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At least 19 recordsLinked to original sources
PubMed1997

Predictors of early and overall outcome in coronary artery bypass without cardiopulmonary bypass.

OBJECTIVE: Cardiopulmonary bypass in coronary artery bypass graft operations may adversely affect the outcome especially in high-risk patients. The purpose of this study is to evaluate results of coronary artery bypass performed without cardiopulmonary bypass, in a relatively high-risk cohort, and to identify predictors of unfavorable outcome. METHOD: Three hundred and thirteen (313) patients, 246 (79%) of whom had high-risk conditions, who have a coronary anatomy suitable for coronary artery bypass surgery without cardiopulmonary bypass, underwent this procedure between December 1991 and July 1995. Mean number of grafts/patient was 1.8 (1-5), and only 71 patients (23%) received a graft to the circumflex coronary system. RESULTS: Early unfavorable outcome events included operative mortality (12 patients, 3.8%), nonfatal perioperative myocardial infarction (eight patients, 2.6%), emergency reoperation (three patients, 0.9%), sternal infection (five patients, 1.6%), and nonfatal stroke (two patients, 0.6%). Multivariate analysis revealed angina pectoris class IV (odds ratio 5.4) and age > or = 70 years (odds ratio 5.0) as independent predictors of early mortality. Preoperative risk factors such as repeat coronary artery bypass grafting (50 patients, 16%), ejection fraction < or = 0.35 (85 patients, 27%), acute myocardial infarction (86 patients, 28%), cardiogenic shock (ten patients, 3.2%), chronic renal failure (25 patients, 8%), chronic obstructive pulmonary disease (20 patients, 6%), and peripheral vascular disease (51 patients, 16%) did not increase early mortality. During 33 months of follow-up (range 1-57 months), there were 42 deaths, at least 16 cardiac-related (one and four years actuarial survival of 90% and 76% respectively), and 39 patients (12.5%) in whom angina returned. Calcified aorta (odds ratio 2.6) and old myocardial infarction (odds ratio 1.8) were independent predictors of overall unfavorable events. CONCLUSIONS: Coronary artery bypass grafting without cardiopulmonary bypass can be performed with relatively low operative mortality in certain high-risk subgroups of patients; however, an increased risk of graft occlusion is a potential disadvantage. This procedure should therefore be considered only for patients with suitable coronary anatomy, in whom cardiopulmonary bypass poses a high risk. Although the risk of stroke is relatively low, the procedure is still hazardous for patients aged 70 years and over.

Adult↗
PubMed1995

P-selectin expression in myocardium of children undergoing cardiopulmonary bypass.

Cardiopulmonary bypass is a planned support technique that results in a period of myocardial ischemia and reperfusion. In addition, it is associated with an inflammatory response likely involving endothelial cell activation. In previous studies, we showed that E-selectin and intercellular adhesion molecule-1 (ICAM-1) messenger ribonucleic acid (mRNA) are increased in human myocardium after cardiopulmonary bypass. We have now examined the expression of P-selectin mRNA by ribonuclease protection in paired atrial biopsy specimens from 12 patients before and after cardiopulmonary bypass. By means of immunocytochemistry, we have also examined the endothelial cell surface expression of P-selectin protein, as well as that of E-selectin and ICAM-1 in three additional patients. Patient ages ranged from 1 day to 8.5 years (median 12 months), and cardiopulmonary bypass times ranged from 46 to 196 minutes (median 144 minutes). By ribonuclease protection, there was marked variability in the expression of P-selectin in biopsy specimens before bypass. However, when compared with prebypass levels, P-selectin mRNA decreased modestly in 10 of 12 patients after bypass (median decrease 1.5-fold, p = 0.016). As seen with immunocytochemistry, P-selectin protein was distributed diffusely through the vascular bed on large vessels and small vessels before bypass but was virtually absent on capillaries in specimens taken after bypass. E-selectin, which was absent in prebypass biopsy specimens, was induced in one of the three specimens after bypass, but no change in ICAM-1 protein expression above baseline was noted. We also find that cultured human endothelial cells treated with tumor necrosis factor-alpha in doses which induce ICAM-1 mRNA simultaneously decrease their expression of P-selectin mRNA as compared with untreated cells. These observations suggest that endothelial P-selectin is transcriptionally downregulated after cardiopulmonary bypass at times when E-selectin and ICAM-1 are induced. Furthermore, we find that E-selectin and ICAM-1 are expressed at times and at sites where P-selectin is absent. Although it is possible that P-selectin may have been induced and lost at early times before reperfusion, these data suggest that endothelial P-selectin plays a limited role in the inflammatory response that ensues after cardiopulmonary bypass.

Adolescent↗
PubMed1994

Platelet-leukocyte activation and modulation of adhesion receptors in pediatric patients with congenital heart disease undergoing cardiopulmonary bypass.

Cardiopulmonary bypass has been shown in adults to activate platelets and leukocytes, lead to the formation of circulating platelet-leukocyte conjugates, and alter adhesive receptors on both cell types. Pediatric patients with congenital heart disease undergoing cardiopulmonary bypass, however, have not been extensively studied and may represent a group at particular clinical risk for bleeding and pulmonary dysfunction. We studied 13 patients with congenital heart disease undergoing operations necessitating bypass, 7 with cyanotic and 6 with noncyanotic congenital heart disease. We determined that (1) the surface density of platelet glycoprotein Ib was significantly lower at baseline and throughout bypass in patients with cyanotic heart disease than in noncyanotic patients; (2) platelet glycoprotein Ib in both cyanotic and noncyanotic congenital heart disease decreased significantly during bypass, with a nadir of 75% of baseline values; (3) platelets were activated to a high degree, comparable with that seen in adults; (4) mean circulating monocyte-platelet conjugates rose significantly during bypass, increasing from 36% to 66% by the end of bypass, whereas neutrophil-platelet conjugates and lymphocyte-platelet conjugates declined; and (5) both monocytes and neutrophils were activated by cardiopulmonary bypass, as assessed by increased surface expression of CD11b and, in the case of monocytes, CD11b expression continued to increase even after termination of bypass. Patients with cyanotic and noncyanotic heart disease did not differ with respect to platelet or leukocyte activation or the formation of platelet-leukocyte conjugates. We conclude that in children with congenital heart disease cardiopulmonary bypass causes loss of platelet adhesion receptors, activation of platelets, formation of platelet-leukocyte conjugates, and leukocyte activation. Cyanotic and noncyanotic patients are qualitatively similarly affected; however, cyanotic patients demonstrate a baseline deficit in the platelet adhesion receptor glycoprotein Ib. These cellular changes may contribute to both the hemostatic and inflammatory complications associated with cardiopulmonary bypass.

Blood Platelets↗
PubMed1993

Heparin-coated circuits reduce the inflammatory response to cardiopulmonary bypass.

Cardiopulmonary bypass generates a systemic inflammatory response including the activation of the complement cascade and leukocytes contributing to postoperative morbidity. To evaluate whether the use of heparin-coated extracorporeal circuits could reduce these activation processes, we performed a study on 30 patients undergoing coronary artery bypass grafting who were randomly perfused with a heparin-coated circuit (Duraflo II, n = 15) or with a similar noncoated circuit (control, n = 15). Standardized systemic heparinization was applied for every patient before cardiopulmonary bypass. The use of heparin-coated circuits resulted in a reduction of systemic leukocyte activation during cardiopulmonary bypass reflected by reduced elastase release (p < 0.05) and tumor necrosis factor generation (p < 0.05) manifest after release of the aortic cross-clamp. In addition, blood samples taken from both the right and left atria after reperfusion revealed that the elastase release from the pulmonary microcirculation was absent in the Duraflo II group in contrast to the control group (p < 0.05). The pattern of complement activation, likely initiating this inflammatory reaction, was modified by heparin coating in two different aspects. There was a significant reduction of C3a generation after protamine administration in patients perfused with heparin-coated circuits, and there was a decrease of complement hemolytic capacity in pooled human serum incubated with heparin-coated tubing. These observations suggest that heparin coating might bind some of the complement components from the classic pathway, thereby reducing the inflammatory response to cardiopulmonary bypass.

Aged↗
PubMed1999

Lung injury and acute respiratory distress syndrome after cardiopulmonary bypass.

Cardiopulmonary bypass is often followed by pulmonary dysfunction as assessed by measuring the alveolar-arterial oxygenation gradient, intrapulmonary shunt, degree of pulmonary edema, pulmonary compliance, and pulmonary vascular resistance. It is also regarded as a risk factor for development of acute respiratory distress syndrome. On the other hand, cardiopulmonary bypass is associated with a whole body inflammatory response, which involves activation of complement, leukocytes, and endothelial cells with secretion of cytokines, proteases, arachidonic acid metabolites, and oxygen free radicals. Leukocyte adhesion to microvascular endothelium, leukocyte extravasation, and tissue damage are the final steps. Although the inflammatory response to cardiopulmonary bypass often remains at subclinical levels, it can also lead to major organ dysfunction and multiple organ failure. This review article summarizes the recent literature on the molecular and cellular mechanisms involved in the phenomenon of pulmonary dysfunction after cardiopulmonary bypass. It also summarizes reports on the prevalence and mortality of acute respiratory distress syndrome after cardiac surgery.

Cardiopulmonary Bypass↗
PubMed2004

Capillary leakage in cardiac surgery with cardiopulmonary bypass.

Cardiopulmonary bypass causes a systemic inflammatory response, which can lead to capillary leak syndrome. In 15 adults undergoing elective cardiac surgery with cardiopulmonary bypass, we determined the volume and peak time of capillary leakage from the measurements of extracellular fluid volume and circulating blood volume taken preoperatively, at various intervals up to 24 hours after surgery, and on the 7th postoperative day. Extracellular fluid volume rose from 15.5 +/- 2.7 L preoperatively to a peak 4 hours after surgery of 18.3 +/- 3.2 L and remained elevated at 24 hours. Circulating blood volume fell from 4.10 +/- 0.68 L preoperatively to 3.20 +/- 0.58 L at the end of surgery. Fluid administered intraoperatively did not raise the circulating blood volume. Intraoperative fluid balance was positive at 2.62 +/- 0.72 L but negative at all time points postoperatively. There was significant postoperative capillary leakage, increasing from 4.7% +/- 2.3% of body weight at the end of surgery to a peak 4 hours later of 5.4% +/- 2.0% and falling to 2.8% +/- 3.3% at 24 hours. This knowledge of the pattern of change in capillary leakage after cardiac surgery with cardiopulmonary bypass might serve as a valuable guide for postoperative management.

Adult↗
PubMed1992

Release of vasoactive substances during cardiopulmonary bypass.

Cardiopulmonary bypass is associated with bleeding and thrombotic complications, massive fluid shifts, and cellular and hormonal defense reactions that are collectively termed "the whole body inflammatory response." A host of vasoactive substances are produced, released or altered during cardiopulmonary bypass. These hormones, autacoids, and cytokines react with specific receptor proteins distributed throughout the body, and mediate the vascular smooth muscle and endothelial cell contractions that are responsible for much of the morbidity associated with open heart operations. This essay briefly reviews the actions, sources, and perturbations of the approximately 25 vasoactive substances known or believed to be altered by cardiopulmonary bypass, and provides an introductory reference list.

Cardiopulmonary Bypass↗
PubMed2002

Aprotinin: antifibrinolytic and anti-inflammatory mechanisms of action in cardiac surgery with cardiopulmonary bypass.

Cardiopulmonary bypass results in activation of the coagulation, fibrinolytic, inflammatory, and complement cascades. These activated cascades result in a decrease in the number of circulating coagulation factors, hyperfibrinolysis, thrombocytopenia, platelet defects, coagulopathies, and an acute inflammatory response. Patients experiencing cardiac surgery with cardiopulmonary bypass are at risk for many potential problems. The use of aprotinin, an antifibrinolytic agent, has multiple effects that tend to reduce hematological defects and blunts the inflammatory response that is associated with cardiac surgery. The pathophysiological consequences of cellular activation associated with cardiopulmonary bypass, basic mechanisms of action of aprotinin, pharmacodynamic and pharmacokinetic properties, dosing, adverse reactions, and cost/benefit ratio are discussed in this article. Critical care nurses need to know about aprotinin to understand its role in reducing blood loss and transfusions during and after cardiac surgery.

Aprotinin↗
PubMed2001

Aprotinin and the systemic inflammatory response after cardiopulmonary bypass.

Cardiopulmonary bypass is associated with a systemic inflammatory response, a spectrum of pathophysiologic changes ranging from mild organ dysfunction to multisystem organ failure. Complications include coagulation disorders (bleeding diathesis, hyperfibrinolysis) from platelet defects and plasmin activation, as well as pulmonary dysfunction from neutrophil sequestration and degranulation. Diverse injuries are a consequence of multiple inflammatory mediators (complement, kinins, kallikrein, cytokines). Both plasmin and kallikrein amplify the inflammatory response by activating components of the contact activation system. The full-Hammersmith (high dose) of aprotinin, a serine protease inhibitor approved for reducing blood loss and transfusion requirements in cardiopulmonary bypass, inhibits kallikrein and plasmin, resulting in suppression of multiple systems involved in the inflammatory response. Specifically, inhibition of factor XII, bradykinin, C5a, neutrophil integrin expression, elastase activity, and airway nitric oxide production are observed. Clinical correlates include reduced capillary leak, preserved systemic vascular resistance and blood pressure, and improved myocardial recovery following ischemia. Overall, evidence indicates that aprotinin attenuates the systemic inflammatory response associated with cardiopulmonary bypass.

Animals↗
PubMed1997

Reoperative coronary artery bypass without cardiopulmonary bypass.

BACKGROUND: Conventional reoperative coronary artery bypass grafting using cardiopulmonary bypass carries relatively high mortality and morbidity. METHODS: Seventy-seven patients underwent coronary artery bypass grafting without cardiopulmonary bypass in two centers between 1988 and 1994. Mean age was 65 +/- 8 years (mean +/- SD). Twenty-three (30%) were operated on urgently and 7 (9%) emergently. Nine (12%) were referred for operation up to 2 weeks after acute myocardial infarction. Fifteen patients (19%) had an ejection fraction less than or equal to 0.35. The mean number of grafts per patient was 1.7 (range, 1 to 3), and the internal mammary artery was used in 66 patients (86%). Only 18 patients (23%) received at least one graft to the circumflex artery. Hospital stay was 7.4 +/- 6.5 days. RESULTS: Early events included operative death in 4 patients (5.2%), nonfatal myocardial infarction in 3 (3.9%), sternal infection in 2 (2.6%), and stroke in 0 (0%). Follow-up (30 +/- 15 months) showed 11 deaths (5 cardiac, 6 noncardiac), 2 (2.8%) nonfatal myocardial infarctions, and return of angina in 9 patients (12.8%). One- and 4-year actuarial survival rates were 90% and 69%, respectively. CONCLUSIONS: Reoperative coronary artery bypass grafting without cardiopulmonary bypass has acceptable early and midterm outcome, and should be considered a viable alternative for properly selected patients.

Aged↗
PubMed1979

Effects of phenylephrine on transmural distribution of myocardial blood flow in regions supplied by normal and collateral arteries during cardiopulmonary bypass.

Cardiopulmonary bypass is frequently accompanied by decreased peripheral vascular resistance with resultant hypotension that is unresponsive to increased flow rates. Alpha adrenergic agonists are routinely used to increase peripheral vascular resistance and augment blood pressure. In this study, the effects of the alpha adrenergic stimulant phenylephrine on blood flow distribution during cardiopulmonary bypass in myocardium supplied by normal and collateral arteries were studied in eight mongrel dogs. Microsphere determinations of blood flow were made following augmentation of perfusion pressure with phenylephrine and were compared with intraoperative normotensive and hypotensive control levels. With systemic flow rates held constant, phenylephrine was infused in doses adequate to raise perfusion pressure to normotensive levels following hypotension. In the normal region (NR), blood flow was returned to normotensive control levels with flow favoring the subendocardium. In the region supplied by collateral vessels (CR), however, phenylephrine infusion failed to return flow to the normotensive control level in the subendocardial layer, and the flow imbalance present during hypotension was not corrected. An analogue model of the calculable resistances in the CR is presented, which indicates that phenylephrine increased resistance in the collateral vessels. Associated with this inflow restriction is decreased resistance or vasodilatation of the intramyocardial vessels supplied by collateral coronary arteries.

Animals↗
PubMed2001

Evidence of increased matrix metalloproteinase-9 concentration in patients following cardiopulmonary bypass.

Cardiopulmonary bypass (CPB) is associated with a systemic inflammatory response, which can result in acute lung injury known as "postperfusion syndrome." Neutrophil activation with concomitant serine protease release has been implicated in the pathogenesis of "postperfusion syndrome." Increased plasma levels of neutrophil elastase (NE) have been demonstrated in patients undergoing CPB, and it is well documented that both NE and matrix metalloproteinase-9 (MMP-9) have a synergistic role in pulmonary injury. We, therefore, hypothesized that plasma levels of MMP-9 would be elevated in patients after CPB. Human plasma was obtained after informed consent from eight patients undergoing CPB. Plasma was collected at the start of CPB, 5 minutes after the initiation of CPB, and at the termination of CPB (156 +/- 17 min). All samples were analyzed by both standard enzyme-linked immunosorbent assay (ELISA) and gelatin zymography for MMP-9 (free and total enzyme) concentration. Data were expressed as means +/-SE and assessed by analysis of variance (ANOVA). Plasma MMP-9 concentration was significantly increased at the end of CPB (191 +/- 30.4 ng/mL; p <.05) as compared to both the start of CPB (28.3 +/- 13.2 ng/mL) and 5 minutes after the initiation of CPB (44.3 +/- 15.4 ng/mL). Patients undergoing CPB show an increase in serum MMP-9 levels. Prior studies utilizing an animal model of "postperfusion syndrome" have shown that inhibition of MMP-9 and NE prevented pulmonary injury following CPB. The results of the current study suggest that such an approach may also have merit in the clinical setting of cardiopulmonary bypass.

Adult↗
PubMed2003

Strategic leukocyte depletion reduces pulmonary microvascular pressure and improves pulmonary status post-cardiopulmonary bypass.

Cardiopulmonary bypass (CPB) precipitates inflammation that causes marked pulmonary dysfunction. Leukocyte filtration has been proposed to reduce these deleterious effects. Other studies show an improvement with aprotinin. We proposed that a combination of these two therapies would synergistically improve pulmonary outcomes. Two hundred and twenty-five patients participated in a randomized prospective study comparing pulmonary microvascular function and pulmonary shunt fraction postcoronary artery bypass grafting (CABG). The study group underwent leukocyte depletion with aprotinin during the procedure. Pulmonary microvascular function was assessed by pulmonary microvascular pressure (PMVP), a measure of pulmonary capillary edema, and pulmonary function was evaluated by comparing pulmonary shunt fractions. Elevated PMVP and increased pulmonary shunting compromise pulmonary performance. The leukocyte-depleted group had significantly reduced PMVP and pulmonary shunt fraction for at least the first 24 hours postbypass. The combination of strategic leukocyte filtration and aprotinin therapy can effectively reduce postoperative decline in pulmonary function. Cardiopulmonary bypass precipitates a variety of inflammatory effects that can cause marked pulmonary dysfunction to the point of respiratory failure, necessitating prolonged mechanical ventilation. Leukocyte filtration has been investigated previously and appears to be beneficial in improving pulmonary outcome by preventing direct neutrophil-induced inflammatory injury. Recent studies of leukocyte reduction profiles suggest that leukoreduction via leukofiltration is short lived with filter saturation occurring 30-45 minutes after onset of filtration. This phenomenon may explain the limited utility observed with higher risk patients. These patients typically require longer pump runs, so leukocyte reduction capability is suboptimal at the time of pulmonary vascular reperfusion. To more effectively protect the lung from reperfusion injury, leukocyte filtration can be delayed so that reduction of activated neutrophils is maximal at the time of pulmonary vascular reperfusion. It is, thus, conceivable that a timely use of arterial line leukoreducing filters may improve, more substantially, pulmonary function postbypass. Two hundred and twenty-five isolated coronary revascularization patients participated in this prospective, randomized trial. The patients received moderately hypothermic CBP alone (control group: n = 110) or combined with leukocyte depletion, initiated 30 minutes before crossclamp release, with filters placed in the bypass circuit (study group: n = 115). All patients also received full Hammersmith aprotinin dosing during the operation. Pulmonary microvascular pressures were lower in the study group at three hours postbypass, and continued to fall until 24 hours postbypass. In contrast, the control group measured a rise in PMVP and a continued plateau throughout 24 hours postbypass (p < 0.028). The calculated pulmonary shunt fraction also was reduced significantly throughout the study interval, with the greatest reduction occurring approximately three to six hours post-CPB (p < 0.002). Shunt fractions eventually converged at 24 hours postbypass. Outcome measures included hospital charges and length of stay, which were also markedly reduced in the treatment group. Increasing PMVPs are a direct reflection of pulmonary capillary edema, which, in conjunction with increased pulmonary shunt ratio, lead to an overall worsening of pulmonary function. Intraoperative strategic leukocyte filtration combined with aprotinin treatment improves post-CPB lung performance by reducing significantly the reperfusion inflammatory response and its sequelae. These benefits are manifested by reductions in ventilator times, hospital stay and patient morbidity.

Aged↗
PubMed1995

Coronary artery bypass without cardiopulmonary bypass: analysis of short-term and mid-term outcome in 220 patients.

Two hundred twenty patients, preferentially those with high-risk conditions, underwent coronary artery bypass grafting without cardiopulmonary bypass. Early unfavorable outcome events included operative mortality (7 patients, 3.2%), nonfatal perioperative myocardial infarction (6 patients, 2.7%), cerebrovascular accident (1 patient, 0.4%), and sternal infection (3 patients, 1.4%). There were two deaths (13%) among 15 patients with calcified aorta and four (12%) in 33 patients who underwent emergency operation. Multivariate analysis revealed these two risk factors to be the only predictors of early mortality (odds ratios, 8.0 and 9.8, respectively). Preoperative risk factors such as left ventricular dysfunction (ejection fraction < or = 35%) (40 patients, 18%), congestive heart failure (46 patients, 21%), acute myocardial infarction (59 patients, 27%), cardiogenic shock (7 patients, 3%), age 70 years or older (59 patients, 27%), renal failure (19 patients, 9%), and cerebrovascular accident and carotid disease (11 patients, 5%) were not found to be major predictors of early mortality or unfavorable outcome. During 12 months of follow-up (range 1 to 21 months), there were four cardiac and three noncardiac deaths (1-year actuarial survival 93%) and 17 cases (7.7%) of early return of angina. Calcified aorta, nonuse of the internal mammary artery, reoperation, and diabetes mellitus were independent predictors of unfavorable events. We conclude that coronary artery bypass grafting without cardiopulmonary bypass can be done with relatively low operative mortality, although there seems to be an increased risk for early return of angina. This procedure should therefore be considered for patients with appropriate coronary anatomy, in whom cardiopulmonary bypass poses a high risk. This procedure is still hazardous with calcified aorta or emergency operation.

Adult↗
PubMedDate not supplied

Cardiac pathology following resuscitative circulatory support. Direct mechanical ventricular actuation versus cardiopulmonary bypass.

Cardiopulmonary bypass (CPB) is currently advocated for treating refractory cardiac arrest. Direct Mechanical Ventricular Actuation (DMVA) is an alternative method that does not contact the blood and has other unique advantages for providing resuscitative circulatory support, including rapid application and relative technical simplicity. The purpose of this study was to assess pathologic changes in the heart following resuscitation with either CPB or DMVA. Dogs (n = 22) received 1 hr of CPB (n = 11) or DMVA (n = 11) following a 12.5 min cardiac arrest. All deaths [4/11 (CPB) vs. 2/11 (DMVA), p = 0.31] occurred during the initial 24 postoperative hours. At 7 days, survivors had magnetic resonance imaging to determine cardiac ejection fraction [46% (CPB) vs. 51% (DMVA), p = 0.39], as well as the presence of cardiac wall motion abnormalities [50% (CPB) vs. 33% (DMVA), p = 0.57] and gross cardiac lesions [17% (CPB) vs. 17% (DMVA)]. The survivor's hearts were then extirpated, fixed, and examined for gross lesions [2/7 (CPB) vs. 0/9 (DMVA), p = 0.17]. Transmural sections of the anterior and posterior papillary muscles were histologically evaluated. The severity and extent of epicardial fibrosis and focal myocyte necrosis did not differ between groups. These data demonstrate that DMVA does not cause more myocardial trauma than CPB when used to provide resuscitative circulatory support. Therefore, the unique attributes of DMVA may improve resuscitation outcome in patients who suffer refractory cardiac arrest, without additional risk of cardiac injury.

Animals↗
PubMed1999

Coronary artery bypass without cardiopulmonary bypass for patients with acute myocardial infarction.

OBJECTIVE: Between January 1992 and December 1994, 57 patients having an acute myocardial infarction with coronary anatomy suitable for coronary artery bypass grafting without cardiopulmonary bypass underwent this procedure within 1 week of the infarction. We describe the surgical results of these high-risk patients. METHODS: The study population included 43 male patients (75%) and 14 female patients (25%) whose mean age was 58.5 +/- 10.4 years. Thirty-two patients (56%) underwent emergency bypass grafting within 48 hours of an acute myocardial infarction, 4 of them (12.5%) as a bailout procedure after complicated percutaneous transluminal coronary angioplasty. Of these 32 patients, 7 patients (22%) were in cardiogenic shock, and 10 patients (31%) required preoperative intra-aortic balloon pump. Twenty-five patients (44%) underwent coronary bypass grafting 2 to 7 days after an acute myocardial infarction. The mean number of grafts per patient was 1.8 (range, 1-4), and the internal thoracic artery was used in 47 patients (82%). Only 7 patients (12%) received grafts to a circumflex marginal branch. RESULTS: Operative mortality was 1.7% (1 patient), and the mean postoperative hospital stay was 6.8 +/- 3 days. One- and 5-year actuarial survivals were 94.7% and 82.3%, respectively. Angina returned in 7 patients (12%), 1 of whom underwent reoperation. Multivariate analysis revealed renal failure and preoperative cardiogenic shock to be independent predictors of overall mortality. Old myocardial infarction and operation within the first 48 hours were independent predictors of overall unfavorable outcome events. CONCLUSIONS: These results suggest that coronary artery bypass grafting without cardiopulmonary bypass is a relatively low-risk procedure for patients having an infarction with coronary anatomy suitable for this technique.

Actuarial Analysis↗
PubMed2005

A case of transient diabetes insipidus following cardiopulmonary bypass.

Cardiopulmonary bypass surgery has been linked with a number of postoperative complications. One of the frequently reported physiological alterations is the relative diuresis seen in the immediate post-op period. Rarely reported though is the development of full-blown diabetes insipidus in such patients. The etiology is unknown and has only been hypothesized in the past. We present the clinical course of a 54 year old male who developed transient diabetes insipidus post bypass surgery with subsequent recovery following exogenous vasopressin administration. The physiological alteration leading to the development of diabetes insipidus in a small fraction of bypass patients remains unknown. We propose that the variation in natriuretic peptide levels in the post-bypass period could account for the transient event.

Cardiopulmonary Bypass↗