RESUMEN
Atrial fibrillation, the most common cardiac arrhythmia in the Western world, confers a 5-fold increase in stroke, mainly due to thrombus formation in the left atrial appendage. Early rhythm control is often beneficial in reducing adverse cardiovascular events in higher-risk populations. Here, we present a patient who was found to have a 1 cm stalk-like lesion in the left atrial appendage on transesophageal echocardiogram prior to electrical cardioversion. Using multiple cardiac imaging modalities, including cardiac magnetic resonance imaging and computed tomography, the mass was eventually determined to be a chronic resolving thrombus.
RESUMEN
Patients suffering blunt cardiac trauma vary widely in the severity of their condition on presentation. Although some may present with mild sternal bruising, others may present with acute valvular rupture or malignant arrhythmia. Disposition for these patients ranges from discharge home to admission for urgent cardiac surgery. This article discusses some of the common types of blunt cardiac trauma and reviews the current literature and guidelines for their triage and initial management.
Asunto(s)
Ecocardiografía/métodos , Lesiones Cardíacas/diagnóstico , Heridas no Penetrantes , Salud Global , Lesiones Cardíacas/epidemiología , Lesiones Cardíacas/terapia , Humanos , Morbilidad , Tasa de Supervivencia , Índices de Gravedad del Trauma , Heridas no Penetrantes/diagnóstico , Heridas no Penetrantes/epidemiología , Heridas no Penetrantes/terapiaRESUMEN
A specific irreversible inhibitor of both cathepsins B and L, Fmoc-Tyr-Ala-CHN(2) (FYAD) induced apoptosis of neuroblastoma cells but not other tumor cells. Cysteine protease inhibitors that were not efficient inhibitors of both proteases did not cause death of any cell line tested. Apoptosis was preceded by accumulation of large electron dense vesicles and multivesicular bodies in the cytoplasm. Exposure of cells to the cathepsin D inhibitor, pepstatin, failed to rescue cells from FYAD-induced death. These results indicate that inhibition of cathepsins B and L may provide a unique mechanism for selectively inducing death of neuroblastoma with limited toxicity to normal cells and tissues.