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Background Intradepartmental and interdepartmental benchmarking requires scoring systems with reliability (calibration) and stability over the complete spectrum of periprocedural risk. The aim of this single-center study was to assess the performance of the 2000 Bernstein-Parsonnet risk stratification model in cardiac surgery, by itself and against the EuroSCORE. Methods A prospective observational design was used. The study group consisted of 1,639 consecutive patients of mean age 64.6 ± 12.04 years who underwent elective or emergency cardiac surgery from January 2003 to June 2004. The probabilities of hospital death were estimated with the 2000 Bernstein-Parsonnet and EuroSCORE algorithms. The correlation of predicted and observed mortality was compared between the two models, and score validity was assessed by calculating the area under the receiver operating characteristic (ROC) curve. Results The patients were stratified into five risk groups according to their scores in the two models. For the 2000 Bernstein-Parsonnet model, findings were as follows: score 0–10: predicted mortality 0%–2.2%, observed mortality 0.6%; score 10.5–20: predicted 2.3%–4.7%, observed 2.3%; score 20.5–30: predicted 4.8%–10%, observed 6.7%; score 30.5–40: predicted 10.1%–23%, observed 11.5%; and score greater than 40: predicted 23.1%–80%, observed 29.9%. For the EuroSCORE, findings were as follows: score 0%–2%: predicted mortality 1.1%, observed mortality 0.6%; score 3%–5%: predicted 2.1%, observed 3.0%; score 6%–8%: predicted 4.1%, observed 3.5%; score 9–11: predicted 7.6%, observed 6.6.%; and score greater than 12: predicted 13.8%, observed 14.0%. There was good agreement between the observed and expected number of deaths, with both models. The area under the ROC curve was higher for the Bernstein-Parsonnet model (0.83, odds ratio [OR] 2.01, 95% confidence interval [CI] 1.75–2.31, p p Conclusions The 2000 Bernstein-Parsonnet model is a simple, objective system for the estimation of hospital mortality in patients undergoing cardiac surgery, with slightly higher calibration and discrimination than the EuroSCORE additive model.

Objectives: Release of thromboxane (Tx) A2 by platelets may be one of multiple factors that are responsible for lung injury after cardiopulmonary bypass, leading to pulmonary vasoconstriction and impaired oxygenation. In experimental models, the inhibition of Tx receptor or its production improved lung function. The use of aspirin, which is used widely in the treatment of ischemic heart disease because of its antiplatelet activity, is usually discontinued a week before the patient undergoes the operation to restore normal platelet hemostatic function. The purpose of this study was to determine the relationship between the time of cessation of aspirin before coronary artery bypass surgery, and postoperative oxygenation and bleeding. Design: A prospective clinical study comparing the effect of aspirin on postoperative oxygenation in patients who had been treated or had not been treated with aspirin. Setting: Tx levels in the pericardial fluid, oxygenation, and bleeding were compared between the two groups. Patients: Thirty-two patients with coronary artery disease who were undergoing coronary artery bypass grafting. Fourteen of these patients received aspirin until the day of the operation, whereas 18 patients stopped receiving aspirin at least 1 week before undergoing the operation. Main results: Mean ( SD) Tx levels in the pericardial fluid were significantly lower in the aspirin group (117 47 pg/mL) compared to those in the control group (1,306 2,048 pg/mL; p 0.02). The duration of ventilation after the operation was significantly longer in the nonaspirin group (9.6 5.6 h vs 3.8 1.4 h, respectively; p 0.0004). PO2 reached a higher level while patients breathed 100% O2 in the aspirin group (235 54 mm Hg vs 176 27 mm Hg, respectively; p 0.001). The mean amount of bleeding during the first 24 h after surgery was increased in the aspirin group (710 202 mL) compared with the nonaspirin group (539 143 mL; p 0.01), but these patients did not require more transfusions. Conclusions: The administration of aspirin until the operation may improve oxygenation with only a slight increase in bleeding. This improvement is probably mediated by antiplatelet activity and Tx inhibition by aspirin. (CHEST 2005; 127:1622–1626)

Background Cardioplegia is known to affect coronary vascular reactivity. We examined the effects of intermittent cold and continuous warm blood cardioplegia on β-adrenoceptor–mediated, adenosine triphosphate–sensitive K + (K + ATP )–channel–mediated, and endothelium-dependent relaxation and on the myogenic tone of coronary arterioles. Methods Pigs were placed on cardiopulmonary bypass. Hearts were arrested for 1 hour with a cold blood cardioplegic solution administered intermittently (n=12; iCB-CP) or with a warm blood cardioplegic solution delivered continuously (n=12; cWB-CP). Selected hearts (n=6 in each group) were then reperfused for 1 hour. In vitro relaxation responses of precontracted microvessels (50 to 160μm) were studied in a pressurized no-flow state. Results Relaxation in response to isoproterenol (β-adrenergic agonist) was similar after iCB-CP and cWB-CP, whereas forskolin (adenylate cyclase activator)–induced relaxation was impaired more after iCB-CP than after cWB-CP. After reperfusion the respective responses were similar. Both iCB-CP and cWB-CP preserved receptor-mediated, endothelium-dependent relaxation in response to adenosine, 5 * -diphosphate; non–receptor-mediated endothelium-dependent relaxation in response to A23187; endothelium-independent cyclic guanosine monophosphate–mediated relaxation in response to sodium nitroprusside, and K + ATP -channel–mediated relaxation. Relaxations in response to 8-bromo-cyclic guanosine monophosphate (a cyclic guanosine monophosphate–dependent protein kinase activator) and to 8-bromo-cyclic adenosine monophosphate (a cyclic adenosine monophosphate–dependent protein kinase activator) were impaired after iCB-CP alone and after reperfusion, whereas the respective responses were not affected after cWB-CP. Myogenic tone was decreased similarly after iCB-CP and cWB-CP but was not further altered after reperfusion. Cardiac function was similar after iCB-CP and cWB-CP. Conclusions These results suggest that cWB-CP is similar to iCB-CP in its ability to preserve endothelium-dependent relaxation and K + ATP -channel function. The superior preservation of β-adrenergic-cyclic adenosine monophosphate–mediated coronary responses after cWB-CP is brief and associated with minimal improvement of myocardial function and myogenic tone.

Background. Cardiopulmonary bypass (CPB) is associated with alterations in the regulation of organ perfusion and vascular permeability. The purpose of this study was to examine the effects of hypothermic CPB on the regulation of the skeletal muscle microcirculation and the modulating influence of the priming solution. Methods. Sheep were placed on hypothermic CPB with a prime of either Pentastarch hydroxylethyl starch (HS) solution (n = 7), a solution in which HS is conjugated with deferoxamine (n = 7), or Ringer's lactate solution (n = 7). Sheep were placed on hypothermic CPB (27°C) for 90 minutes while the heart was protected with cold blood cardioplegia. Sheep were then separated from CPB and perfused for an additional 3 hours off CPB. Hemodynamics and total water content were measured. Results. In vitro relaxation responses of gracilis muscle arterioles (70 to 180 μm) to the endothelium-dependent agent acetylcholine, the endothelium-independent cyclic GMP-mediated vasodilator sodium nitroprusside, the β-adrenergic agonist isoproterenol, and the adenylate cyclase activator forskolin were studied. No statistically significant hemodynamic differences were observed between groups. However, weight gain was significantly less when the priming solution was HS or HS-deferoxamine compared to when Ringer's lactate was used. Skeletal muscle arteriolar relaxations to the endothelium-dependent vasodilator acetylcholine and the βadrenergic agonist isoproterenol were impaired after CPB in the HS and Ringer's lactate groups. Acetylcholine response was preserved in the HS-deferoxamine group, whereas the response to isoproterenol remained impaired. The responses to sodium nitroprusside and forskolin were similar in all groups. Conclusions. Skeletal muscle microvascular endothelium-dependent relaxation and β-adrenergic relaxation are reduced after CPB using either a crystalloid or HS prime. Skeletal muscle microvascular endothelial dysfunction may be attributable to oxygen-derived free radical-mediated injury, whereas altered β-adrenergic regulation is attributable to mechanisms other than the generation of oxygen-derived free radicals during CPB.

We compared the effect of hypermagnesium and hyperkalemic crystalloid cardioplegia on beta-adrenoceptor-mediated and endothelium-dependent relaxation and myogenic responses of coronary arterioles. Pigs were placed on cardiopulmonary bypass. Hearts were arrested with cold hypermagnesium (25 mM Mg2+, hyper-Mg, n = 12) or hyperkalemic (25 mM K+, hyper-K, n = 12) crystalloid cardioplegia for 1 hr. Hearts of selected pigs (n = 6 in each group) were then reperfused for 1 hr. In vitro relaxation responses of acetylcholine-pre-contracted arterioles were studied in a pressurized no-flow state with video-microscopy. Relaxation of pre-contracted coronary microvessels (70-150 microns) to isoproterenol (beta-adrenergic agonist) and forskolin (adenylate cyclase activator) was preserved after cardioplegia using a hyper-Mg solution. In contrast, responses were impaired to isoproterenol [P0.01 (two-factor ANOVA) vs. controls, n = 6] and forskolin (P0.01) after hyper-K cardioplegia. After 1 hr of reperfusion, relaxation responses to isoproterenol and forskolin were partially recovered. Hyper-Mg cardioplegia and post-cardioplegic reperfusion did not affect receptor-mediated endothelium-dependent relaxation to ADP, non-receptor-mediated endothelium-dependent relaxation to A23187, and endothelium-independent relaxation to nitroprusside. However, responses to ADP (P0.01) and A23187 (P0.05) were selectively impaired after hyper-K cardioplegia. Myogenic contraction was impaired after either hyper-Mg or hyper-K cardioplegia. Left ventricular systolic pressure, coronary blood flow, and +dP/dt were similar after hyper-Mg or hyper-K cardioplegia. These results suggest that hyper-Mg cardioplegia is superior to hyper-K cardioplegia in terms of preserving beta-adrenoceptor-mediated and endothelium-dependent regulation of the coronary microcirculation, yet it has minimal if any additional beneficial effect on preserving myogenic responses or myocardial contractile function.

A 48-year-old man undergoing orthotopic heart transplantation for ischemic cardiomyopathy developed severe right heart failure. Severe intractable bleeding complicated implantation of a right ventricular assist device. Treatment with 9.6 mg of recombinant activated factor VII stopped the bleeding, and the patient could be transferred to the intensive care unit. This is the first reported case of the successful use of recombinant activated factor VII to control bleeding with subsequent right ventricular assist device function.

The effect of periadventitial administration of acidic fibroblast growth factor (FGF) on coronary microvascular reactivity and blood flow was examined in the collateral-dependent and normally perfused myocardium.Ameroid constrictors were placed on the proximal left circumflex (LCx) coronary artery in 14 pigs. In seven pigs acidic FGF (10 micrograms) was administered into the perivascular space of the proximal LCx artery by using an ethylene vinyl acetate copolymer slow release device. After 7 to 9 weeks coronary arterial microvessels (70 to 150 microns) were studied in a pressurized (40 mm Hg) no-flow state with video microscopy.Relaxation mediated by beta-adrenoceptors and induced by isoproterenol (p0.05), and endothelium-dependent relaxation induced by adenosine 5' diphosphate (ADP) (p0.05) of isolated microvessels from the collateral-dependent LCx region were markedly reduced compared with the respective responses of vessels from the normally perfused left anterior descending (LAD) artery region. Relaxation induced by the adenylate cyclase activator forskolin and the guanylate cyclase activator sodium nitroprusside were unaltered. Chronic treatment with acidic FGF normalized responses to isoproterenol (p0.001 versus nontreated LCx) and ADP (p0.001 versus nontreated LCx) in the collateral-dependent LCx region, whereas responses to forskolin and sodium nitroprusside were not changed. Blood flow in the collateral-dependent LCx region (0.49 +/- 0.24 ml/min/gm) was less than that in the normally perfused LAD region (0.80 +/- 0.24 ml/min/gm, p0.05). Treatment with acidic FGF improved perfusion in the LCx region (0.80 +/- 0.06 ml/min/gm, p0.05) but did not significantly affect blood flow in the LAD territory (0.89 +/- 0.09 ml/min/gm).The periadventitial delivery of acidic FGF normalizes vasomotor regulation by beta-adrenergic and endothelium-dependent mechanisms and improves myocardial perfusion to the collateral-dependent myocardium. This may have implications regarding the treatment of patients with severe coronary artery disease who are not ameneable to conventional methods of revascularization.

Patients who undergo cardiopulmonary bypass frequently have neuropsychologic dysfunction. This study was undertaken to determine whether altered cerebral perfusion and vascular responses may in part lead to these neuropsychologic changes. Pigs were placed on normothermic cardiopulmonary bypass for 2 hours. Basal cerebral blood flow and in vivo responses to administration by internal carotid artery of neuronally released vasoactive substances were evaluated before and 5 to 15 minutes after termination of cardiopulmonary bypass. Another group of pigs were placed on cardiopulmonary bypass for 2 hours and then perfused off bypass for 1 additional hour. In vitro responses of cerebral arterial microvessels (100 to 175 μm) from both groups were examined in a pressurized (40 mm Hg) no-flow state with videomicroscopy. Vessels from uninstrumented pigs served as control preparations for in vitro studies. Cerebrovascular resistance and cerebral perfusion were maintained constant during cardiopulmonary bypass and after separation from bypass. The internal carotid artery infusion of acetylcholine (cholinergic agonist) caused increased internal carotid artery blood flow before cardiopulmonary bypass but decreased blood flow after cardiopulmonary bypass. After 2 hours of cardiopulmonary bypass, the increase in internal carotid artery blood flow induced by isoproterenol (a β-adrenoceptor agonist) was reduced, whereas the response to sodium nitroprusside (a guanylate cyclase activator) was unchanged. In vitro acetylcholine-induced microvascular vasodilation was converted to a contractile response and isoproterenol elicited less relaxation after 2 hours of cardiopulmonary bypass. One hour of cerebral perfusion after cardiopulmonary bypass caused a further reduction in isoproterenol-induced relaxation but had no further effect on the cholinergically mediated response. In vitro relaxation responses to sodium nitroprusside and forskolin (an adenylate cyclase activator) were similar in all experimental groups, suggesting that second-messenger mechanisms remain intact after normothermic cardiopulmonary bypass. In conclusion, basal cerebrovascular resistance and internal carotid artery blood flow are maintained if the systemic circulation and pressure are supported with fluid administration after cardiopulmonary bypass. Agonist-induced vasodilation of cerebral microvessels to cholinergic and β-adrenoceptor stimulation are selectively impaired after normothermic cardiopulmonary bypass, whereas second-messenger mechanisms remain intact. (J Thorac Cardiovasc Surg 1996;112:450-61)

Acute massive pulmonary embolism is associated with a high mortality rate. Prompt diagnosis and treatment are mandatory for a successful outcome. Although thrombolysis is effective, it is associated with a high rate of bleeding complications. This report describes the use of emergent pulmonary embolectomy as an effective and aggressive therapeutic approach to a massive saddle pulmonary embolism in a 66-year-old woman. With the application of specific surgical techniques and good interdisciplinary cooperation, pulmonary embolectomy may serve as more than a last resort for the management of this clinically unstable and dangerous condition.