Multi-organ embolism caused by oscillating aortic valve vegetation: A case report.

INTRODUCTION: Valvular vegetation is often due to rheumatic heart disease and infective endocarditis. However, multi-arterial embolism can happen in older patients with no history of infection, fever, and cardiac symptoms. We describe a case of multi-organ embolism caused by oscillating aortal valve vegetation. PATIENT CONCERNS: An 80-year-old woman without a history of infection, fever, and heart symptoms showed sudden loss of consciousness and symptoms of a multi-vessel embolism. Magnetic resonance imaging revealed multiple patchy ischemic foci in both cerebral hemispheres in the same time-phase, and echocardiography showed regurgitation in the aortic valve due to an abnormally hypo-hyperechoic mass measuring about 7.7 × 17.2 mm and oscillating aortic valve vegetation, which was induced by cardiac contraction. DIAGNOSIS: Multiple organ cardiac embolisms caused by oscillating aortic valve vegetation. INTERVENTIONS: Anti-platelet, fluid-supplement, and vascular-dilating therapies as well as intravenous diazepam were given to the patient. OUTCOME: The patient died of epileptic attack secondary to the cerebral embolism. CONCLUSIONS: The patient's whole-body multi-vessel ischemic events in nearly the same time-phase should have encouraged us to consider the possibility of cardiogenic embolism and thus early examination and treatment, although she was old with a relatively poor response due to early infection and physical discomfort. Clinicians should be aware that aortic valve vegetation induces generalized multi-organ embolism in the setting of infective endocarditis in order to ensure prompt recognition and treatment of this fatal complication.

Lower limb vein thrombosis-induced pulmonary embolism and paradoxical multiple arterial embolisms: A case report with a 10-year follow-up.

INTRODUCTION: Paradoxical embolism (PDE) refers to direct passage of venous thrombi into the arterial circulation through an arteriovenous shunt. It is well-known that the pulmonary thromboembolism (PTE) can cause opening of the foramen ovale leading to paradoxical arterial embolism. Long term follow up of PDE patient over 10 years was not reported in the literature. PATIENT CONCERNS: A 57-year-old woman presented with initial symptoms of numbness/weakness and hypoxemia. Ultrasonography and pulmonary arteriography indicated pulmonary thromboembolism. DIAGNOSIS: Pulmonary embolism and paradoxical multiple arterial embolism or acute PTE concomitant with paradoxical multiple arterial embolism. INTERVENTIONS: Craniectomy and anticoagulation treatment was administered and the patient received low-dose warfarin therapy for 10 years. OUTCOMES: The patient is currently stable with no abnormalities seen in the deep veins of the bilateral lower limbs. The international normalized ratio (INR) was controlled within the range of 1.20 to 1.51. As this is a 10-year follow-up case report, the patient has responded well to the treatment and has been followed-up. The follow-up has been annual and the patient has been stable CONCLUSION:: Low intensity and persistent anticoagulation therapy can inhibit blood thrombophilia and reduce the risk of bleeding. It is noteworthy that such an approach used effectively in this patient. To best our knowledge, it is first report for long term follow up PDE patient successfully over 10 years.

Ca2+-dependent activator protein for secretion 1 is critical for constitutive and regulated exocytosis but not for loading of transmitters into dense core vesicles.

Although CAPS1 was originally identified as a soluble factor that reconstitutes Ca(2+)-dependent secretion from permeabilized neuroendocrine cells, its exact function in intact mammalian cells remains controversial. Here we investigate the role for CAPS1 by generating stable cell lines in which CAPS1 is strongly down-regulated. In these cells, Ca(2+)-dependent secretion was strongly reduced not only of catecholamine but also of a transfected neuropeptide. These secretion defects were rescued by infusion of CAPS1-containing brain cytosol or by transfection-mediated expression of CAPS1. Whole cell patch clamp recording revealed significant reductions in slow burst and sustained release components of exocytosis in the knockdown cells. Unexpectedly, they also accumulated higher amounts of endogenous and exogenous transmitters, which were attributable to reductions in constitutive secretion. Electron microscopy did not reveal abnormalities in the number or docking of dense core vesicles. Our results indicate that CAPS1 plays critical roles not only in Ca(2+)-dependent, regulated exocytosis but also in constitutive exocytosis downstream of vesicle docking. However, they do not support the role for CAPS1 in loading transmitters into dense core vesicles.

RalA and RalB function as the critical GTP sensors for GTP-dependent exocytosis.

Although it has been established that the activation of GTPases by non-hydrolyzable GTP stimulates neurotransmitter release from many different secretory cell types, the underlying mechanisms remain unclear. In the present study we aimed to elucidate the functional role(s) for endogenous Ras-like protein A (RalA) and RalB GTPases in GTP-dependent exocytosis. For this purpose stable neuroendocrine pheochromocytoma 12 (PC12) cell lines were generated in which the expressions of both RalA and RalB were strongly downregulated. In these double knock-down cells GTP-dependent exocytosis was reduced severely and was restored after the expression of RalA or RalB was reintroduced by transfection. In contrast, Ca2+-dependent exocytosis and the docking of dense core vesicles analyzed by electron microscopy remained unchanged in the double knock-down cells. Furthermore, the transfected RalA and RalB appeared to be localized primarily on the dense core vesicles in undifferentiated and nerve growth factor-differentiated PC12 cells. Our results indicate that endogenous RalA and RalB function specifically as GTP sensors for the GTP-dependent exocytosis of dense core vesicles, but they are not required for the general secretory pathways, including tethering of vesicles to the plasma membrane and Ca2+-dependent exocytosis.