RESUMEN
Intrapericardial hernia is a diaphragmatic hernia that extremely rarely causes cardiac tamponade. We present a case of a cardiac tamponade caused by an intrapericardial hernia in a 78-year-old male patient with a history of coronary artery bypass grafting, mimicking ST-segment elevation myocardial infarction, which was successfully treated by emergent laparotomy.
RESUMEN
BACKGROUND AND OBJECTIVE: Turbulent blood flow in patients with aortic valve stenosis (AS) results in morphological and functional changes in platelets and coagulation factors. The aim of this study is to determine how shear stress affects platelets and coagulation factors. METHODS: We retrospectively evaluated data from 78 patients who underwent AVR to treat AS between March 2008 and July 2017 at Kagoshima University Hospital. RESULTS: Platelet (PLT) count obviously decreased at three days after AVR, and increased above preoperative levels at the time of discharge. In contrast, platelet distribution width (PDW), mean platelet volume (MPV), and platelet large cell ratio (P-LCR) increased three days after AVR, then decreased to below preoperative levels. No differences were evident between groups with higher (HPPGâ>â100âmmHg) and lower (LPPGâ<â100âmmHg) peak pressure gradients (PPG) before AVR, whereas PLT count, PDW, MPV and P-LCR improved more in the HPPG group. Plateletcrit (PCT), which represents the total volume of platelets, increased after AVR due to decreased shear stress. High increasing rate of PCT was associated with lower PLT count, higher PDW and lower fibrinogen. CONCLUSION: Shear stress affects PLT count, PDW, and fibrinogen in patients with AS.
Asunto(s)
Estenosis de la Válvula Aórtica/sangre , Plaquetas/inmunología , Recuento de Plaquetas/métodos , Anciano , Animales , Femenino , Humanos , Masculino , Ratones , Estudios RetrospectivosRESUMEN
Iatrogenic atrial septal defect is an issue after percutaneous interventions for structural heart disease. A 63-year-old man, who had previously received 5 catheter ablations for paroxysmal atrial fibrillation, was found to have an iatrogenic atrial septal defect that persisted after the fourth intervention. Approximately 4 years later, he suffered exertional dyspnea. Pulmonary hypertension was caused by a left-to-right shunt via a large iatrogenic atrial septal defect. We performed surgical closure and the symptom improved. The timing of treatment for persistent iatrogenic atrial septal defect is difficult to determine, but preferable before the appearance of right ventricular dysfunction or embolism.