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Study Objectives: Community-acquired pneumonia is a frequent event in the course of chronic obstructive pulmonary disease (COPD). The aim of the present study was to provide information on clinical and microbiological characteristics and outcome of community-acquired pneumonia in these patients, in a comparative study with the non-COPD population., Design: Prospective study of cases., Setting: A university hospital in Lleida, Spain., Patients: During a 6 year-period, we prospectively studied the clinical and radiological manifestations, microbiological data and outcome of all patients with community-acquired pneumonia. A comparative analysis of characteristics of pneumonia between 132 patients with a definitive diagnosis of COPD and 575 patients who did not have this underlying disease was performed., Measurements and Results: COPD was associated with an older and predominantly male population. These patients frequently had concomitant comorbidities such as diabetes mellitus or chronic heart failure. Clinical presentation was more severe, manifested by septic shock, tachypnea, lower values of pH, pO(2) and oxygen saturation, and greater values of pCO(2). Purulent expectoration was also more frequent in this subset of patients. Admission was usually required for patients with COPD, and length of hospitalization was significantly increased; however, difference in the mortality rate was not observed. Although the spectrum of responsible microorganisms was very similar, the incidence of Pseudomonas aeruginosa and other Gram-negative bacilli was increased in COPD, particularly among patients with advanced situation and/or oral corticosteroid treatment., Conclusions: Community-acquired pneumonia in patients with COPD was associated with epidemiological and clinical particularities mainly related to the underlying disease but showed only minor differences in outcome parameters. Gram-negative bacilli and P. aeruginosa are potential pathogens that need to be considered.

Background: Aprotinin significantly decreases postoperative blood loss, yet its exact mechanism of action remains unproven., Methods: To study the cytoprotective effect on platelets, we collected blood samples from patients during cardiopulmonary bypass (CPB) operations performed with or without aprotinin. Analysis included whole-blood flow cytometry., Results: The highest percentages of activated platelets (positive for GMP-140 expression) were bound to leukocytes and erythrocytes in all CPB patients. Platelet-platelet activation did not reveal any marked differences between groups. However, in the platelet-cell bound region, increased ristocetin-stimulated platelet activation was observed from 30 minutes on CPB to 90 minutes after CPB with aprotinin (11.9% +/- 5.1% to 33.1% +/- 8.6%; p < 0.05), but not without aprotinin (17.5% +/- 0.1% to 17.9% +/- 2.3%). Platelet autoactivation increased more in the untreated group with time on CPB., Conclusions: This study demonstrates that in the presence of aprotinin, platelets remain unstimulated during CPB and the von Willebrand GPIb-mediated activatability of platelets is preserved, thus maintaining a viable platelet population. Most important, this study reveals that these mechanisms are more related to platelet-leukocyte than to platelet-platelet interactions.

Background: Aprotinin is a serine protease inhibitor that reduces blood loss and transfusion requirements when administered prophylactically to cardiac surgical patients. To examine the safety and dose-related efficacy of aprotinin, a prospective, multicenter, placebo-controlled trial was conducted in patients undergoing repeat coronary artery bypass graft (CABG) surgery., Methods and Results: Two hundred eighty-seven patients were randomly assigned to receive either high-dose aprotinin, low-dose aprotinin, pump-prime-only aprotinin, or placebo. Drug efficacy was determined by the reduction in donor-blood transfusion up to postoperative day 12 and in postoperative thoracic-drainage volume. The percentage of patients requiring donor-red-blood-cell (RBC) transfusions in the high- and low-dose aprotinin groups was reduced compared with the pump-prime-only and placebo groups (high-dose aprotinin, 54%; low-dose aprotinin, 46%; pump-prime only, 72%; and placebo, 75%; overall P = .001). The number of units of donor RBCs transfused was significantly lower in the aprotinin-treated patients compared with placebo (high-dose aprotinin, 1.6 +/- 0.2 U; low-dose aprotinin, 1.6 +/- 0.3 U; pump-prime-only, 2.5 +/- 0.3 U; and placebo, 3.4 +/- 0.5 U; P = .0001). There was also a significant difference in total blood-product exposures among treatment groups (high-dose aprotinin, 2.2 +/- 0.4 U; low-dose aprotinin, 3.4 +/- 0.9 U; pump-prime-only, 5.1 +/- 0.9 U; placebo, 10.3 +/- 1.4 U). There were no differences among treatment groups for the incidence of perioperative myocardial infarction (MI)., Conclusions: This study demonstrates that high- and low-dose aprotinin significantly reduces the requirement for donor-blood transfusion in repeat CABG patients without increasing the risk for perioperative MI.

During a 30-month period, 34 premature infants underwent surgical closure of a patent ductus arteriosus. The mean gestational age at birth was 25 +/- 0.3 weeks and the mean age at the time of operation was 3 +/- 0.3 weeks (mean weight, 829 +/- 54 g). Indomethacin therapy had failed in 32 patients, and 2 had contraindications to its use. The initial 8 patients had parascapular incision and ligation of the patent ductus arteriosus; the last 26 patients had a short transaxillary incision and clipping. The average duration of the operation from the time of incision to skin closure was 36 +/- 2 minutes (range, 15 to 65 minutes). One patient (3%) needed chest tube insertion intraoperatively because of visceral pleura disruption. Two patients (5.8%) had a "small pneumothorax" (< 10% of the lung field) that resolved within 24 hours. There was no morbidity or mortality directly related to the operative procedure, although 3 patients (8.8%) ultimately died from problems related to their severe prematurity. We conclude that surgical closure of patent ductus arteriosus without chest tube drainage can be accomplished safely in premature infants. Postoperative nursing care is simplified and the cost is reduced because the need for the chest tube and drainage system is eliminated and the number of chest radiograms needed postoperatively is reduced.

The hemodynamic changes consistent with constrictive pericarditis are often encountered in patients who have undergone cardiac transplantation. We describe here 4 patients who underwent pericardiectomy after cardiac transplantation. All were found to have evidence of a thickened and constricting peel of pericardium at surgical exploration. Their postoperative clinical courses were variable. One patient with primarily effusive constriction experienced marked improvement. Three patients failed to show clinical improvement and had persistently elevated atrial and ventricular end-diastolic pressures. A coexisting restrictive cardiomyopathy secondary to chronic rejection, coronary arteriopathy, or long-standing constriction may have been the cause of this poor outcome. Many patients with transplanted hearts exhibit evidence of poor diastolic ventricular compliance without evidence of classic constriction; some manifest both the restrictive and constrictive components. The careful selection of patients with constrictive pericarditis can optimize the outcome.

Failure to recognize the presence of accessory mitral tissue causing subaortic stenosis can lead to not only the performance of inappropriate operations, but the persistence and recurrence of obstruction or even death. Over a 12-month period, we treated 2 children with severe subaortic stenosis caused by accessory mitral tissue. In 1 patient, who was 4 years old, the echocardiogram showed the accessory mitral tissue to be attached to the anterior mitral leaflet and ballooning into the subaortic area. The other patient, as a newborn, underwent simultaneous repair of a complete canal defect and coarctation. Two years later, the patient was seen because of syncopal episodes, progressive mitral insufficiency, and subaortic stenosis thought to be caused by anterior displacement of the anterior mitral leaflet. Mitral valvuloplasty and a conal enlargement procedure were planned. Intraoperatively, after the mitral valvuloplasty had been done, the subaortic stenosis was found to be due to a tight subaortic ring formed by accessory mitral tissue located at the septum and its fibrous extension to the anterior mitral leaflet. In both patients, excision of the accessory mitral and fibrous tissues resulted in a wide-open subaortic area. Both patients had an uneventful hospital course, and follow-up echocardiography showed no noteworthy residual left ventricular outflow gradient. We believe that increased awareness and sophisticated echocardiographic techniques should lead to an increased recognition of accessory mitral tissue causing subaortic stenosis. Simple resection of the accessory mitral tissue and its secondary fibrous tissues can be curative.

Background: This study was undertaken to determine if a newly developed synthetic peptide thrombin inhibitor (DuP 714; DuPont-Merck, Wilmington, Del) could be used as an anticoagulant in cardiopulmonary bypass (CPB) surgery., Methods and Results: Anesthetized mongrel dogs were placed on CPB for 1 hour and then observed for 2 hours. Following a dose-finding study, the optimal dose (DuP 714 group) and an overdose (DuP-HI group) were studied. The DuP 714 group received 0.25 mg/kg i.v. bolus plus 0.5 mg.kg-1 x h-1 infusion of DuP 714 (n = 10) and the DuP-HI group received 0.5 mg/kg i.v. bolus plus 1.0 mg.kg-1 x h-1 infusion of DuP 714 (n = 6). No neutralizing agent was used. The control group received 2.0 mg/kg intracardiac bolus of heparin with 0.15 mg/kg i.v. bolus injections as needed to maintain the activated clotting time (ACT) at > 300 seconds during CPB (n = 6). Protamine sulfate (2.0 mg/kg) was used to reverse heparin after CPB. Postoperative blood loss for both DuP 714 groups was less than that for heparin (177 +/- 40 and 297 +/- 36 versus 318 +/- 99 g, P = NS). The DuP 714 group revealed higher pump line filter fibrin deposits (15.5 +/- 3.6 mg, P < .032 ANOVA) compared with the heparin group (4.2 +/- 2.4 mg), whereas the DuP-HI group showed equivalent deposits (9.3 +/- 5.3 mg). The ACT levels recorded during and 30 minutes after CPB were 638 +/- 52 and 160 +/- 9 seconds in the DuP 714 group and > 800 and 436 +/- 75 seconds in the DuP-HI group; however, the ACT level only in the DuP-HI group remained elevated 2 hours after CPB. Platelet counts were significantly higher (P < .05) in both DuP 714 groups after CPB. There was nearly complete elimination of all peptide in the urine. No statistical difference was observed in hemodynamics (cardiac index and systemic vascular resistance) in any of the groups., Conclusions: This study reveals that the peptide inhibitor DuP 714 can effectively function as an anticoagulant in a canine CPB model. The efficacy and safety, even when overdosed, are demonstrated by reduced blood loss and lack of platelet count reduction. Clinical monitoring can be achieved by the use of ACT levels. No evidence of hemodynamic compromise was noted with the drug administration.

Infective aortic endocarditis developed in an elderly patient after a percutaneous balloon aortic valvuloplasty. The transesophageal echocardiogram demonstrated a perivalvular abscess. The patient underwent surgical replacement of the infected valve, but later succumbed to renal failure. The development of infective aortic endocarditis should be recognized as a potentially fatal complication of percutaneous balloon aortic valvuloplasty. The important measures in preventing bacteremia during percutaneous balloon aortic valvuloplasty and the appropriate role of operation are discussed.

Background: Photopheresis is a technique in which reinfusion of mononuclear cells exposed to UV-A light ex vivo after in vivo treatment with 8-methoxypsoralen initiates host-immunosuppressive responses., Methods and Results: To determine if photopheresis safely reverses International Society for Heart and Lung Transplantation (ISHLT) rejection grades 2, 3A, and 3B without hemodynamic compromise, 16 heart transplant patients with ISHLT rejection grades 2, 3A, and 3B were randomized to photopheresis or corticosteroid therapy. The average number of mononuclear cells treated with each photopheresis procedure was 9.8 +/- 9.1 x 10(9) (mean +/- SD). Photopheresis and corticosteroids reversed eight of nine and seven of seven episodes of rejection, respectively. The median time from initiation of treatment to rejection reversal was 25 days (range, 6-67 days) in the photopheresis group and 17 days (range, 8-33 days) in the corticosteroid group. Hemodynamics were normal before either treatment and did not change after reversal of rejection. No adverse reactions occurred with photopheresis, and all patients in either treatment group are alive., Conclusions: These preliminary, short-term results in prospectively randomized patients indicate that photopheresis may be as effective as corticosteroids for treating ISHLT rejection grades 2, 3A, and 3B. The apparently low toxicity and potential efficacy of photopheresis warrant further analysis of its role in the prevention and treatment of heart transplant rejection.

Obesity and hypertension frequently develop after heart transplantation. The cardiac adaptation to obesity and hypertension was studied by determining hemodynamic and echocardiographic indexes in 10 obese hypertensive patients (body mass index greater than or equal to 27.8 kg/m2 in men or greater than or equal to 27.3 kg/m2 in women) matched by mean arterial pressure, age and gender with 10 nonobese hypertensive patients 1 year after cardiac transplantation. Cardiac output was 30% greater (p less than 0.02) and systemic vascular resistance 25% lower (p less than 0.01) in the obese than in the nonobese patients. Right ventricular systolic and pulmonary artery systolic, diastolic and mean pressures were also significantly higher (p less than 0.05) in the obese patients. Left ventricular end-diastolic diameter was 25% greater (p less than 0.05), left ventricular mass 28% greater (p less than 0.02) and left ventricular end-diastolic volume 20% higher (p less than 0.01) in the obese subjects. Left ventricular ejection fraction was significantly lower in the obese than in the nonobese subjects (34% vs. 51%, p less than 0.05). These results indicate that the cardiac adaptation to obesity and hypertension after heart transplantation consists of left ventricular dilation and an increase in left ventricular mass associated with an increased cardiac output and lower peripheral vascular resistance. These adaptive changes that occur in obese hypertensive patients after heart transplantation might increase the long-term risk of graft failure, as suggested by their lower left ventricular ejection fraction 1 year after transplantation.

Myocardial infarction remains the leading cause of early and late deaths after abdominal aortic reconstruction in patients with abdominal aortic aneurysm. Our approach for the past 4 years has been combined myocardial revascularization with abdominal aortic aneurysm repair in patients with good left ventricle performance. From July 1984 through June 1989, 128 patients underwent abdominal aortic aneurysm repair. Seventeen patients underwent combined abdominal aortic reconstruction with coronary artery bypass grafting. One patient died (5.9%). The remaining patients are all well at current follow-up. Our experience shows that patients with coronary artery disease and abdominal aortic aneurysm may have both lesions safely repaired as a single operative procedure.

Recombinant (r) hirudin is a potent thrombin-specific inhibitor derived from the natural hirudin of the leech (Hirudo medicinalis). We have studied the efficacy of r-hirudin compared with heparin in a canine model of cardiopulmonary bypass operations. Two administration regimens were used for r-hirudin: group 1, 1.0 mg/kg intracardiac bolus then intravenous bolus at 30 minutes (n = 10); and group 2, 1.0 mg/kg intracardiac bolus with 1.25 +/- 0.04 mg.kg-1.h-1 intravenous infusion (n = 8). Group 3 was given an intracardiac bolus of heparin, 1.66 mg/kg (n = 9). Aspiration of blood from the chest cavity revealed no significant difference between the three groups. Measurement of fibrin deposits in the pump line filter revealed higher amounts in the r-hirudin groups (p = 0.02). Decreases in platelets, fibrinogen, and hematocrit due primarily to hemodilution were the same in each group. The bleeding time assay showed less prolongation for r-hirudin than for heparin (p less than 0.001). No antagonist for r-hirudin was used; however, due to its short half-life all coagulation variables returned to baseline within 30 minutes after cardiopulmonary bypass. Because r-hirudin lacks effect on platelets, is a poor immunogen, does not require a plasma cofactor, and may not require an antagonist, it may provide an alternative anticoagulant to heparin in cardiopulmonary bypass. Additional studies are, however, needed to optimize the dose and to evaluate other clinical aspects of r-hirudin.

Repeat coronary angiography was performed in 42 patients 10 years after randomization to medical (n = 21) or surgical (n = 21) therapy for chronic angina. The native coronary arteries were classified into 15 angiographic segments and 3 arterial trunks for analysis of progression of coronary artery disease. The incidence rate of disease progression in coronary segments was 24% and 28% in medically and surgically treated patients, respectively (p = NS). Grafted segments showed a 38% rate of disease progression, which was higher than the 18% rate of for nongrafted segments (p less than 0.001) and the overall rate of 24% for medically treated patients (p less than 0.01). Similarly, 29 (94%) of 31 grafted arteries exhibited disease progression compared with 19 (59%) of 32 nongrafted arteries (p less than 0.01) and 42 (67%) of 63 arteries in medically treated patients (p less than 0.01). In grafted vessels, disease progression occurred more often in arteries proximal (84%) to the anastomosis than in arteries distal (16%) to graft insertion (p less than 0.001). Progression occurred in 46% of proximal segments compared with 23% of distal segments (p less than 0.02). Progression was seen in 23 (55%) of 43 segments with an occluded graft compared with 30 (31%) of 96 segments with a patent graft (p less than 0.02). Ten years after randomization, medically and surgically treated patients showed a comparable rate of disease progression in coronary segments. However, surgical therapy appeared to significantly accelerate atherosclerotic progression in the grafted vessels, especially in the proximal portions. Occluded grafts also correlated with an adverse effect on disease progression.(ABSTRACT TRUNCATED AT 250 WORDS)

Twenty-six patients on long-term renal dialysis underwent coronary artery bypass grafting. The patients were divided into two groups: group 1, (16 patients) saphenous vein bypass grafts, and group 2, (10 patients) internal mammary artery in combination with saphenous vein bypass grafts. Both groups were similar in terms of cardiac hemodynamics and previous number of myocardial infarctions, though more group 1 patients were in New York Heart Association class III or IV. Patients in group 1 received 2.9 bypass grafts per patient; patients in group 2 received 4.0 bypass grafts per patient (4 with bilateral mammary arteries). No wound healing problems occurred in either group. Blood replacement was similar for both groups (group 1, 5.5 units/patient; group 2, 5.3 units/patient). More platelets were given to group 1 patients (16.2 units/patient) than group 2 patients (3.1 units/patient). We conclude that use of the internal mammary artery in patients on long-term renal dialysis does not alter wound healing or increase blood loss in this subset of patients.

Medical treatment of postinfarction ventricular septal rupture carries a high mortality. Delayed surgery can be done with good results but many patients die awaiting operation. In 1978 we decided that all such patients presenting to us should undergo urgent cardiac catheterization and surgery. Since then we have seen 22 such patients. Two decided against surgery and died in the hospital. Twenty agreed to surgery; in 15 of these an intra-aortic balloon pump was inserted before catheterization and in another four at the time of operation. Catheterization was performed without complication, and surgery was performed within 2 days of septal rupture in all 20 patients. Twelve patients (60%) survived hospitalization. Three patients died of pump failure shortly after surgery; five died after a second operation for free wall rupture (n = 2) or persistent or recurrent septal defect (n = 3). Two other patients survived reoperation. Survivors were significantly younger than nonsurvivors and had a higher cardiac index and a lower shunt ratio. At a mean follow-up of 47.9 months, there has been one late noncardiac death. Eleven patients survive, all in class I or II. We conclude that in patients with septal rupture urgent surgery results in improved near-term survival compared with known survival rates in medically treated patients. Early recurrent rupture is common and often disastrous and requires refinement in operative technique. Age, cardiac index, and shunt volume are related to surgical outcome. Hospital survivors do very well on a long-term basis. We recommend continuation of this aggressive approach.

Factors related to late narrowing of aortocoronary vein grafts are poorly understood. Repeat aortocoronary bypass graft angiography was performed in 34 patients at 13 +/- 5 months and 61 +/- 13 months after surgery. In these patients, 61 of 65 grafts (94%) were patent at 1 year; at 5 years, 39 of these patent grafts (64%) remained unchanged, 21 (34%) had become progressively narrowed and one (2%) was totally occluded. There appeared to be no predilection for progression to occur at specific segments or in particular grafts: Eight of 28 left anterior descending (29%), seven of 17 right coronary artery (41%) and seven of 16 circumflex artery grafts (44%) (NS) showed further narrowing. Progressive graft narrowing occurred in 15 of 34 patients (44%). Risk factors (incidence of smoking, diabetes mellitus, hypertension, and triglyceride and cholesterol levels) in these 15 patients were compared with those in the 19 patients whose grafts were unchanged between 1 and 5 years. The incidence of smoking, diabetes mellitus (fasting blood sugar greater than or equal to 110 mg % or 2-hour postprandial sugar greater than or equal to 140 mg %) and hypertension (systolic blood pressure greater than 140 mm Hg or diastolic pressure greater than or equal to 95 mm Hg) were 46%, 27% and 33%, respectively, in the patients with progressive graft narrowing and 68%, 16%, 26% in the patients whose grafts were unchanged (NS). The average mean triglyceride levels were 617 +/- 785 mg % (+/- SD) and 195 +/- 86 mg %, respectively (p less than 0.05). The average mean cholesterol levels were 279 +/- 53 mg % and 234 +/- 35 mg %, respectively (p less than 0.01). In patients who have had aortocoronary bypass surgery, total graft occlusion is rare between 1 and 5 years after surgery. Progressive narrowing of grafts is common and appears to be associated with elevated blood lipids.

A comparison of the levels of serum epinephrine, norepinephrine and blood pressure was made in 25 patients undergoing aorta-coronary bypass or valve replacement who were anaesthetized with a nitrous oxide-narcotic technique. Serum epinephrine and norepinephrine were measured in arterial samples drawn pre-induction, post-induction, before cardiopulmonary bypass, two and eight minutes after initiation of cardiopulmonary bypass, 20 minutes before termination and after termination of cardiopulmonary bypass. In both patient groups significant increases in epinephrine and norepinephrine occurred befored cardiopulmonary bypass, with accompanying increase of blood pressure in the valve replacement patients. During cardiopulmonary bypass an initial hypotensive response (p less than 0.001) was recorded, followed by a significant increase in blood pressure and epinephrine in both groups. After cardiopulmonary bypass, aorta-coronary bypass patients had epinephrine, norepinephrine and blood pressure equal to levels before cardiopulmonary bypass. In contrast, serum epinephrine continued to rise in the valve replacement patients, with a gradual recovery of blood pressure to pre-bypass levels. These findings demonstrate significant differences in blood pressure and catecholamine response in patients with valvular disease from patients with coronary artery disease.

Repeat angiography was performed at 63 +/- 9 months in 26 medically treated patients and at 66 +/- 10 months in 32 surgically treated patients with chronic angina. The native coronary arteries were divided into three major trunk vessels and 15 angiographic segments. Progression of disease was defined as the appearance of new (greater than 50%) obstruction or significant worsening of existing lesions in a segment or vessel. The incidence of progression was similar in medical and surgical patients, comparing individual segments (69 of 312 [22%] and 91 of [23%], respectively) or vessels (49 of 78 [63%] and 60 of 96 [63%], respectively). In both medical and surgical patients, segments initially free of disease showed a 14% incidence of developing new lesions, compared with the 37% progression in segments initially diseased (p less than 0.001). In the surgical patients, progression occurred in 48 of 219 (22%) nongrafted and 43 of 177 (24%) grafted segments (NS). When analyzed by major trunk vessel, progression occurred in 40 of 57 grafted arteries (70%) and 20 of 39 nongrafted arteries (51%) (NS). The incidence of new total occlusions was similar in medical and surgical patients (6% and 8%, respectively); new total occlusions occurred predominantly in diseases segments (15% and 22%, respectively). In patients with stable angina pectoris who have medical or surgical treatment assigned by randomization, progression of coronary disease at 5 years is not influenced by which mode of therapy was received. Vessels initially free of disease are at relatively low risk for development of disease within 5 years. In surgical patients, grafted and nongrafted vessels show similar rates of progression.

The efficacy of OKT*3 monoclonal antibody in reversing acute cardiac allograft rejection was investigated in 10 cardiac transplant recipients aged 5 to 57 years (mean 34 +/- 18) and treated with the same induction and maintenance immunosuppression. Serial endomyocardial biopsies, right heart catheterization, and echocardiograms were performed for rejection surveillance. After intensified immunosuppression with equine antithymocyte globulins and steroids, nine patients showed persistent rejection (lymphocytic infiltration and myocyte necrosis). Conventional immunosuppression was contraindicated in one patient. OKT*3 (5 mg by intravenous push daily for 14 days) resulted in complete resolution of rejection in nine of 10 patients (90%). After therapy with OKT*3 mean right atrial and pulmonary arterial wedge pressure were significantly lower (9.1 +/- 4.0 vs 4.8 +/- 2.0 mm Hg and 13.4 +/- 4.3 vs 8.0 +/- 3.3 mm Hg, respectively; p less than .05). Cardiac index was doubled in two patients with rejection-induced cardiac dysfunction (1.5 vs 3.2 and 1.6 vs 2.7 liters/min/m2). Only two patients developed antibodies to OKT*3. Fever, nausea and headache occurred with the first three doses of OKT*3 and did not recur. One patient developed aseptic meningitis. OKT*3 effectively reverses refractory cardiac allograft rejection before the development of irreversible graft dysfunction. Patients who do not develop antibodies to OKT*3 can be retreated with this drug. Adverse reactions to OKT*3 are self-limited.

Qualitative distribution of coronary flow using thallium-201 perfusion scans immediately postintubation was studied in 22 patients scheduled for elective coronary artery bypass surgery. Ten patients received a thiopental (4 mg/kg) and halothane induction. Twelve patients received a fentanyl (100 micrograms/kg) induction. Baseline thallium-201 perfusion scans were performed 24 h prior to surgery. These scans were compared with the scans performed postintubation. A thallium-positive scan was accepted as evidence of relative hypoperfusion. Baseline hemodynamic and ECG data were obtained prior to induction of anesthesia. These data were compared with the data obtained postintubation. Ten patients developed postintubation thallium-perfusion scan defects (thallium-positive scan), even though there was no statistical difference between their baseline hemodynamics and hemodynamics at the time of intubation. There was no difference in the incidence of thallium-positive scans between those patients anesthetized by fentanyl and those patients anesthetized with thiopental-halothane. The authors conclude that relative hypoperfusion, and possibly ischemia, occurred in 45% of patients studied, despite stable hemodynamics, and that the incidence of these events was the same with two different anesthetic techniques.

A total of 145 patients with greater than 50% obstruction of the left main coronary artery (LMC) were studied by coronary arteriography. Of the 140 who survived cardiac catheterization, 121 were considered operable by coronary arteriography, and 19 were inoperable. Of the 121 operable patients, 32 were treated medically, and 89 had aortocoronary bypass surgery. Surgical mortality was 11%. The follow-up was from 1 to 72 months with a mean follow-up of 15 months. A survival table was plotted over a 24-month period. At 90 days survival in surgical patients was 85%, medical patients 72%, and inoperable patients 64%. At one year 82% of surgical patients were alive compared with 61% of medically treated operable patients (P less than 0.05). Thereafter, the survival rate remained stable up to 23 months. Survival in inoperable patients was 38% at one year. Improved surgical survival was associated with the presence of preoperative collateral vessels and a left ventricular stroke index greater than 18 g-m/m2. The study demonstrates that survival is improved significantly by surgery in LMC patients. Since mortality occurs early after coronary arteriography, surgery should be offered early to operable patients.

A series of 12 consecutive patients who underwent aortic valve replacement (AVR) for aortic stenosis complicated by severe left ventricular dysfunction was reviewed. Ventricular dysfunction was reflected by pulmonary congestion, edema, renal and hepatic dysfunction, and by severely depressed ejection fractions (mean, 13%; range equal to 0-20%). Aortic valve replacement was accompanied by mitral commissurotomy in 1 patient and aortocoronary bypass in 5. Three of 5 patients with greater than 50% coronary obstruction died without reversal of heart failure, and 1 of the 5 died after a stroke. The 1 survivor of this group has done well. All 7 patients with minimal or no coronary disease survived operation and are now in New York Heart Association Class I or II. Postoperative catheterization (2 to 12 months) in 6 patients showed improved cardiac index and filling pressures. Left ventricular diastolic volume fell from 159 to 82 ml/m2, and ejection fraction rose from 13 to 45%. We conclude that left ventricular dysfunction owing to aortic stenosis alone is reversible and that AVR results in great clinical improvement. When coronary disease is present, survival may be accompanied by great improvement but the operative mortality is much higher.