Repair of aortic regurgitation caused by spontaneous avulsion of aortic valve commissure in a patient with idiopathic thrombocytopenic purpura.

We describe a case of severe acute aortic regurgitation in a 60-year-old woman due to spontaneous avulsion of an aortic valve commissure. She presented with spontaneous bleeding and a platelet count of 4 000/microl caused by idiopathic thrombocytopenic purpura and developed acute heart failure and respiratory insufficiency. Preoperative transesophageal echocardiography was not diagnostic for the exact mechanism of aortic regurgitation. She received a 2-day course of intravenous immunoglobulin (0.5 mg/kg/d) to increase platelet count. At operation detachment (avulsion) of the commissure between the left and the right coronary cusp was evident. Aortic valve repair was performed with resuspension of the commissure. The postoperative course was uneventful. During a 24-month follow-up period, the patient has remained in NYHA class I.

Evidence for the ''paradox'' association between hypertensive lower esophageal sphincter and gastroesophageal reflux disease.

There are several studies suggesting the paradoxical simultaneous presence of hypertensive lower oesophageal sphincter and gastroesophageal reflux disease. We present a case of a 22-year-old male patient who was examined in our outpatient clinic with oesophageal food bolus impaction during a meal, severe chest pain and drooling. Manometry revealed a hypertensive lower esophageal sphincter pressure (resting pressure 35 mmHg) and pHmetry revealed a DeMeester score > 14.72 (43.27). Six months after therapy with lansoprazole, manometry revealed a normal lower oesophageal sphincter (resting pressure 14 mmHg) and the DeMeester score was < 14.72 (5.89). The patient is now asymptomatic. This report is the only published case which exhibits the normalization of lower oesophageal pressure 6 months after gastroesophageal reflux disease management with lansoprazole, thus proving and establishing the above ''paradox''.

The role of SOAT-1 polymorphisms in cognitive decline and delirium after bypass heart surgery.

BACKGROUND: Cognitive decline (CD) and delirium (PD) are commonly observed complications after bypass heart surgery. In this study we aimed to investigate whether certain genetic factors (alleles of the SOAT-1 gene) play a role in their appearance. PATIENTS AND METHODS: We examined 137 patients receiving coronary bypass surgery with a neuropsychiatric test battery consisting of the Mini Mental State Examination (MMSE), the Brief Psychiatric Rating Scale (BPRS), the Wechsler's Memory Scale-Revised (WMS-R) on admission and one month after surgery, and the Delirium Rating Scale postoperatively, when indicated, and genotyped them in relation to the SOAT-1 genotypes (AA positive group with augmented protection of the nerve cells against stress and the AA negative group--AC and CC subgroups--with diminished protection against stress). RESULTS: We noted a significant decline in test results postoperatively and a high frequency of delirium (29.92% of the patients). None of these complications could be associated to the SOAT-1 genotypes. CONCLUSIONS: Our study confirmed the expected cognitive decline and highly frequent delirium after bypass heart surgery and excluded the possible role of SOAT-1 genotype polymorphisms in their genesis.