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We have described a case in which closure of an aspergilloma cavity was done internally when it was determined that pulmonary resection was too hazardous. There was an intense inflammatory reaction surrounding the aorta and pulmonary artery. In the absence of gross purulence and underlying parenchymal infection, this technique may be used to avoid the prolonged hospitalization and bronchopleural fistulas associated with external drainage procedures.

Warm blood cardioplegia has emerged as a substitute for cold blood cardioplegia as a method of myocardial protection. However, the continuous infusion of blood in this technique may obscure the operative field and necessitate interruption of warm blood cardioplegia. This experimental study was therefore undertaken to determine whether interrupting warm blood cardioplegia during coronary revascularization would increase myocardial damage. In 30 adult pigs, the second and third diagonal vessels were occluded with snares for 90 minutes. All animals underwent cardiopulmonary bypass and 45 minutes of cardioplegic arrest. During the period of cardioplegic arrest, 10 pigs received intermittent antegrade/retrograde infusion of cold blood cardioplegic solution (4 degrees C) 10 pigs received continuous retrograde infusion of warm blood cardioplegic solution (37 degrees C) at 100 ml/min, and 10 pigs received retrograde infusion of warm blood cardioplegic solution that was interrupted for three 7-minute periods. After aortic unclamping, the coronary snares were released and all hearts were reperfused for 180 minutes. Interrupting retrograde warm blood cardioplegia resulted in more tissue acidosis during cardioplegic arrest (6.20 +/- 0.16 interrupted retrograde warm blood cardioplegia and 6.45 +/- 0.12 continuous retrograde warm blood cardioplegia, both p < 0.05 compared with 6.98 +/- 0.17 intermittent antegrade and retrograde cold blood cardioplegia), decreased echocardiographic wall-motion scores (4 [normal] to -1 [dyskinesis]; 2.06 +/- 0.30 interrupted retrograde warm blood cardioplegia, p < 0.05 compared with 3.30 +/- 0.40 intermittent antegrade and retrograde cold blood cardioplegia, 2.80 +/- 0.40 continuous retrograde warm blood cardioplegia), and increased tissue necrosis as measured by the area of necrosis/area at risk (38% +/- 5% interrupted retrograde warm blood cardioplegia, p < 0.05 compared with 21% +/- 2% intermittent antegrade and retrograde cold blood cardioplegia; 25% +/- 2% continuous retrograde warm blood cardioplegia). We concluded that interrupting warm blood cardioplegia during coronary revascularization diminishes the effectiveness of warm blood cardioplegia and results in increased ischemic damage.

This experimental study sought to compare the effectiveness of warm blood cardioplegia versus cold blood cardioplegia in protecting areas of ischemic myocardium during urgent coronary revascularization. In 40 adult pigs, the second and third diagonal vessels were occluded with snares for 90 minutes. All animals were then placed on cardiopulmonary bypass and underwent 45 minutes of cardioplegic arrest followed by 3 hours of reperfusion during which time the coronary snares were released. During the period of cardioplegic arrest, 10 pigs received antegrade continuous warm blood cardioplegic solution (37° C) at 100 ml/min; 10 animals received retrograde warm blood cardioplegic solution at 100 ml/min; 10 received intermittent, antegrade cold blood cardioplegic solution (4° C), and 10 animals received intermittent, antegrade/retrograde cold blood cardioplegic solution. Hearts protected with antegrade warm blood cardioplegic solution had the lowest pH values in the area at risk (6.59 ± 0.10 antegrade warm blood cardioplegia versus 6.80 ± 0.10 retrograde warm blood cardioplegia versus 6.72 ± 0.18 antegrade cold blood cardioplegia versus 6.85 ± 0.15 antegrade/retrograde cold blood cardioplegia and the highest area of necrosis (42 % ± 3 % antegrade warm blood cardioplegia versus 26% ± 2% [p

As more high-risk patients undergo percutaneous transluminal coronary angioplasty (PTCA), the changing profiles of PTCA patients who may require emergent coronary artery bypass grafting may alter operative morbidity and mortality. This study compared profiles of recent patients undergoing emergent coronary artery bypass grafting after a failed PTCA with earlier patients to determine their impact on operative results. From 1980 to 1988, 53 patients underwent emergent coronary artery bypass grafting after a failed PTCA at the Boston University Medical Center. These patients were divided into two groups based on the year of the PTCA: group I, 1980 to 1985 (n = 18); and group II, 1986 to 1988 (n = 35). Group II patients tended to be older (age greater than or equal to 65 years, 47% group II versus 11% group I), were more likely to have unstable angina before PTCA (74% versus 33%), and had lower ejection fractions (0.53 +/- 0.02 versus 0.63 +/- 0.05) and more vessels with 50% or greater stenosis (2.1 +/- 0.2 versus 1.6 +/- 0.2). Nevertheless, there was no significant difference in the incidence of perioperative myocardial infarcts using enzyme and electrocardiographic criteria (37% in group II versus 39% in group I), 30-day operative mortality (11% in group II versus 11% in group I), or major postoperative complications (14% in group II versus 22% in group I). We conclude that despite the changing profiles of patients undergoing PTCA, which include older patients with more extensive coronary artery disease and lower ejection fractions, operative results after emergent coronary artery bypass grafting for failed PTCAs remain unchanged.

We report the case of a patient who presented with sudden onset of paraplegia following an acute ascending aortic dissection extending to the arch, descending, and abdominal aorta. The paraplegia was fully reversed following an emergent replacement of the ascending aorta and hemi-arch repair.(J Card Surg 2010;25:65-66)

Because antegrade cardioplegia may limit the distribution of cardioplegia beyond a coronary occlusion, this study was undertaken to determine whether retrograde coronary sinus cardioplegia provides superior myocardial protection during revascularization of an acute coronary occlusion. In 20 adult pigs, the second and third diagonal branches were occluded with a snare for 1 1/2 hours. Animals were then placed on cardiopulmonary bypass and underwent 30 minutes of ischemic arrest with multidose, potassium, crystalloid cardioplegia. In 10 animals, the cardioplegia was given antegrade through the aortic root, whereas in 10 others, it was given retrograde through the coronary sinus. After the arrest period, the coronary snares were released and all hearts were reperfused for 3 hours. Postischemic damage in the myocardium beyond the occlusions was assessed by wall motion scores using two-dimensional echocardiography (4 = normal to -1 = dyskinesia), the change in myocardial pH from preischemia, and the area of necrosis/area of risk (histochemical staining). Hearts protected with retrograde coronary sinus cardioplegia had less tissue acidosis (change in pH = 0.08 +/- 0.03 versus 0.41 +/- 0.13; p less than 0.05), higher wall motion scores (2.0 +/- 0.6 versus 1.3 +/- 0.3; not significant), and less myocardial necrosis (43.4% +/- 3.6% versus 73.3% +/- 3.5%; p less than 0.0001). We conclude that retrograde coronary sinus cardioplegia provides more optimal myocardial protection than is possible with antegrade cardioplegia after revascularization of an acute coronary occlusion.

Nesiritide, a recombinant human B-type natriuretic peptide, has been used in conjunction with inotropic agents in the postoperative management of low cardiac output and pulmonary hypertension. However, its effects on intraoperative myocardial protection are unknown. This study was therefore undertaken to determine whether Nesiritide could enhance myocardial protection when given intraoperatively in a porcine model simulating urgent CABG surgery. Twenty pigs underwent occlusion of the second and third diagonal coronary arteries using snares for 90 minutes followed by 45 minutes of antegrade, cold blood cardioplegic arrest and 180 minutes of reperfusion on cardiopulmonary bypass(CPB) during which time the snares were released. Ten animals received an IV bolus of Nesiritide(2ug/kg) at the initiation of coronary occlusion followed by a 0.01ug/kg/min IV infusion during coronary occlusion, cardioplegic arrest, and reperfusion on CPB. Ten other animals underwent the same protocal without Nesiritide(placebo). Infarct size was assessed by the area of necrosis/area of risk(AN/AR) using histochemical staining, endothelial function by the % change in coronary vasodilation using ring chamber methodology, and lung edema using % change in wet/dry weights. The data is expressed as the mean+/− standard deviation. Nesiritide treated hearts had significantly decreased infarct size, better preservation of endothelial function, and less lung edema. In a porcine model of acute coronary occlusion simulating urgent CABG surgery, the intraoperative infusion of Nesiritide limited myocardial damage. These data suggest that IV Nesiritide infusions may afford increased myocardial protection when administered intraoperatively during the revascularization of acutely ischemic myocardium. RESULTS

Maintaining glycemic control(120 –180mg/dl)with GIK solutions in patients with diabetes undergoing CABG decreases perioperative morbidity and enhances long-term survival. The mechanism by which GIK exerts its protective effects is unknown. This study was undertaken to determine whether it is substrate enhancement with glucose, glycemic control with insulin, or the combination of glucose + insulin + potassium which contributes to improved outcomes with GIK in CABG patients with diabetes. One hundred-twenty diabetic patients undergoing isolated CABG surgery were prospectively randomized to achieve glycemic control(120 –180mg/dl)using an INSULIN infusion(100units/100mlNS),LOW GIK(500mlD5W + 80units insulin + 40mEqKCL), and HIGH GIK(D20W + 200units insulin + 80mEqKCL) beginning on anesthetic induction and continuing for 18 hours after surgery. Variables assessed included Major Adverse Events(MAE=death, MI, CVA, atrial fibrillation, infection, ventilation > 24 hours, inotropic usage > 24hours,lenght of stay > 7days), serum glucose, the amount of insulin infused, and serum free fatty acids(ffa).Values are mean+/− standard deviation. HIGH GIK delivered more insulin and resulted in significantly lower levels of glucose and ffa. However, it had no effect on the incidence of MAEs compared to INSULIN infusions without glucose and potassium. Insulin, rather than substrate enhancement with glucose and potassium, is the key element in GIK used in CABG patients with diabetes. Augmenting insulin delivery results in lower levels of glucose and ffa, but has no effect on clinical outcomes as long as gylcemic control(120 –180mg/dl) is achieved. This research has received full or partial funding support from the American Heart Association, AHA National Center. RESULTS

Background And Aims: New techniques for skin closure that minimize tissue inflammation and avoid foreign material may decrease morbidity following saphenous vein harvesting. The 3M™ Steri-Strip™ S surgical skin closure system is a new, noninvasive method of wound closure, which consists of polymeric components coated with a pressure-sensitive skin adhesive. This prospective, randomized study was undertaken to compare the results of the noninvasive skin closure method to the traditional subcuticular skin closure technique on saphenous vein harvest sites. Methods: Twenty-six patients undergoing coronary artery bypass surgery with saphenous vein harvesting were prospectively randomized to skin closure using 3M Steri-Strip S Surgical Skin Closure System or subcuticular suture closure with a skin sealant. Wounds were evaluated on postoperative days 7 and 2l for erythema, edema, pain, cosmesis, and the time taken to close the incision. Results: Skin closure with 3M Steri-Strip S was significantly faster, resulted in significantly less erythema, edema, and significantly improved cosmesis. Conclusions: 3M Steri-Strip S Skin Closure improves wound healing of saphenous vein sites, compared to traditional subcuticular skin closure techniques.

Background— TP10, a potent inhibitor of complement activation during cardiopulmonary bypass (CPB) has been shown to significantly reduce the incidence of death and myocardial infarction (MI) in high-risk male patients undergoing cardiac surgery. However, the effect of TP10 in females was undefined because of the limited number of females studied. To examine the possibility of a gender effect, this phase 2 multi-center trial was undertaken to determine whether TP10 would also limit ischemic damage in a larger sample size of high-risk females undergoing cardiac surgery on cardiopulmonary bypass (CPB). Methods and Results— This prospective, double-blind, placebo-controlled, multi-center trial involved 297 high-risk (urgent surgery, CABG + Valve, reoperations, ejection fraction P =0.0001; SC5b-9 (ng/mL) 917±1067 placebo versus 204±79 TP10; P =0.0001), there was no difference in the primary end point between the groups (17% placebo versus 21% TP10; P =0.2550). Conclusions— The benefits of TP10 appear to be gender-related. and mechanisms other than complement activation may be responsible for myocardial injury in high-risk female patients during cardiac surgery on CPB.

Background and Aim: Cardioprotective strategies implemented to prevent ischemic events in patients at risk for cardiovascular disease have decreased morbidity and prolonged survival. In this review, we have used evidence-based medicine and number-needed-to-treat (NNT) analyses to determine which interventions are most beneficial in minimizing ischemic events and prolonging survival following coronary artery bypass graft (CABG) surgery. Methods: Therapeutic interventions available to minimize ischemic events in the post-CABG patient were analyzed using ACC/AHA Classifications and Level of Evidence Criteria. Based on these recommendations, NNT analyses were performed to determine the effectiveness of each intervention compared to the number of patients needed to be treated before a benefit was apparent. Results: The most beneficial intervention to improve mortality following CABG was the use of high tissue angiotensin-converting enzyme inhibitors, followed by statins and smoking cessation. Conclusions: NNT analyses and evidence-based medicine recommendations provide surgeons with cardioprotective strategies to improve long-term outcomes following CABG surgery.

The leading causes of accidental hypothermia in urban medical centers in the United States are exposure due to alcoholism, drug addiction, or mental illness and accidents involving immersion in col...

Angiotensin-converting enzyme inhibitors have been shown to prolong survival and decrease infarct size in patients after acute coronary syndromes. Now there is evidence to suggest that angiotensin-converting enzyme inhibition is beneficial in coronary artery bypass patients. This review will summarize the beneficial effects of angiotensin-converting enzyme inhibition in patients with ischemic heart disease and provide evidence to show that the routine use of angiotensin-converting enzyme inhibition in coronary artery bypass patients can improve clinical outcomes.

Several of the manufacturers of cardiopulmonary bypass equipment have recently introduced new miniature cardiopulmonary bypass systems. New advancements in cardiopulmonary bypass technology are almost always of interest to the perfusion community. However, the question arises, what advantages do these systems offer over our present technology? The manufacturers claim that these new systems will add to our perfusion armamentarium by offering us an opportunity to further reduce priming volume and the surface area to which the blood is exposed. Our group, in the Department of Cardiac Surgery at Boston Medical Center has been involved in the development of a comprehensive blood conservation strategy since 1994. Our published data clearly demonstrates improved clinical outcomes using coated circuit technology as part of a comprehensive blood conservation strategy. In an effort to clearly evaluate this new technology, in this article we review our current technique at Boston Medical Center.

Larry R. Kaiser, Sunil Singhal 366 pp. Philadelphia, Pa: Elsevier Mosby; 2004. $79.00. ISBN 0-8151-2613-1 Kaiser and Singhal have chosen not to write an authoritative reference on the practice of thoracic surgery, but instead have produced an easily readable text that would be useful to readers such as medical students and surgical residents who wish to acquire the basic fundamentals of the practice of thoracic surgery. The beginning of each chapter contains a list of key topics that focus on the most important areas to be covered in that chapter. Key references are provided at the end of each chapter to supplement the information provided in the text. The first 2 chapters provide an excellent review of thoracic anatomy …

BACKGROUND: Off-pump coronary revascularization (OPCAB) has been shown to reduce markers of acute inflammation but its effect on coronary endothelial function is unknown. This experimental study sought to determine whether OPCAB reduces endothelial dysfunction, compared to standard cardiopulmonary bypass (CPB) with and without the anticomplement agent soluble complement receptor-1 (sCR(1)). METHODS: In 10 pigs, OPCAB was simulated by snaring the left anterior descending (LAD) artery for 15 minutes followed by 3 hours of reperfusion. On-pump revascularization was simulated in 20 pigs by 15 minutes of LAD occlusion on CPB with cold blood cardioplegic arrest followed by 3 hours of reperfusion. Ten of these animals received sCR(1) (10 mg/kg) prior to CPB. Inflammatory response was monitored by percent (%) lung water increase, wall motion scores (WMS) with transthoracic echocardiography where 4 = normal to -1 = dyskinesia, and endothelial function in the distal LAD with bradykinin-induced coronary artery relaxation using organ chamber methodology. RESULTS: OPCAB had no effect on lung edema (% increase = 1.7 +/- 1.4 OPCAB vs. 3.4 +/- 0.5 CPB vs. 2.3 +/- 0.9 CPB + sCR(1)) and failed to prevent wall motion changes (WMS = 2.65 +/- 0.08 OPCAB vs. 2.70 +/- 0.04 CPB vs. 3.10 +/- 0.07* CPB + sCR(1), *p < 0.01) and coronary endothelial dysfunction (% relaxation = 41 +/- 9 OPCAB vs. 40 +/- 9 CPB vs. 78 +/- 8** CPB + sCR(1), **p < 0.001), which was best preserved with sCR(1). CONCLUSIONS: This study suggests that agents which directly inhibit complement activation such as sCR(1) are more important in preventing endothelial dysfunction during coronary revascularization than merely avoiding CPB.

Background— This study was undertaken to determine whether soluble human complement receptor type 1 (TP10), a potent inhibitor of complement activation, would reduce morbidity and mortality in high-risk patients undergoing cardiac surgery on cardiopulmonary bypass (CPB). Methods— This was a randomized multicenter, prospective, placebo-controlled, double-blind study in which 564 high-risk patients undergoing cardiac surgery on CPB received an intravenous bolus of TP10 (1, 3, 5, 10 mg/kg) or placebo immediately before CPB. The primary endpoint was the composite events of death, myocardial infarction (MI), prolonged (≥24 hours) intra-aortic balloon pump support (IABP), and prolonged intubation. Results— TP10 significantly inhibited complement activity after 10 to 15 minutes of CPB and this inhibition persisted for 3 days postoperatively. However, there was no difference in the primary endpoint between the 2 groups (33.7% placebo versus 31.4% TP10; P =0.31). The primary composite endpoint was, however, reduced in all male TP10 patients by 30% ( P =0.025). TP10 reduced the incidence of death or MI in males by 36% ( P =0.026), the incidence of death or MI in CABG males by 43% ( P =0.043) and the need for prolonged IABP support in male CABG and valve patients by 100% ( P =0.019). There was, however, no improvement seen in female TP10 patients. There were no significant differences in adverse events between the groups. Conclusion— TP10 effectively inhibits complement activation during CPB; however, this was not associated with an improvement in the primary endpoint of the study. Nevertheless, TP10 did significantly decrease the incidence of mortality and MI in male patients.

Background— This study sought to determine whether tight glycemic control with a modified glucose-insulin-potassium (GIK) solution in diabetic coronary artery bypass graft (CABG) patients would improve perioperative outcomes. Methods and Results— One hundred forty-one diabetic patients undergoing CABG were prospectively randomized to tight glycemic control (serum glucose, 125 to 200 mg/dL) with GIK or standard therapy (serum glucose P P =0.0017), and a shorter postoperative length of stay (6.5±0.1 versus 9.2±0.3 days; P =0.003). GIK patients also showed a survival advantage over the initial 2 years after surgery ( P =0.04) and decreased episodes of recurrent ischemia (5% versus 19%; P =0.01) and developed fewer recurrent wound infections (1% versus 10%, P =0.03). Conclusions— Tight glycemic control with GIK in diabetic CABG patients improves perioperative outcomes, enhances survival, and decreases the incidence of ischemic events and wound complications.

Recent studies suggest that the U-Clip interrupted coronary artery anastomosis is superior to continuous suture. However, clinical experience with this device is limited.To evaluate our initial clinical experience with the U-Clip technology.Outcomes of 59 patients undergoing isolated coronary artery bypass grafting (CABG) using U-Clips (UCs) were compared to outcomes of 138 patients undergoing CABG using conventional sutures (Conv).The average number of distal anastomoses was similar in the groups (UC, 2.9; Conv, 3.2; P = .33). Also similar were the number of arterial grafts (1.6 versus 1.5, P = .4), percentage of sequential anastomoses (22% versus 12%, P = .058), and percentage performed off pump (27% versus 28%, P = .74). Cardiopulmonary bypass and aortic crossclamp times were longer in the UC group (98 +/- 27 versus 81 +/- 20 minutes, P = .001; 63 +/- 25 versus 54 +/- 24 minutes, P = .028). Rates of operative mortality (UC, 1.69%; Conv, 0.7%), postoperative myocardial infarction (0% each), stroke (0% each), renal failure (2% versus 1.4%), and blood transfusion (53% versus 58%) were not statistically different. Average follow-up in 36 (61%) of UC patients was 5 +/- 2 months (range, 1-7 months). One patient died from a non-cardiacrelated cause. At the time of follow-up 90% of patients were in angina class I-II.The U-Clip interrupted anastomosis technique is versatile and safe and is associated with excellent short-term outcomes.

Objective: This experimental study was undertaken to determine whether pretreatment with statins would enhance myocardial protection and minimize ischemic injury during revascularization of acutely ischemic myocardium. Methods: In 20 pigs the second and third diagonal arteries were occluded for 90 minutes, followed by 45 minutes of blood cardioplegic arrest and 180 minutes of reperfusion. Ten pigs received atorvastatin (40 mg orally every day) for 21 days before surgical intervention; 10 others received no statins. Ischemic damage was assessed on the basis of the need for cardioversions for ventricular arrhythmias, regional wall-motion scores (4 = normal to −1 = dyskinesia) were determined by means of 2-dimensional echocardiography, endothelial function was assessed on the basis of bradykinin-induced coronary artery relaxation, and infarct size was calculated by determining the area of necrosis to the area of risk by means of histochemical staining. Results are given as means ± SE. Results: Statin-treated animals required fewer cardioversions (0.11 ± 0.01 vs 2.87 ± 0.20, P = .0001), had improved wall-motion scores (2.81 ± 0.10 vs 1.52 ± 0.08, P = .01), had lower infarct size (21% ± 2% vs 41% ± 2%, P = .0001), and had more complete coronary artery relaxation (34% ± 5% vs 8% ± 4%, P = .01). Total serum cholesterol levels were similar between the groups (62 ± 5 mg/dL for statin-treated animals vs 68 ± 5 mg/dL for non-statin-treated animals, P = .30). Conclusions: Pretreatment with statins enhances myocardial protection during revascularization by means of mechanisms that are independent of their cholesterol-lowering properties. J Thorac Cardiovasc Surg 2003;125:1037-42

Antioxidants improve endothelial function in hypercholesterolemia (HC); however, whether this includes improvement of the vascular smooth muscle response to NO is unknown. NO relaxes arteries, in part, by stimulating Ca 2+ uptake via sarco/endoplasmic reticulum Ca 2+ -ATPase (SERCA) in aortic smooth muscle, and HC impairs SERCA function and the response to NO. HC induces oxidative stress, which could impair SERCA function. To study the effect of antioxidants, which are known to improve endothelium-dependent relaxation in HC, smooth muscle SERCA activity and NO-induced relaxation were studied in rabbits fed normal chow or a 0.5% cholesterol diet for 13 weeks. The antioxidant t -butylhydroxytoluene (BHT, 1%) was mixed with the HC diet in the last 3 weeks. HC impaired acetylcholine- and NO-induced relaxation, and these were restored by BHT. After inhibiting SERCA with thapsigargin, no difference existed in NO-induced relaxation among the three groups. Reduced aortic SERCA activity in HC was restored by BHT without changing SERCA protein expression. 3-Nitrotyrosine was notably increased in the media of the HC aorta, where it colocalized with SERCA. Tyrosine-nitrated SERCA protein was immunoprecipitated in the aortas of HC rabbits, where it was decreased by BHT, and it was also detected in the aortas of atherosclerotic humans. Thus, the antioxidant reverses impaired smooth muscle SERCA function in HC, and this is correlated with the improved relaxation to NO. These beneficial effects may depend on reducing the direct effects on SERCA of reactive oxygen species that are augmented in HC.

The Heart Outcomes Prevention Evaluation (HOPE) trial demonstrated that ischemic events are decreased in patients receiving angiotensin-converting enzyme (ACE) inhibitors. This study sought to determine whether pretreatment with ACE inhibitors would attentuate ischemic injury during surgical revascularization of ischemic myocardium.In a porcine model, the second and third diagonal vessels were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest, and 180 minutes of reperfusion. Ten pigs received quinapril (20 mg p.o. q.d.) for 7 days prior to surgery; 10 others received no-ACE inhibitors.Quinapril-treated animals required less cardioversions for ventricular arrhythmias (1.58 +/- 0.40 vs 2.77 +/- 0.22; p0.05), had higher wall motion scores assessed by two-dimensional echocardiography (4 = normal to -1 = dyskinesia; 2.11 +/- 0.10 vs 1.50 +/- 0.07; p0.05), more complete coronary artery endothelial relaxation to bradykinin (45% +/- 3% vs 7% +/- 4%; p0.005), and lower infarct size (24.0% +/- 3.0% vs 40.0% +/- 1.7%; p0.0001).ACE inhibition prior to coronary revascularization enhances myocardial protection by decreasing ventricular irritability, improving regional wall motion, lowering infarct size, and preserving endothelial function.

Amiodarone-induced pulmonary toxicity is usually seen in cardiac surgical patients who have received large doses of amiodarone for ventricular arrhythmias over prolonged periods. In this report, we describe a case of amiodarone-induced pulmonary toxicity after a short course of therapy for postoperative atrial fibrillation.

Angiotensin-converting enzyme (ACE) is primarily localized (>90%) in various tissues and organs, most notably on the endothelium but also within parenchyma and inflammatory cells. Tissue ACE is now recognized as a key factor in cardiovascular and renal diseases. Endothelial dysfunction, in response to a number of risk factors or injury such as hypertension, diabetes mellitus, hypercholesteremia, and cigarette smoking, disrupts the balance of vasodilation and vasoconstriction, vascular smooth muscle cell growth, the inflammatory and oxidative state of the vessel wall, and is associated with activation of tissue ACE. Pathologic activation of local ACE can have deleterious effects on the heart, vasculature, and the kidneys. The imbalance resulting from increased local formation of angiotensin II and increased bradykinin degradation favors cardiovascular disease. Indeed, ACE inhibitors effectively reduce high blood pressure and exert cardio- and renoprotective actions. Recent evidence suggests that a principal target of ACE inhibitor action is at the tissue sites. Pharmacokinetic properties of various ACE inhibitors indicate that there are differences in their binding characteristics for tissue ACE. Clinical studies comparing the effects of antihypertensives (especially ACE inhibitors) on endothelial function suggest differences. More comparative experimental and clinical studies should address the significance of these drug differences and their impact on clinical events.

Aortic-valve replacement is the most effective treatment to alleviate symptoms and improve survival in patients with critical aortic stenosis. The incidence of aortic stenosis multiplies with age, and as the life span of our population increases, a larger number of elderly patients will require aortic-valve replacement. However, a substantial number of these patients will have coexisting conditions that preclude surgery. Since outcomes with medical management are uniformly poor, a less invasive and safer alternative to surgical aortic-valve replacement is needed for this expanding group of patients. Transcatheter aortic-valve implantation (TAVI) has emerged as an alternative treatment for aortic stenosis in . . .

Acute papillary muscle rupture is usually associated with a myocardial infarction and involves the posteromedial muscle. We present a case of spontaneous rupture of the anterolateral papillary muscle due to an isolated infarct of the papillary muscle in the absence of epicardial coronary artery disease.

Background. Coronary artery bypass grafting (CABG) with coronary endarterectomy (CE) has been associated with increased morbidity and mortality. We sought to evaluate the impact of recent advances in operative and perioperative management on outcomes after CE. Methods. One hundred fifty-one consecutive patients undergoing first-time CABG with CE between 1991 and 1997 were compared with a concurrent group of 757 patients undergoing CABG without CE (Control). Results. Age, gender, left ventricular ejection fraction, percent nonelective were similar in both groups. Compared with control, the CE group had a higher incidence of hypertension (80% versus 71%, p = 0.02), diabetes (42% versus 32%, p = 0.01), prior myocardial infarction (MI) (68% versus 59%, p = 0.05), peripheral vascular disease (36% versus 16%, p < 0.001), renal failure (15% versus 4%, p < 0.001), and three-vessel coronary disease (81% versus 70%, p = 0.007), resulting in higher Society of Thoracic Surgeons database predicted mortality (4.9 ± 5.9% versus 3.9 ± 4.6%, p = 0.05). Despite the higher risk profile of the CE group, hospital mortality (CE 2.0%, Control 1.2%) and the incidence of major complications such as cerebrovascular accident (CVA) (0.7% versus 1.5%), major respiratory complications (8% versus 5%), and postoperative MI (3% versus 1.4%) were similar between the groups (all p = NS). In a multiple logistic regression analysis, prolonged cardiopulmonary bypass time was an independent predictor of postoperative MI (odds ratio 1.2, CI 1.05 to 1.39, p < 0.01) and the use of heparin-bonded cardiopulmonary bypass circuits of reduced MI rate (odds ratio 0.25, CI 0.08 to 0.76, p < 0.01). Mean follow-up for 94% of patients was 30 ± 19 months (range 1 to 83 months). Five-year survival after CE was 70 ± 5%, with 96% of patients in Canadian Cardiovascular Society class I/II. Conclusions. In a contemporary series of carefully selected patients, mortality and major complications after CE are now similar to CABG without CE. CE itself is not an independent predictor of postoperative MI. Functional class of hospital survivors is excellent.

Pulmonary hyalinizing granulomata are unusual, noninfectious lesions of the lung of uncertain etiology that probably represent an exaggerated immune response. They present radiographically as noncalcified solitary or multiple pulmonary nodules, thereby mimicking primary or metastatic malignancy. The article discusses a case of this rare entity that presented as a solitary pulmonary nodule.

Background —Activation of complement during revascularization of ischemic myocardium accentuates myocardial dysfunction. Soluble human complement receptor type 1 (sCR1) is a potent inhibitor of complement, as are heparin-bonded (HB) cardiopulmonary bypass (CPB) circuits. This study sought to determine whether total complement inhibition with the combination of sCR1 and HB-CPB limits damage during the revascularization of ischemic myocardium. Methods and Results —In 40 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 pigs, sCR1 (10 mg/kg) was infused 5 minutes after the onset of coronary occlusion (sCR1), 10 received HB-CPB only (HB-CPB), 10 received sCR1 and HB-CPB (sCR1+HB), and 10 received neither sCR1 or HB-CPB (unmodified). Addition of sCR1 to the HB group resulted in less myocardial tissue acidosis (ΔpH=−0.72±0.03 for unmodified; −0.46±0.05* for HB; −0.18±0.04*† for sCR1; −0.13±0.01*† for sCR1+HB), better recovery of wall motion scores (4=normal to −1=dyskinesia; 1.67±0.17 for unmodified; 2.80±0.08* for HB; 3.35±0.10*† for sCR1; 3.59±0.08*† for sCR1+HB), less lung water accumulation (5.46±0.28% for unmodified; 2.39±0.34%* for HB; 1.22±0.07%*† for sCR1; 1.24±0.13%*† for sCR1+HB), and smaller infarct size (area necrosis/area risk=44.6±0.7% for unmodified; 33.2±1.9%* for HB; 19.0±2.4%*† for sCR1; 20±1.0%*† for sCR1+HB) (* P P Conclusions —Total complement inhibition with sCR1 and sCR1+HB circuits optimizes recovery during the revascularization of ischemic myocardium.

This experimental study sought to determine whether heparin-bonding of intraaortic balloons (IAB) would decrease the incidence of arterial thrombosis in the absence of systemic heparinization.In 25 adult pigs, a 9F, 40-mL IAB was inserted into the femoral artery and positioned just below the takeoff of the left subclavian artery for 9 hours. Five animals received systemic heparin, 10 animals had no heparin, and another 10 animals received no heparin but the IAB was heparin-bonded (Duraflo II). Thrombus formation was assessed using a numerical scoring system (0 = no thrombosis to 3 = thrombus5 cm or evidence of luminal compromise).Animals receiving heparin and heparin-bonded IAB had no thrombus formation around the IAB (mean +/- SE; 0 +/- 0.00 heparin versus 1.55 +/- 0.29 no heparin versus 0 +/- 0.00 heparin-bonded; p0.005), at the insertion site (0 +/- 0.00 heparin versus 1.55 +/- 0.29 no heparin versus 0 +/- 0.0 heparin-bonded; p0.005), and in the distal femoral artery (0 +/- 0.00 heparin versus 2.00 +/- 0.23 no heparin versus 0 +/- 0.00 heparin-bonded; p0.005).Heparin-bonding of the IAB significantly decreases thrombus formation in the absence of systemic heparinization.

The incidence of carotid artery disease in patients undergoing coronary artery bypass grafting appears to be increasing as our population ages. The optimal treatment for these high-risk patients with concomitant carotid and coronary artery disease remains controversial. This review focuses on the management of patients with coexistent carotid and coronary arteriosclerosis. The significance and management of the patient with an asymptomatic carotid stenosis in patients undergoing coronary artery bypass grafting and the role of combined coronary artery bypass grafting and carotid endarterectomy in these patients will be discussed.

Compared to patients undergoing elective or urgent coronary artery bypass grafting (CABG), those undergoing emergency CABG (EM-CABG) have a higher morbidity and mortality. The use of heparin-bonded circuits (HBC) has been shown to improve clinical outcomes in nonemergent CABG patients. It is not known, however, whether the improved hemostasis and attenuation of the inflammatory response to cardiopulmonary bypass, conferred by HBC, can overcome the high incidence of comorbid risk factors in (EM-CABG) patients and improve their outcomes. A retrospective analysis of 206 consecutive patients undergoing EM-CABG over 4 years (1993-1997) at one institution was performed. Eighty-one patients were treated with conventional non-heparin-bonded circuits (NHBC) with full anticoagulation protocol (FAP, activated clotting time [ACT] > 480 sec); 125 patients were treated with HBC and a lower anticoagulation protocol (LAP, ACT > 280 seconds). Outcomes and results were collected prospectively and are presented as mean +/- SD. Preoperative risk profiles were similar in both treatment groups. Postoperatively, compared with the NHBC group, patients treated with HBC/LAP required fewer homologous donor units (4.1 +/- 10.7 vs 8.2 +/- 13.6 units, p = 0.005), were less likely to require inotropic support (18.6% vs 38.3%, p = 0.005), and had a lower incidence of perioperative myocardial infarction (MI, 3.2% vs 12.3%, p = 0.04) and pulmonary complications (4.0% vs 12.3%, p = 0.04). The use of HBC/LAP resulted in a decreased incidence of postoperative complications (12.8% vs 28.4%, p = 0.01, odds ratio 0.37 with 95% confidence interval [CI] 0.18-0.76). This resulted in a shorter duration of ventilatory support (30.5 +/- 54.0 vs 72.8 +/- 16.7 hours, p = 0.009), ICU stay (38.2 +/- 36.5 vs 91.5 +/- 68.7 hours, p = 0.009), hospital stay (8.0 +/- 7.1 vs 11.0 +/- 8.9 days, p = 0.008), and therefore cost. In conclusion, the use of HBC/LAP in EM-CABG resulted in a reduction of homologous transfusion and postoperative complications associated with decreased hospital stays and cost.

This study was undertaken to determine whether suppression of complement activation with soluble human complement receptor type I reduces myocardial damage during the revascularization of ischemic myocardium.In 20 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 pigs, soluble human complement receptor type I (10 mg/kg) was infused over 30 minutes before the period of coronary occlusion; 10 other pigs received no soluble human complement receptor type I. Complement activation was measured by total hemolytic complement activity (expressed as a percentage of preischemic values). Ischemic damage was assessed by changes in myocardial tissue pH, wall motion scores (range, 4=normal to -1=dyskinesia), and infarct size (area of necrosis versus area at risk).After 180 minutes of reperfusion, hearts treated with soluble human complement receptor type I had significantly less complement activation than nontreated hearts (1.1%+/-0.09% versus 7.8%+/-0.04%, respectively; p0.002), less myocardial acidosis (-0.41+/-0.03 versus -0.72+/-0.03, respectively; p0.0001), higher wall motion scores (3.1+/-0.09 versus 1.67+/-0.16, respectively; p0.0001), and smaller infarct size (24.6%+/-2.0% versus 41%+/-1.3%, respectively; p0.0001).Complement inhibition with soluble human complement receptor type I significantly limits ischemic damage during the revascularization of acutely ischemic myocardium.

Background. Emergency coronary artery bypass grafting after failed percutaneous transluminal coronary angioplasty is associated with increased mortality. Methods. From 1981 through 1995, 117 patients at our institution underwent emergency coronary artery bypass grafting after failed percutaneous transluminal coronary angioplasty, with an in-hospital mortality rate of 13.6%. Univariate and multivariate analyses were used to identify the factors that influenced the risk of death. Results. Univariate analysis revealed that patients who died more often were women and had chronic renal failure, lower ejection fractions, and more diffuse coronary artery disease; less often received an internal mammary artery graft or an antegrade perfusion catheter; required inotropic support in the cardiac catheterization laboratory; and experienced myocardial infarction. Multivariate analysis demonstrated that the need for inotropic support in the cardiac catheterization laboratory was the best predictor of perioperative death. Conclusions. Patients with a reduced ejection fraction in whom percutaneous transluminal coronary angioplasty fails, antegrade perfusion does not produce a response, and myocardial infarction occurs are more likely to die after coronary artery bypass grafting. The risk appears to be highest for patients who require inotropic support in the cardiac catheterization laboratory.

Although the primary energy source for normal myocardium is free fatty acids, glucose appears to be a more favorable energy substrate for the myocardium during ischemia and reperfusion. Glucose-insulin-potassium (GIK) solutions have been shown to limit ischemic damage in experimental models of ischemia. This review summarizes our experimental and clinical studies involving GIK solutions during urgent surgical revascularization of ischemic myocardium. A pig model was used to simulate the conditions of urgent coronary artery bypass graft (CABG) surgery. The second and third diagonal vessels were occluded with snares for 90 minutes followed by 30 minutes of cardioplegic arrest and 180 minutes of reperfusion. Animals receiving GIK during the periods of coronary occlusion and reperfusion had significantly less tissue acidosis, better recovery of wall motion scores, and smaller infarct size. In a prospective, randomized, clinical study involving patients undergoing CABG surgery for unstable angina, GIK therapy resulted in higher cardiac indices, less weight gain, earlier extubation, lower incidence of atrial arrhythmia, and shorter ICU and hospital stays. In conclusion, GIK enhances myocardial performance during ischemia and results in faster recovery after CABG surgery for unstable angina.

Heparin-bonded cardiopulmonary bypass circuits reduce complement activation, but their effect on myocardial function is unknown. This study was undertaken to determine whether heparin-bonded circuits reduce myocardial damage during acute surgical revascularization.In 16 pigs, the second and third diagonal vessels were occluded with snares for 90 minutes followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion with the snares released. During the period of coronary occlusion, all animals were placed on percutaneous bypass followed by standard cardiopulmonary bypass during the periods of cardioplegic arrest and reperfusion. In 8 pigs, heparin-bonded circuits were used, whereas 8 other pigs received nonbonded circuits.Animals treated with heparin-bonded circuits had the best preservation of wall motion scores (3.5 +/- 0.3 versus 2.3 +/- 0.2; 4 = normal to -1 = dyskinesis; p0.05), least tissue acidosis (change in pH = -0.31 +/- 0.02 versus -0.64 +/- 0.08; p0.05), smallest increase in lung H2O (1.7% +/- 0.7% versus 6.1% +/- .5%; p0.05), and the lowest area of necrosis/area of risk (20.3% +/- 2.2% versus 40.4% +/- 1.6%; p0.05).We conclude that heparin-bonded circuits significantly decrease myocardial ischemic damage during acute surgical revascularization.

Objective: This prospective, randomized, clinical study was undertaken to determine whether glucose-insulin-potassium solutions would benefit patients undergoing coronary artery bypass grafting because of unstable angina.Methods: The study group consisted of 30 patients with unstable angina who required coronary artery bypass grafting. In 15 patients, glucose-insulin-potassium solution (30% dextrose in water; K+, 80 mEq/L; regular insulin, 50 units) was given intravenously at 1 ml/kg per hour after induction of anesthesia and administration continued for 12 hours after aortic unclamping. Fifteen patients in a separate group received 5% dextrose in water intravenously at 50 ml/hr.Results: Patients treated with glucose-insulin-potassium solution had higher cardiac indices (2.8 ± 0.1 vs 2.0 ± 1 L/min per square meter; p < 0.001), lower inotrope scores (0.06 ± 0.01 vs 0.46 ± 0.19; p = 0.041), and less weight gain (6.4 ± 9 vs 11.6 ± 1.1 pounds; p < 0.001) and had shorter times of ventilator support (8.3 ± 0.6 vs 14.2 ± 0.2 hours; p = 0.003). They had a significantly lower incidence of atrial fibrillation (13.3% vs 53.3%; p = 0.020) and had shorter stays in the intensive care unit (14.8 ± 1.3 vs 31.6 ± 5.2 hours; p = 0.002) and in the hospital (6.0 ± 0.4 vs 8.0 ± 0.7 days; p = 0.010).Conclusions: We conclude that glucose-insulin-potassium therapy enhances myocardial performance and results in faster recovery from urgent coronary artery bypass grafting. (J Thorac Cardiovasc Surg 1997;113:354-62)

Despite many advances in blood conservation techniques, a significant proportion of patients undergoing primary coronary revascularization still require homologous transfusions. Based on a large clinical experience with high-risk patients during coronary artery bypass, a comprehensive strategy to diminish perioperative blood loss was developed by integrating many individual components. An integral component in this strategy is the use of lower heparinization (activated clotting time [ACT] > 280 sec) in conjunction with "tip-to-tip" heparin-bonded cardiopulmonary bypass (CPB) circuits (HBC). This technique was prospectively applied to a group of Jehovah's Witnesses (JW) patients who refuse blood transfusion on religious grounds (n = 9). Outcome was compared to a matched group of patients treated with full heparinization (ACT > 480 sec) used with conventional, nonheparin-bonded CPB circuits (NHBC) performed within the same academic year (n = 455). There were no complications in JW patients who had a significantly lower mediastinal and pleural tube output in the first 24 hours (323 67 mL vs 984 616 mL, p < 0.01). In comparison to JW patients who received no transfusions, 68.1% of patients treated with NHBC were transfused (p 0.0001). In summary, HBC in conjunction with lower anticoagulation was effectively and safely applied to JW patients undergoing coronary artery bypass grafting. This technique should be considered for broader clinical use.

Background. Leukocyte depletion (LD) has been shown to be beneficial during the reperfusion of acutely ischemic myocardium; however, its role during cardiopulmonary bypass (CPB) in hearts protected with blood cardioplegia (BCP) is unknwon. This experimental study sought to determine whether LD filters inserted in the CPB circuit before cardioplegic arrest and in the BCP circuit during arrest would decrease ischemic myocardial damage. Methods. In 20 pigs, the second and third diagonal vessels were occluded for 90 minutes, followed by 45 minutes of BCP arrest and 180 minutes of reperfusion on CPB. In 5 pigs, LD filters were inserted in both the CPB and BCP circuits (LD-CPB+BCP). Five pigs had LD during BCP (LD-BCP), 5 pigs had LD during CPB (LD-CPB), and 5 pigs had no LD. Ischemic damage was assessed by wall motion scores using two-dimensional echocardiography and the area of necrosis/area of risk. Results. The LD-CPB and LD-CPB+BCP groups had the highest wall motion scores and the lowest area of necrosis/area of risk. The addition of LD to BCP alone did not significantly alter wall motion scores or the area of necrosis/area of risk. Conclusions. Leukocyte depletion filters significantly reduce ischemic damage during acute surgical revascularization and appear to be most effective when placed in the CPB circuit before cardoplegic arrest.

Occult cardiac injury following blunt trauma is underestimated in frequency of occurrence. Recent reports indicate that it rivals thoracic aortic transection as the cause of death following traffic fatalities. The most common mechanisms include rapid cardiac rotation while the great vessels remain fixed, transfer of hydraulic pressure from the abdomen or extremities, and direct myocardial compression by the sternum. Presentation can be diverse and findings can include jugular venous distention, upper extremity cyanosis, unexplained hypotension, and muffled heart sounds. An enlarged cardiac silhouette is occasionally seen on roentgenographic evaluation. A surprisingly large number of these patients are noted to have no significant signs of external thoracic trauma. Possible mechanisms include rapid rotation and deceleration of the heart with fixation of the great vessels, transmission of a large venous pressure wave to the heart following abdominal or extremity compression, and direct compression of the heart by the sternum. Following prompt diagnosis and rapid surgical intervention, a large number of these patients can be expected to survive this otherwise fatal injury.

This study sought to determine which factors influence the mortality rate in patients developing gastrointestinal complications following cardiac surgery. Between July 1988 and January 1992, 2054 patients underwent cardiac surgical procedures at the Boston University Medical Center. Of these, 29 (1.4%) developed postoperative gastrointestinal complications. The overall mortality rate among these patients was 27% (829). Those who died following such complications had a higher incidence of New York Heart Association (NYHA) class IV and unstable symptoms (88, 100% versus 321, 14%; P < 0.0001), and an increased need for preoperative intra-aortic balloon pump support (48. 50% versus 121, 5%; P < 0.004). The need for gastrointestinal surgical intervention increased the mortality rate significantly compared with patients managed medically (818, 44% versus 0/11, 0%; P < 0.01). Patients with ischemic bowel also had a significantly higher mortality (55, 100% versus 324, 12%; P < 0.001). It is concluded that most patients with gastrointestinal complications following cardiac surgery can be treated, and with acceptable mortality rates. The presence of unstable symptoms, preoperative intra-aortic balloon pump support, ischemic bowel and the need for gastrointestinal surgical intervention adversely affect mortality.

Although percutaneous bypass (PB) can support the failing myocardium, regional ischemic damage may still occur beyond a coronary occlusion. This study sought to determine whether the addition of intraaortic balloon pump (IABP) support to PB would result in more optimal salvage of ischemic myocardium. In 30 pigs, the second and third diagonal vessels were occluded with snares for 90 minutes followed by 30 minutes of cardioplegic arrest and 3 hours of reperfusion with the snares released. During the period of coronary artery occlusion, 10 pigs were placed on PB, 10 pigs received PB plus IABP support, and 10 pigs received no support (the unmodified group). The hearts treated with the combination of PB and IABP support exhibited the highest wall motion scores (3.3 +/- 0.20 for the PB plus IABP group [p0.05 from the unmodified group and from the PB group]; versus 1.40 +/- 0.30 for the PB group versus 1.37 +/- 0.33 for the unmodified group), the least tissue acidosis (change in pH, -0.30 +/- 0.2 for the PB plus IABP group [p0.05 from the PB group] versus -0.60 +/- 0.10 for the PB group versus -0.41 +/- 0.13 for the unmodified group), and the least area of necrosis (25% +/- 5% for the PB plus IABP group [p0.05 from the unmodified group and from the PB group]; versus 43% +/- 2% for the PB group [p0.05 from the unmodified group] versus 73% +/- 3% for the unmodified group).(ABSTRACT TRUNCATED AT 250 WORDS)