The differences in electroencephalographic changes in patients undergoing carotid endarterectomies while under local versus general anesthesia

OBJECTIVE: This study compared the electroencephalographic (EEG) changes occurring during carotid occlusion in 225 consecutive patients undergoing carotid endarterectomies performed by two surgeons, one using local and the other using general anesthesia. METHODS: A retrospective review of patients undergoing carotid endarterectomies for carotid occlusive disease was conducted. EEG changes associated with intraoperative ischemia (decreased amplitude, generalized slowing, and loss of fast activity) resulting in the need for an indwelling arterial shunt were recorded for the two anesthesia groups. To determine the similarities or differences between the two groups, the groups were compared regarding age, risk factors, and indications for surgery. RESULTS: Significant EEG changes were noted in 6 of 96 patients (6.3%) in the local anesthesia group versus 19 of 121 patients (15.7%) in the general anesthesia group. EEG changes consisted solely of generalized slowing in the local anesthesia group, whereas a more varied spectrum was observed in the general anesthesia group. The two groups were similar regarding age and risk factors. Although the local anesthesia group had more asymptomatic patients, symptomatic patients did not have a greater incidence of EEG changes. CONCLUSION: There is a large difference in EEG changes potentially requiring shunt placement in patients undergoing surgery while under local (6.3%) versus general (15.7%) anesthesia. This could not be explained based on age, risk factors, interpretation of EEG findings, or indications between the two groups. We conclude that EEG monitoring may be insensitive and may fail to detect ischemia in patients who are under regional anesthesia. Alternately, the presence of general anesthetics may alter the character of the EEG findings and increase the sensitivity of EEG monitoring to ischemic events.     

Heart, brain and hypertension

Hypertension is one of the most important cardiovascular risk factors. Without therapy hypertension leads to stroke, coronary heart disease with angina pectoris and myocardial infarction, kidney failure and/or peripheral vascular disease. The association between blood pressure and these cardiovascular complications can be demonstrated over the entire blood pressure range. The risk of stroke, myocardial infarction, renal failure or peripheral vascular disease increases with increasing blood pressure. Additional cardiovascular risk factors such as hyperlipidemia, smoking and diabetes involve a further increase in risk. Today hypertension can be effectively treated. To that end, diuretics, betablockers, ACE-inhibitors or calcium antagonists can be used. Alpha receptor antagonists and angiotensin AT1 receptor antagonists are also of value. The antihypertensive effectiveness of these drugs is comparable but may vary in individual patients. During antihypertensive therapy, a reduction in cerebrovascular and cardiac complications has been demonstrated for alpha methyldopa, diuretics and betablockers. In these studies, fatal and non-fatal strokes were reduced by 42%, while the reduction in cardiac events was less pronounced (14%). The reasons for this greater efficacy of antihypertensive therapy in the cerebral circulation are not clear. Other risk factors may be particularly important in the pathogenesis of coronary artery disease (e.g. genetic factors, hyperlipidemia and others) or hypertensive vascular changes in the coronary circulation may not be as reversible as they are in the cerebral circulation. The well documented correlation between stroke, myocardial infarction and hypertension, as well as the proven efficacy of antihypertensive therapy in preventing cardiovascular events, underscores the importance of effective and sustained blood pressure control in these patients.     

Effects of pentoxifylline on renal function and blood pressure in cardiac transplant recipients: a randomized trial

BACKGROUND: The current success of cardiac transplantation is in part attributable to the development of effective immunosuppressive agents such as cyclosporine. However, concern remains regarding the potential for cyclosporine-induced nephrotoxicity. Animal studies and early reports of renal protective effects of pentoxifylline in bone marrow transplant recipients prompted a randomized trial in cardiac transplant recipients. METHODS: Twenty-nine patients were randomized to receive pentoxifylline 400 mg p.o. t.i.d. or matching placebo for 1 year after cardiac transplantation. Renal function was assessed preoperatively and at 1, 6, and 12 months postoperatively. Glomerular filtration rate and renal plasma flow were measured with iothalamate and para-aminohippurate, respectively. Serum creatinine was also measured. Ambulatory blood pressure monitoring after withdrawal of antihypertensives for 3 days was performed 12 months postoperatively. RESULTS: Twenty-seven patients completed the study. Glomerular filtration rate rose between 1 and 6 months after transplantation, presumably due to the reduction in goal cyclosporine level in that period, and then fell modestly between 6 and 12 months, presumably due to ongoing nephrotoxic effects of cyclosporine. No difference in glomerular filtration rate or creatinine was seen between pentoxifylline and placebo groups at any interval. Renal plasma flow increased modestly between baseline and 6 months in the pentoxifylline group, but not in the placebo group, and then fell between 6 and 12 months. Serum creatinine increased between baseline and 6 months in both groups, apparently due to increased body weight. Results of 18-hr ambulatory blood pressure monitoring obtained 1 year after transplantation was not different between groups. CONCLUSIONS: Renal function declines only modestly in the first year after cardiac transplantation. Pentoxifylline did not attenuate this process and had no effect on blood pressure. The modest decline in renal function may be related to current immunosuppressive strategies.     

Acidic sphingomyelinase mediates entry of N. gonorrhoeae into nonphagocytic cells

Invasion of human mucosal cells by N. gonorrhoeae via the binding to heparansulfate proteoglycan receptors is considered a crucial event of the infection. Using different human epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol and ceramide. Genetic and/or pharmacological blockade of ASM and PC-PLC cause inhibition of cellular invasion by N. gonorrhoeae. Complementation of ASM-deficient fibroblasts from Niemann-Pick disease patients restored N. gonorrhoeae-induced signaling and entry processes. The activation of PC-PLC and ASM, therefore, is an essential requirement for the entry of N. gonorrhoeae into distinct nonphagocytic human cell types including several epithelial cells and primary fibroblasts.