Faculty Bibliography

Twenty-five patients who underwent resection of a thoraco-abdominal aneurysm between 1985-1993 were reviewed to study determinants of survival in patients undergoing the procedure in a community hospital. Twelve procedures were performed electively, six urgently and seven emergently. Type I aneurysm was present in one patient (n = 1), Type II n = 7; Type III n = 5 and Type IV = 12. Hypertension (n = 17), cardiac disease (n = 10) and renal insufficiency (n = 4) were most common risk factors. Aneurysms were repaired using inclusion method without special techniques for renal or spinal cord preservation. Eighteen patients survived and were discharged; four patients died 30 days and three patients died 30 days. Causes of death were multisystem failure (n = 3), acute myocardial infarction (n = 2) coagulopathy (n = 1) and bowel infarction (n = 1). Major complications included renal failure (n = 2) myocardial infarction (n = 3), bleeding (n = 3), paraplegia (n = 1). Statistical significance was determined using Fisher's exact test-2 tail. Risk factors for death and complication included emergency or urgent surgery (4 deaths-emergent, 2 deaths-urgent) and preoperative renal insufficiency (2 deaths; 1 dialysis) 52% of patients in a community hospital setting underwent emergent or urgent operation and this accounted for 87% of deaths and most morbidity. Mortality in elective procedures was 8%. Based on this data, we believe that thoracoabdominal aneurysm resection can be reasonably undertaken in a community-type hospital.

Spontaneous dissection of the infradiaphragmatic abdominal aorta is a rare form of aortic dissection. Its natural history and management are not well defined. We have recently treated five patients with spontaneous aortic dissection. Two patients had acute dissections and three had chronic dissections. Three patients developed saccular aneurysms and underwent resection. Two patients had stable dissections and were treated medically. All patients are alive and well at 6 months to 5 years. We think that spontaneous aortic dissection can be treated as a variant of type III dissection with initial medical management, reserving surgery for those patients in whom a saccular aneurysm or a complication of the dissection develops.

The effect of descending thoracic aortomyoplasty using conditioned latissimus dorsi muscle on cardiac output in five mongrel dogs with pharmacologically induced congestive heart failure was evaluated. A neurovascular left latissimus dorsi flap was lifted and through a left thoracotomy placed around the proximal descending thoracic aorta. The flap was conditioned for 4-6 weeks with a neurostimulator using the following parameters: amplitude 0.5 V, pulse width 210 microseconds and frequency 2 Hz. The neurostimulator was then removed and a cardiomyostimulator inserted and programmed to burst-stimulate the muscle during diastole. Baseline measurements of central venous pressure, heart rate, mean arterial blood pressure, pulmonary capillary wedge pressure, and cardiac output were obtained with the cardiomyostimulator off and on (study 1). Heart failure was induced with a combination of propranolol and verapamil, and measurements again taken with the stimulator off and on. The neurostimulator was reimplanted to continue stimulation of the latissimus dorsi muscle, and another set of measurements taken at 6 weeks with the cardiomyostimulator off and on (study 2). Counterpulsation in control conditions (before cardiac failure) in both studies demonstrated no significant increase in cardiac output. However, mean(s.d.) cardiac output was significantly (P < 0.1) increased by muscle stimulation in dogs with heart failure (study 1: from 2.39(1.10) to 3.14(1.41)l/min; study 2: from 1.89(0.64) to 2.38(0.57)l/min). There was no significant difference in the increase in cardiac output associated with muscle stimulation between studies 1 and 2. The results indicate that the model can increase cardiac output in heart failure and that this improvement is constant over a 4-6 week period, suggesting that muscle fatigue may not occur.

This study attempted to evaluate the efficacy of chronic extra-aortic counterpulsation with a latissimus dorsi neuro vascular flap. Five dogs had a preliminary procedure consisting of the creation of a latissimus dorsi flap and a thoracotomy in which the flap was wrapped around the descending aorta just distal to the left subclavian artery. An epicardial lead was placed on the left ventricle and a nerve stimulating lead placed around the thoraco-dorsal nerve. Three weeks later, both leads were connected to a cardiomyostimulator programmed to function in a counterpulsation mode with a 1:2 assist frequency. Hemodynamic measurements were made at 6 and 8 and 10 and 12 weeks and the dogs were sacrificed. Three dogs had all sets of hemodynamic measurements made. Two of the three dogs demonstrated diastolic augmentation at 6 and 8 and 10 and 12 weeks average 20 to 25 mmHg. The third dog failed to demonstrate any change. All dogs were sacrificed at 12 weeks and specimens were submitted for histologic evaluation. The muscle flap was preserved in all animals. The aorta subjacent to the flap showed, (1) normal intima with no evidence of disruption or thrombus in all animals, (2) in the animals in whom counterpulsation was observed, there appeared to be thinning of the media in the aorta subjacent to the muscle flap, and (3) no evidence of distal emboli. This study demonstrated that chronic counterpulsation can be obtained with a latissimus dorsi flap. The actual hemodynamic benefits are not determined from this study. The medial thinning in the aortic wall may limit the long-term benefit of this procedure.

The aim of this study was to evaluate the hemodynamic effects of extraaortic counterpulsation with a latissimus dorsi (LD) neurovascular flap in a canine heart failure model. Five dogs (8-18 kg) had a left LD neurovascular muscle flap raised. The muscle was brought into the chest through the second interspace and wrapped around the aorta. Parameters studied were heart rate (HR), systolic pressure (SP), diastolic pressure (DP) pulmonary artery pressure (PAP), mixed venous oxygen saturation (MVO2), and cardiac output (CO). Baseline measurements were obtained with the muscle nonstimulated and stimulated by a prototype burst stimulation. The only parameter that changed significantly with muscle stimulation was DP (55.8 +/- 3.8 mmHg to 72.4 +/- 4.8 mmHg, p less than 0.05). Propranolol (3-4 mg/kg) and verapamil (2-3 mg) were given intravenously to induce heart failure. Mean blood pressure decreased from 64.12 +/- 5.03 mmHg to 43.3 +/- 9.28 mmHg (p less than 0.05). Repeat measurements were obtained. With stimulation of the muscle flap there was an increase in DP from 36.8 +/- 9.2 mmHg to 55.4 +/- 19.3 mmHg (p less than 0.05). Although CO increased from 8% to 18% in all animals (1.42 +/- 0.33 L/mm to 1.58 +/- 0.34 L/mm) this did not reach statistical significance. This data indicates that both DP and CO can be improved by this method of cardiac assist in a heart failure model.

Changes in atrial adenosine triphosphate (ATP) and the presence of postoperative arrhythmias were studied in 14 patients during routine coronary artery bypass grafting to 1) attempt to evaluate atrial preservation, and 2) determine if a relationship exists between changes in ATP and the development of postoperative arrhythmias. Atrial biopsies were obtained at the time of cannulation (preischemic sample) and after the removal of the aortic crossclamp (postischemic sample). Methods of myocardial protection included systemic hypothermia (28 degrees C), periodic reinfusion of crystalloid cardioplegia into the aortic root and completed vein grafts, and iced slush in the pericardial well. Atrial temperature was monitored. Preischemic ATP was 0.412 +/- 0.32 mu mol/gm, and the postischemic value was 0.220 +/- 0.13 mu mol/gm (p less than .02). Atrial temperature routinely decreased to 13-18 degrees C after cardioplegic infusion but rose to 24 degrees C between infusions. There was no correlation between postoperative supraventricular arrhythmias (4 patients) and changes in ATP. In conclusion, routine coronary artery bypass grafting with standard methods of cardiac preservation does not appear to satisfactorily preserve atrial tissue. The clinical correlation and significance of this remains to be elucidated.