Acute cardiac inflammatory responses to postischemic reperfusion during cardiopulmonary bypass

Objectives: The investigation centers on whether there is a reperfusion-induced specific cardiac inflammatory reaction after bypass surgery. Background: Cardiopulmonary bypass (CPB) leads to systemic inflammation. Additionally, cardiac inflammation due to reperfusion could occur. Knowledge about nature and time course of this reaction might help to develop cardioprotective interventions. Methods: In 12 patients receiving coronary bypass grafts, arterial and coronary venous blood was obtained before onset of CPB, and 1, 5, 10, 25, 35 and 75 min after cardiac reperfusion. Plasma levels of IL6 and IL8 were measured by immunoassay. CD11b, CD41, and CD62 on blood cells were quantified by flow cytometry. Measurement of CD41, a platelet marker, on neutrophils and monocytes allowed detection of leukocyte–platelet microaggregates. Results: Transcardiac veno–arterial difference of IL6 rose in the 10th and 25th min of reperfusion (from 0 to 7 pg/ml; p<0.05), and after 75 min (15 pg/ml). IL8 did not change. CD11b on neutrophils (PMN) decreased transcardially to 95, 88 and 82% of the initial level in the 5th, 10th, and 75th min, respectively, suggesting sequestration of activated neutrophils. CD62 on platelets rose about 30% in the 75th min. Initially, leukocyte–platelet microaggregates were formed during coronary passage (+31% of the arterial level for PMN, +23% for monocytes). During reperfusion, coaggregates were retained (PMN: -1% and -7% in the 5th and 10th min, monocytes: -22%, -13% and -12% in the 1st, 5th and 10th min. Conclusions: During early reperfusion after aortic declamping, the coronary bed is already a source of proinflammatory stimuli and target for activated leukocytes, partly in conjunction with platelets. Mitigation of these phenomena might help to improve cardiac function after CPB especially in patients at risk

Acute cardiac inflammatory responses to postischemic reperfusion during cardiopulmonary bypass

Objectives: The investigation centers on whether there is a reperfusion-induced specific cardiac inflammatory reaction after bypass surgery. Background: Cardiopulmonary bypass (CPB) leads to systemic inflammation. Additionally, cardiac inflammation due to reperfusion could occur. Knowledge about nature and time course of this reaction might help to develop cardioprotective interventions. Methods: In 12 patients receiving coronary bypass grafts, arterial and coronary venous blood was obtained before onset of CPB, and 1, 5, 10, 25, 35 and 75 min after cardiac reperfusion. Plasma levels of IL6 and IL8 were measured by immunoassay. CD11b, CD41, and CD62 on blood cells were quantified by flow cytometry. Measurement of CD41, a platelet marker, on neutrophils and monocytes allowed detection of leukocyte–platelet microaggregates. Results: Transcardiac veno–arterial difference of IL6 rose in the 10th and 25th min of reperfusion (from 0 to 7 pg/ml; p<0.05), and after 75 min (15 pg/ml). IL8 did not change. CD11b on neutrophils (PMN) decreased transcardially to 95, 88 and 82% of the initial level in the 5th, 10th, and 75th min, respectively, suggesting sequestration of activated neutrophils. CD62 on platelets rose about 30% in the 75th min. Initially, leukocyte–platelet microaggregates were formed during coronary passage (+31% of the arterial level for PMN, +23% for monocytes). During reperfusion, coaggregates were retained (PMN: -1% and -7% in the 5th and 10th min, monocytes: -22%, -13% and -12% in the 1st, 5th and 10th min. Conclusions: During early reperfusion after aortic declamping, the coronary bed is already a source of proinflammatory stimuli and target for activated leukocytes, partly in conjunction with platelets. Mitigation of these phenomena might help to improve cardiac function after CPB especially in patients at risk

Impact of the interval between coronary angiography and off-pump coronary bypass surgery on postoperative renal function

BACKGROUND: Postoperative acute kidney injury (AKI) is a significant complication after coronary artery bypass surgery. Prior coronary angiography increases the likelihood of AKI due to the use of a radiocontrast dye. This study examined the effect of coronary angiography on the postoperative renal function after off-pump coronary artery bypass surgery (OPCAB). METHODS: The records of 110 patients who required OPCAB were reviewed. These patients also had at least two of the following conditions: chronic kidney disease, hypertension, diabetes mellitus, emergency surgery, congestive heart failure, age >75 years, hematocrit /=50% or >/=0.3 mg/dl within 48 hours. RESULTS: The postoperative changes in the SCr, cystatin C and eGFR were similar in the two groups. The incidence of AKI and renal replacement therapy were similar in the two groups. CONCLUSIONS: Coronary angiography performed within two days of OPCAB does not affect the postoperative renal functionope

Impact of repeated percutaneous coronary intervention on long-term survival after subsequent coronary artery bypass surgery

<p>Abstract</p> <p>(Background)</p> <p>In the current stent era, aggressive repeated percutaneous coronary intervention (PCI) has become more common. The aim of this study was to investigate the impact of previous repeated PCI on the subsequent coronary artery bypass grafting (CABG).</p> <p>(Methods)</p> <p>Between January 1990 and January 2008, a total of 894 patients underwent first-time isolated elective CABG. Among the 894 patients, 515 patients had had no PCI (group A), 179 patients had had single PCI (Group B), and 200 patients had had multiple PCI (2-15 times, mean 3.6 ± 2.3 times) (group C) before CABG. These groups were compared in terms of early and late clinical results.</p> <p>(Results)</p> <p>Preoperative left ventricular ejection fraction was significantly higher in group A (group A;58 ± 13%, group B;54 ± 12%, and group C;54 ± 12%). Number of bypass grafts was significantly smaller in group C (A:3.3 ± 1.0, B 3.4 ± 0.9, C 3.1 ± 1.0). Although there was no statistically significant difference among the groups, in-hospital mortality in group C was higher than that in group A and B (A:1.6%, B:1.1%, C:3.5%, p = 0.16). Survival analysis by Kaplan-Meier method (mean follow-up: 58 ± 43 methods) revealed that freedom from all-cause death and cardiac death was significantly lower in group C in comparison with group A. Freedom from cardiac event was significantly higher in group C than that in group A. Multivariate analysis identified a number of previous PCI as an independent risk factor for cardiac death.</p> <p>(Conclusions)</p> <p>Repeated PCI increased risk for long-term prognosis of subsequent CABG.</p

Thrombotic gene polymorphisms and postoperative outcome after coronary artery bypass graft surgery

<p>Abstract</p> <p>Background</p> <p>Emerging perioperative genomics may influence the direction of risk assessment and surgical strategies in cardiac surgery. The aim of this study was to investigate whether single nucleotide polymorphisms (SNP) affect the clinical presentation and predispose to increased risk for postoperative adverse events in patients undergoing coronary artery bypass grafting surgery (CABG).</p> <p>Methods</p> <p>A total of 220 patients undergoing first-time CABG between January 2005 and May 2008 were screened for factor V gene G1691A (FVL), prothrombin/factor II G20210A (PT G20210A), angiotensin I-converting enzyme insertion/deletion (ACE-ins/del) polymorphisms by PCR and Real Time PCR. End points were defined as death, myocardial infarction, stroke, postoperative bleeding, respiratory and renal insufficiency and event-free survival. Patients were compared to assess for any independent association between genotypes for thrombosis and postoperative phenotypes.</p> <p>Results</p> <p>Among 220 patients, the prevalence of the heterozygous FVL mutation was 10.9% (n = 24), and 3.6% (n = 8) were heterozygous carriers of the PT G20210A mutation. Genotype distribution of ACE-ins/del was 16.6%, 51.9%, and 31.5% in genotypes I/I, I/D, and D/D, respectively. FVL and PT G20210A mutations were associated with higher prevalence of totally occluded coronary arteries (p < 0.001). Furthermore the risk of left ventricular aneurysm formation was significantly higher in FVL heterozygote group compared to FVL G1691G (<it>p </it>= 0.002). ACE D/D genotype was associated with hypertension (<it>p </it>= 0.004), peripheral vascular disease (p = 0.006), and previous myocardial infarction (<it>p </it>= 0.007).</p> <p>Conclusions</p> <p>FVL and PT G20210A genotypes had a higher prevalence of totally occluded vessels potentially as a result of atherothrombotic events. However, none of the genotypes investigated were independently associated with mortality.</p

Mechanisms of pulmonary dysfunction after on-pump and off-pump cardiac surgery: a prospective cohort study

BACKGROUND: Pulmonary dysfunction following cardiac surgery is believed to be caused, at least in part, by a lung vascular injury and/or atelectasis following cardiopulmonary bypass (CPB) perfusion and collapse of non-ventilated lungs. METHODS: To test this hypothesis, we studied the postoperative pulmonary leak index (PLI) for (67)Ga-transferrin and (transpulmonary) extravascular lung water (EVLW) in consecutive patients undergoing on-pump (n = 31) and off-pump (n = 8) cardiac surgery. We also studied transfusion history, radiographs, ventilatory and gas exchange variables. RESULTS: The postoperative PLI and EVLW were elevated above normal in 42 and 29% after on-pump surgery and 63 and 37% after off-pump surgery, respectively (ns). Transfusion of red blood cell (RBC) concentrates, PLI, EVLW, occurrence of atelectasis, ventilatory variables and duration of mechanical ventilation did not differ between groups, whereas patients with atelectasis had higher venous admixture and airway pressures than patients without atelectasis (P = 0.037 and 0.049). The PLI related to number of RBC concentrates infused (P = 0.025). CONCLUSION: The lung vascular injury in about half of patients after cardiac surgery is not caused by CPB perfusion but by trauma necessitating RBC transfusion, so that off-pump surgery may not afford a benefit in this respect. However, atelectasis rather than lung vascular injury is a major determinant of postoperative pulmonary dysfunction, irrespective of CPB perfusion

Strategies to prevent intraoperative lung injury during cardiopulmonary bypass

During open heart surgery the influence of a series of factors such as cardiopulmonary bypass (CPB), hypothermia, operation and anaesthesia, as well as medication and transfusion can cause a diffuse trauma in the lungs. This injury leads mostly to a postoperative interstitial pulmonary oedema and abnormal gas exchange. Substantial improvements in all of the above mentioned factors may lead to a better lung function postoperatively. By avoiding CPB, reducing its time, or by minimizing the extracorporeal surface area with the use of miniaturized circuits of CPB, beneficial effects on lung function are reported. In addition, replacement of circuit surface with biocompatible surfaces like heparin-coated, and material-independent sources of blood activation, a better postoperative lung function is observed. Meticulous myocardial protection by using hypothermia and cardioplegia methods during ischemia and reperfusion remain one of the cornerstones of postoperative lung function. The partial restoration of pulmonary artery perfusion during CPB possibly contributes to prevent pulmonary ischemia and lung dysfunction. Using medication such as corticosteroids and aprotinin, which protect the lungs during CPB, and leukocyte depletion filters for operations expected to exceed 90 minutes in CPB-time appear to be protective against the toxic impact of CPB in the lungs. The newer methods of ultrafiltration used to scavenge pro-inflammatory factors seem to be protective for the lung function. In a similar way, reducing the use of cardiotomy suction device, as well as the contact-time between free blood and pericardium, it is expected that the postoperative lung function will be improved