Left ventricular outflow tract obstruction due to anomalous insertion of papillary muscle.

A 56-year-old man who complained of quadrantic hemianopsia was admitted to determine its etiology. Cerebral angiography revealed no organic stenosis. Echocardiography showed clear direct continuity between a hypertrophied anterolateral papillary muscle and the anterior mitral leaflet, and the left ventricular (LV) outflow tract (LVOT) was narrowed by the presence of an accessory papillary muscle. The LVOT obstruction caused an intra-LV pressure overload that resulted in LV concentric hypertrophy. Arrhythmia, such as paroxysmal atrial fibrillation (PAF), was thought to have caused a cerebral embolism. Mitral valve replacement (MVR), septal myectomy, and myectomy of the abnormal papillary muscle were performed, and complete release of the LVOT obstruction was accomplished. Anomalous insertion of papillary muscle is a rare cause of LVOT obstruction. Echocardiography was useful in identifying the papillary muscle malformation, and surgery was completely curative.

Bradykinin inhibits serum-depletion-induced apoptosis of human vascular endothelial cells by inducing nitric oxide via calcium ion kinetics.

Vascular endothelial cells play important roles in atherogenesis, and bradykinin is associated with atherosclerosis. The effect of bradykinin on apoptosis in human umbilical vein endothelial cells (HUVECs) was investigated, with a focus on Ca2+ kinetics and nitric oxide production. In serum-free conditions, the number of apoptotic cells increased in a time-dependent manner, but this increase was inhibited by bradykinin in a dose-dependent manner. The apoptosis inhibited by bradykinin was reduced by nitric oxide inhibitor N(G)-monomethyl-L-arginine (L-NMMA) and consequently restored by combined treatment with L-NMMA and L-arginine. Bradykinin increased influx of extracellular Ca2+, generation of inositol 1,4,5-trisphosphate, and release of Ca2+ from intracellular storage sites, thus increasing the total intracellular Ca2+ concentration ([Ca2+]i). Bradykinin increased nitric oxide production, which was inhibited by L-NMMA and restored by combined treatment with L-NMMA and L-arginine. Sodium nitroprusside (SNP) dose-dependently increased nitric oxide production and inhibited apoptosis; however, 10(-5) M SNP did not inhibit apoptosis. Caspase-3 inhibitor, acetyl-Asp-Met-Gln-Asp-aldehyde, enhanced bradykinin-induced inhibition of apoptosis but did not effect bradykinin-induced nitric oxide production. These findings suggest that bradykinin inhibits serum-depletion-induced apoptosis in HUVECs by enhancing nitric oxide production via an increase in [Ca2+]i.