIVE: Right ventricular (RV) failure is the leading cause of death in various cardiopulmonary diseases, including pulmonary hypertension. It is generally considered that the RV is vulnerable to pressure overload as compared with the left ventricle (LV). However, as compared with LV failure, the molecular mechanisms of RV failure are poorly understood, and hence therapeutic targets of the disorder remain to be elucidated. Thus, we aimed to identify molecular therapeutic targets for RV failure in a mouse model of pressure overload. APPROACH AND RESULTS: To induce pressure overload to respective ventricles, we performed pulmonary artery constriction or transverse aortic constriction in mice. We first performed microarray analysis and found that the molecules related to RhoA/Rho-kinase and integrin pathways were significantly upregulated in the RV with pulmonary artery constriction compared with the LV with transverse aortic constriction. Then, we examined the responses of both ventricles to chronic pressure overload in vivo. We demonstrated that compared with transverse aortic constriction, pulmonary artery constriction caused greater extents of mortality, Rho-kinase expression (especially ROCK2 isoform), and oxidative stress in pressure-overloaded RV, reflecting the weakness of the RV in response to pressure overload. Furthermore, mice with myocardial-specific overexpression of dominant-negative Rho-kinase showed resistance to pressure overload-induced hypertrophy and dysfunction associated with reduced oxidative stress. Finally, dominant-negative Rho-kinase mice showed a significantly improved long-term survival in both pulmonary artery constriction and transverse aortic constriction as compared with littermate controls. CONCLUSION: These results indicate that the Rho-kinase pathway plays a crucial role in RV hypertrophy and dysfunction, suggesting that the pathway is a novel therapeutic target of RV failure in humans.

A Case of Intracardiac Thymic Carcinoma Presenting as Congestive Hepatopathy / 대한내과학회지

Thymic carcinoma is a rare but aggressive epithelial neoplasm with a strong propensity for early local invasion and widespread metastasis. It is common for thymic carcinomas to invade the lungs, pericardium, and great vessels. However, invasion of thymic carcinoma into the right atrium, right ventricle, mediastinum, and superior vena cava is very rare. There have been sporadic reports on intracardiac thymic carcinomas globally and only one case report in South Korea to date. We herein report a case of intracardiac thymic carcinoma presenting as right-sided heart failure with congestive hepatopathy.