Intraaortic balloon counterpulsation as a temporary support measure in decompensated critical aortic stenosis

Intraaortic balloon counterpulsation was instituted in two adult patients whose condition was rapidly deteriorating because of critical decompensated valvular aortic stenosis. The acute hemodynamic effect of counterpulsation in these patients was compared with the effect of counterpulsation in three control patients with unstable angina and no aortic valve disease. Augmentation of aortic diastolic pressure was similar in both groups; however, in contrast to the patients with unstable angina, the patients with aortic stenosis had no decrease in left ventricular systolic pressure. Counterpulsation resulted in an increase in the transvalvular pressure gradient, which was associated with a slight increase in stroke volume. In both patients with aortic stenosis, the institution of counterpulsation resulted in marked clinical improvement, which facilitated successful valve replacement surgery.The benefit from counterpulsation in critically decompensated aortic stenosis appears to be derived almost entirely from augmentation of the diastolic coronary filling gradient. The improvement that results from counterpulsation suggests that ischemia is the major cause of decompensation

Hemodynamic effects of nitroglycerin in an experimental model of acute aortic regurgitation

AbstractAfterload reduction is an accepted therapeutic modality for the treatment of congestive heart failure caused by chronic aortic regurgitation. However, the role of vasodilator therapy in acute aortic incompetence has not been established. To investigate this, left ventricular volume overload was produced in 18 dogs by constructing a valved conduit from the descending thoracic aorta to the left ventricular apex. The time course of aortic, pulmonary and conduit flows was analyzed in eight control studies and established stability of the experimental model.In the remaining 10 dogs, intravenous nitroglycerin, titrated to reduce mean aortic blood pressure by 40%, and placebo (ethanol) were each infused for 20 min periods. Compared with placebo, nitroglycerin significantly reduced aortic flow (3,945 ± 324 to 3,397 ± 362 ml/min, p < 0.01), regurgitant flow (1,304 ± 131 to 764 ± 90 ml/min, p < 0.001), septal-lateral end-diastolic diameter (47.5 ± 1.8 to 46.5 ± 1.8 mm, p < 0.001), left ventricular end-diastolic pressure (6.9 ± 0.8 to 6.0 ± 0.6 mm Hg, p < 0.05), left ventricular stroke work (19.0 ± 2.6 to 10.8 ± 1.7 g-m/beat, p < 0.001) and systemic vascular resistance (2,253 ± 173 to 1,433 ± 117 dyne-s/cm5, p < 0.001). In contrast, pulmonary flow, left anterior descending coronary flow and subendocardial pH did not change during infusion of either nitroglycerin or placebo.These data indicate that by decreasing preload and afterload, and by preserving coronary flow and tissue pH, nitroglycerin effectively reduced ventricular and regurgitant volumes in the setting of acute volume overload. This study supports the clinical use of nitroglycerin in severe acute aortic incompetence

Modest serum creatinine elevation affects adverse outcome after general surgery

Modest serum creatinine elevation affects adverse outcome after general surgery.BackgroundModest preoperative serum creatinine elevation (1.5 to 3.0 mg/dL) has been recently shown to be independently associated with morbidity and mortality after cardiac surgery. It is important to know if this association can be applied more broadly to general surgery cases.MethodsMultivariable logistic regression analyses of 46 risk variables in 49,081 cases from the Veterans Affairs National Surgical Quality Improvement Program, undergoing major general surgery from 10/1/96 through 9/30/98.ResultsThirty day mortality and several cardiac, respiratory, infectious and hemorrhagic morbidities were significantly (P < 0.001) higher in patients with a serum creatinine>1.5 mg/dL. With multivariable analysis, the adjusted odds ratio for mortality for patients with a serum creatinine of 1.5 to 3.0 mg/dL was 1.44 [95% confidence interval (95% CI) 1.22 to 1.71] and for creatinine>3.0 mg/dL was 1.93 (95% CI 1.51 to 2.46). The adjusted odds ratio for morbidity (one or more postoperative complications) for patients with a serum creatinine of 1.5 to 3.0 mg/dL was 1.18 (95% CI 1.06 to 1.32) and for creatinine>3.0 mg/dL was 1.19 (95% CI 0.99 to 1.43). Further stratification and recursive partitioning of creatinine levels revealed that a serum creatinine level>1.5 mg/dL was the approximate threshold for both increased morbidity and mortality.ConclusionsModest preoperative serum creatinine elevation (>1.5 mg/dL) is a significant predictor of risk-adjusted morbidity and mortality after general surgery. A preoperative serum creatinine of 1.5 mg/dL or higher is a readily available marker for potential adverse outcomes after general surgery

Laparoscopic Versus Open Gastric Bypass for Morbid Obesity: A Multicenter, Prospective, Risk-Adjusted Analysis From the National Surgical Quality Improvement Program

OBJECTIVE: To compare laparoscopic versus open gastric bypass procedures with respect to 30-day morbidity and mortality rates, using multi-institutional, prospective, risk-adjusted data. SUMMARY BACKGROUND DATA: Laparoscopic Roux-en-Y gastric bypass for weight loss is being performed with increasing frequency, partly driven by consumer demand. However, there are no multi-institutional, risk-adjusted, prospective studies comparing laparoscopic and open gastric bypass outcomes. METHODS: A multi-institutional, prospective, risk-adjusted cohort study of patients undergoing laparoscopic and open gastric bypass procedures was performed from hospitals (n = 15) involved in the Private Sector Study of the National Surgical Quality Improvement Program (NSQIP). Data points have been extensively validated, are based on standardized definitions, and were collected by nurse reviewers who are audited for accuracy. RESULTS: From 2000 to 2003, data from 1356 gastric bypass procedures was collected. The 30-day mortality rate was zero in the laparoscopic group (n = 401), and 0.6% in the open group (n = 955) (P = not significant). The 30-day complication rate was significantly lower in the laparoscopic group as compared with the open group: 7% versus 14.5% (P < 0.0001). Multivariate logistic regression analysis was performed to control for potential confounding variables and showed that patients undergoing an open procedure were more likely to develop a complication, as compared with patients undergoing an laparoscopic procedure (odds ratio = 2.08; 95% confidence interval, 1.33–3.25). Propensity score modeling revealed similar results. A prediction model was derived, and variables that significantly predict higher complication rates after gastric bypass included an open procedure, a high ASA class (III, IV, V), functionally dependent patient, and hypertension as a comorbid illness. CONCLUSIONS: Multicenter, prospective, risk-adjusted data show that laparoscopic gastric bypass is safer than open gastric bypass, with respect to 30-day complication rate

The effects of aspirin and hypothermia on platelet function in vivo

Patients undergoing hypothermic cardiopulmonary bypass are often receiving aspirin therapy. Hypothermia, aspirin and cardiopulmonary bypass can each induce a platelet function defect, but it is not known if the effects of aspirin and hypothermia are additive in this regard. To address this question in humans in vivo, the forearm skin temperature of healthy volunteers was equilibrated and maintained at either normothermia (32 degrees C) or hypothermia (28 degrees C or 22 degrees C) before and 16 h after the ingestion of 650 mg aspirin. A standardized template bleeding time was performed on the forearm and the shed blood emerging from the wound was assayed for platelet surface P-selectin expression by whole blood flow cytometry (reflecting alpha granule secretion) and thromboxane B2 (the stable metabolite of thromboxane A2) by radioimmunoassay. Hypothermia resulted in marked prolongation of the bleeding time. Aspirin resulted in prolongation of the bleeding time under normothermic conditions, but only minimally augmented the hypothermia-induced prolongation of the bleeding time. Platelet surface P-selectin up-regulation in shed blood was abolished by hypothermia. Aspirin had no effect on maximal platelet surface P-selectin expression under normothermic or hypothermic conditions. Both hypothermia and aspirin resulted in markedly reduced shed blood thromboxane B2. Although aspirin slightly augmented the hypothermia-induced reduction in shed blood thromboxane B2, the concentration of thromboxane generated in shed blood under hypothermic conditions in the absence of aspirin had no effect on platelet surface P-selectin or platelet aggregation in whole blood. In conclusion, as determined by three independent parameters of the shed blood emerging from a standardized bleeding time wound (bleeding time, platelet surface P-selectin, and thromboxane B2), aspirin did not significantly augment hypothermia-induced platelet dysfunction in vivo