Beating aortic valve replacement surgery as an alternative to transcatheter aortic valve implantation in a patient with severe aortic stenosis and left ventricular dysfunction.

BACKGROUND: Transcatheter aortic valve implantation (TAVI) is the standard treatment for high-risk patients with aortic stenosis (AS); however, alternative treatments for patients who are ineligible for TAVI are controversial. CASE PRESENTATION: 56 year-old female who required 6 γ dobutamine support due to congestive heart failure was diagnosed as severe aortic stenosis with bicuspid valve. Echocardiography revealed left ventricular ejection fraction (LVEF) was 15%. The patient was relatively young for TAVI, and TAVI was not licensed for patient presenting with a bicuspid aortic valve in places other than the limited institutions in Japan. On pump beating aortic valve replacement (AVR) was performed with selective antegrade coronary artery blood perfusion. She resumed a completely normal lifestyle by 3 weeks after the operation. CONCLUSIONS: A relatively young patient for TAVI who was diagnosed as aortic stenosis with severely reduced ejection fraction and bicuspid valve is reported. Beating AVR with a continuously selective antegrade-perfusion was achieved safely with good clinical results in a patient with severely reduced left ventricular (LV) function. Beating AVR can be considered as a potential alternative for patients who are ineligible for conventional surgical aortic valve replacement (SAVR) and TAVI.

Molecular and electrical remodeling of L- and T-type Ca(2+) channels in rat right atrium with monocrotaline-induced pulmonary hypertension.

BACKGROUND: Atrial arrhythmia is often encountered in chronic pulmonary disease with pulmonary hypertension (PH), but few studies have investigated the electrical remodeling of atrial Ca(2+) channels under PH. METHODS AND RESULTS: Wistar rats were injected with monocrotaline (MCT), resulting in PH with right atrial and ventricular hypertrophy. The L-type Ca(2+) channel current density was significantly decreased in right atrial cells of MCT-treated rats, accompanied by a significant reduction in mRNA expression of the CaV1.2 (alpha(1C)) subunit and accessory beta(2) subunit. Conversely, the low voltage-activated Ca(2+) current was more marked in the right atrial cells of MCT-treated rats than in those of control rats. The current-voltage relationship and the time course of inactivation closely resembled those of T-type Ca(2+) channels, although the current was only slightly inhibited by 10-100 micromol/L Ni(2+). No significant differences were observed in the mRNA expression levels of CaV3.1 (alpha(1G)) and CaV3.2 (alpha(1H)) or the protein level of the CaV3.1 subunit. In left atrial cells, the electrophysiological molecular properties of Ca(2+) channels were unaffected by MCT treatment. CONCLUSIONS: PH causes right atrial hypertrophy, associated with alteration of the electrophysiological molecular properties of Ca(2+) channels.