Myocardial bridging prevents safe laparoscopy? A case report.

A 49-year-old male presented with atypical chest pain. Complete cardiac evaluation was normal except for cardiac catheterization, which revealed a myocardial bridge across the LAD (left anterior descending coronary artery) that caused a 50% systolic stenosis. Abdominal ultrasound revealed cholelithiasis. The patient became asymptomatic and was discharged only to return with biliary pancreatitis, which resolved over 2 weeks and laparoscopic cholecystectomy was attempted. Upon establishment of a pneumoperitoneum, he began to suffer cardiac ischemia, which immediately resolved upon desufflation. The procedure was converted to an uneventful open cholecystectomy. He did well without any further problems. This is the first report of myocardial bridging, a well-known cardiac anomaly, possibly preventing safe laparoscopy. This was possibly due to transmitted intraperitoneal pressure effect on the pericardium pushing closed that myocardial bridge.

Role of adrenal steroidogenesis in etiology of hypertension in the spontaneously hypertensive rat.

We measured peripheral adrenal steroid levels in spontaneously hypertensive rats (SHR), killed by nitrogen suffocation, at different ages during the development of hypertension. SHR became hypertensive by 8 weeks of age. Circulating plasma aldosterone (Aldo) levels of SHR gradually declined with age compared to their male Wistar-Kyoto (WKY) normotensive controls. On the other hand, corticosterone (B) concentrations rose relatively as the rats grew older, however, they were significantly lower in SHR at 16 weeks of age. Deoxycorticosterone (DOC) levels were significantly lower at 8 weeks and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) were lower at 16 weeks of age. Steroid ratios at age 4 weeks showed significantly higher B to 18-OH-DOC and lower B to DOC, 18-OH-DOC to Aldo, and 18-OH-DOC to DOC values in SHR. Furthermore, the B to 18-OH-DOC ratio remained significantly higher at 12 weeks and the B to DOC ratio remained lower at 16 weeks. These data imply the possibility of the secretion of an unknown steroid(s) and the existence of another, fourth pathway of Aldo biosynthesis in young SHR. Thus, major alterations of adrenal steroidogenesis exist in young SHR which may be causative in the development of hypertension. After the onset of hypertension, steroidogenesis tends to return to normal, by which time, however, SHR may have developed metacorticoid hypertension.