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We evaluated the hemodynamic effects of amiodarone on left ventricular (LV) function after global ischemia. Amiodarone was administered orally at 15 mg/kg/day for an average of 28 days to a group of 10 dogs. The concentration of amiodarone in serum and LV myocardium was 0.40 +/- 0.24 micrograms/ml and 44 +/- 27.0 micrograms/g, respectively. This experimental group and a control group of 10 dogs each underwent 120 min of aortic cross-clamping with cold crystalloid cardioplegia resulting in an average myocardial temperature of 15 degrees C. LV function measurements by pulse-transit sonomicrometry and Millar solid-state micromanometers were processed by a minicomputer. Compared to the nontreated control group, oral amiodarone for 28 days produced depression of LV contractility which was reflected by lower slope of the end-systolic pressure-volume relation (Evmax), percentage shortening of segment length, left ventricular pressure-segment length loop area, and slope of the end-systolic pressure-segment length relation (Esmax). After ischemia, percentage recovery of LV global function (Evmax and mean velocity of circumferential fiber shortening) and regional function (Esmax) was significantly better in the amiodarone group than in the control group. We conclude that oral amiodarone for 28 days results in a depression of LV contractility but the combination of amiodarone and ischemia does not act synergistically to further depress postischemic LV function.

Over the 3-year period from Jan. 1, 1986, through Dec. 31, 1988, we have implanted 101 automatic implantable cardioverter-defibrillators into patients with life-threatening ventricular arrhythmias. There were 82 male patients and 19 female patients. The mean age was 58 years with a range of 25 to 82 years. The indication for implantation was ventricular fibrillation in 89 patients and recurrent ventricular tachycardia in 12 patients. Seventy-seven patients had a history of prior myocardial infarction or coronary artery disease, or both. Eighteen patients had nonischemic cardiomyopathy. One patient had a prolonged QT syndrome and five patients had no evidence of preexisting structural heart disease. The mean injection fraction was 37% ± 17%. Forty-one of the automatic implantable cardioverter-defibrillator implantations were associated with procedures necessitating cardiopulmonary bypass. The hospital mortality rate was 4% and the morbidity rate was 15%. The only statistical difference between those patients who did and did not have postoperative complications was a history of a prior myocardial infarction (90% versus 54%, p

TABAYASHI, K., MCKEOWN, P.P., MIYAMOTO, M., LUEDTKE, A.E., THOMAS, R., BREAZEALE, D.G., MISBACH, G.A., ALLEN, M. and IVEY, T.D. Myocardial Preservation: A Comparison of Oxygenated Crystalloid and Blood Cardioplegia. Tohoku J. Exp. Med., 1990, 161 (3), 185-197-The purpose of this experiment was to compare myocardial protective effect after global ischemia using oxygenatedcrystalloid (CCcO2) and an oxygenated blood (BCcO2) cardioplegic solutions. Post-ischemic ventricular performance was studied in 2 equal (n=7) groups of dogs subjected to 120min of global ischemia induced at average myocardial temperatures of 8°C in the CCcO2 group and 18°C in the BCcO2 group. Left ventricular (LV) function included analysis of LV systolic function (global and regional function), LV diastolic function (chamber and myocardial stiffness) and LV relaxation was measured by sonomicrometry and Millar micrometers. Data were processed with a Dec PDP-11/23 computer. In vitro oxygen content (Vol%) measured 3.2±1.0 (CCcO2) and 9.5±0.3 (BCcO2). Percent recoveries of LV global function (LVSP, loop area, % shortening, LV dp/dt, mean VCF and E max) in the CCcO2 group were approximately the same as those in the BCcO2 group. There were no significant differences in LV regional function (loop area and % shortening) after ischemia between the two groups. The chamber and myocardial stiffness after ischemia in the CCcO2 group were almost the same as the baseline values. Values in the BCcO2 group were reduced significantly compared to the baseline level. There were significant differences in post-ischemic chamber and myocardial stiffness between the two groups. Post-ischemic maximum negative LV dp/dt in both groups decreased significantly compared to the baseline values. However, the time constant and diastolic interval after ischemia in both groups were approximately the same as the baseline values. We conclude that there were no significant differences in myocardial protective effect between the CCcO2 and BCcO2 groups, and both methods preserved the ischemic myocardium well.

The optimal management of patients with small aortic anulus or left ventricular outflow tract obstruction remains unclear. Between 1976 and March, 1982, 18 patients have undergone enlargement of their left ventricular outflow tract by means of the Konno or a modification of the Konno procedure. Fourteen of these 18 patients had previous operations for aortic stenosis or tunnel left ventricular outflow tract, and two patients had undergone three previous operations. All 18 patients had symptoms of either heart failure or chest pain, or had electrocardiographic evidence of strain. They ranged in age from 4 years to 58 years, with 13 of the 18 patients being less than 20 years of age. A Dacron patch was used to enlarge the left ventricular outflow tract after incising down the ventricular septum. In all patients, at least a 21 mm valve could be placed, with between 50% and 65% of the valve anulus being made up of natural tissue. The remaining portion of the valve anulus was constructed from the Dacron patch. The patch was extended up to enlarge the ascending aorta, and a pericardial patch was used to close the defect in the right ventricular outflow tract. In all 18 patients the gradient was obliterated at the time of operation. There was one early death in a patient who had previous insertion of a left ventricular apical-aortic conduit in which the heterograft valve had degenerated. There has been one late death because of bacterial endocarditis in a child who also had a parachute mitral valve and evidence of pulmonary hypertension. The remaining 16 patients are functioning well after the Konno procedure. Three are receiving warfarin sodium, and 13 are receiving aspirin. These results suggest that this is an acceptable method of treating patients with small aortic anulus or left ventricular outflow tract obstructions and would appear to have advantages over a left ventricular apical-aortic conduit.

To determine if the prophylactic administration of oral verapamil is effective in reducing the incidence of supraventricular tachycardia after myocardial revascularization, 141 patients were entered into a double-blind randomized trial. Seventy patients received verapamil 80 mg every 8 hours beginning immediately after operation and continuing for 5 days, and 71 patients received placebo. Patients were monitored during the study period and observed for the occurrence of supraventricular tachycardia. The verapamil and placebo groups were similar with regard to sex, age, preoperative antianginal drugs, number of bypass grafts, average bypass time, and average occlusion time. A total of 39 patients had supraventricular tachycardia, 20 were receiving verapamil, and 19 were receiving placebo. The average ventricular rate was 127 +/- 13 beats/min for the verapamil group with supraventricular tachycardia compared with 140 +/- 12 beats/min for the placebo group with the mean differences not significant (p = 0.10). On the basis of these data, it is concluded that verapamil 80 mg every 8 hours beginning early after myocardial revascularization is not effective in reducing the incidence of supraventricular tachycardia.

In general, it has been thought that pulmonary valve insufficiency is well tolerated when the valve is excised or when the pulmonary annulus has been widened with an outflow patch during repair of tetralogy of Fallot. However, when pulmonary regurgitation is massive or when it is combined with other causes of right ventricular failure, progressive right ventricular dilation may occur in some patients. Pulmonary valve replacement has not been commonly used in the past. From January, 1980, to August, 1982, 12 patients, 11 months to 17 years old, had pulmonary regurgitation treated by insertion of a valve in the pulmonary position 4½ months to 11 years after initial repair of tetralogy of Fallot. All patients had progressive right ventricular failure not responsive to medical management. There were no major outflow tract obstructions, residual ventricular septal defects, or persistent aortopulmonary shunts. All 12 patients underwent patch reconstruction of the right ventricular outflow tract that allowed placement of a larger valve. There have been no operative or late deaths, and each patient has had improvement in functional status. One patient required tricuspid valve replacement 1½ years after pulmonary valve replacement to achieve sustained relief of symptoms. Only 1 other patient required subsequent operation; this was for pacemaker lead changes. These early results suggest that in patients with right ventricular failure, attention should be directed to pulmonary regurgitation since this is a component of failure that is reversible; pulmonary valve replacement carries a low risk, and it can relieve symptoms and prevent further deterioration of right ventricular function.

Most reports of operations for ventricular arrhythmia have dealt with patients with anterior myocardial infarction. Patients with previous remote inferior myocardial infarction and recurrent ventricular tachycardia or fibrillation are a difficult subset of patients to treat with surgical ablative procedures. Over a 2 year period, 11 patients with prior inferior myocardial infarction and drug-refractory ventricular tachycardia or fibrillation underwent elective operation to control the arrhythmia. Five patients had monomorphic ventricular tachycardia. Three of these five patients had localized endocardial resection and/or cryoablative procedures when the ventricular tachycardia was well localized intraoperatively. In the remaining two patients, ventricular tachycardia was noninducible intraoperatively, and the patients underwent extensive endocardial resection and mitral valve replacement because of sites suspected near the posterior papillary muscle from preoperative catheter mapping. None of these five patients had inducible ventricular tachycardia postoperatively, and all are clinically free of the arrhythmia over a 24 month follow-up period. One patient with two morphologies of ventricular tachycardia previously had an unsuccessful blind endocardial resection. She underwent map-directed cryoablation of both sites of ventricular tachycardia. Postoperatively, the patient was free of inducible arrhythmia and has been asymptomatic over 8 months. Five patients had pleomorphic ventricular tachycardia or fibrillation that could not be electrically localized. One patient with ventricular fibrillation underwent extensive endocardial resection, but the posterior papillary muscle was spared. Postoperative electrophysiological study was positive. The patient has had no clinical ventricular arrhythmias on a regimen of amiodarone, however. Two patients had extensive endocardial resection and mitral valve replacement. One died early in the postoperative course and the other is clinically well. The remaining two patients had an encircling endocardial ventriculotomy. Both are clinically stable although one had inducible ventricular fibrillation postoperatively. We conclude that well-defined monomorphic ventricular tachycardia in patients with a previous inferior myocardial infarction can be successfully treated with localized endocardial resection and/or cryoablation. However, patients with poorly localized monomorphic ventricular tachycardia or pleomorphic ventricular tachycardia or fibrillation may require more extensive procedures. The role of posterior papillary muscle sacrifice with mitral valve replacement remains undefined. The exact procedure cannot be anticipated and depends on both the type of clinical arrhythmia and the surgical anatomy.

Twenty-three patients with bacterial endocarditis and mycotic aneurysms of the aortic annulus were treated between 1978 and 1985. There were 18 men and 5 women ranging from 24 to 72 years old. All patients had congestive heart failure and positive blood cultures as a complication of the endocarditis and were in New York Heart Association (NYHA) Functional Class III or IV. The aneurysm complicated late prosthetic valve endocarditis in 7 patients and native valve endocarditis in 16. The most common infecting organisms were streptococci (12 patients) and staphylococci (7 patients). The noncoronary sinus was the most frequent site for aneurysm formation. Following debridement of the abscess cavity, the orifice of the aneurysm was closed with a patch of Dacron in 20 patients and autologous pericardium in 3. A prosthetic valve (18 bioprosthetic and 5 mechanical) was secured to the noninfected portion of the native annulus and to the patch at the level of annulus. There were 3 deaths, 1 perioperative and 2 late, each without evidence of residual infection or aortic insufficiency. There are 20 late survivors (87%). After a mean follow-up of 1 year, all patients are in NYHA Functional Class I. Patch closure of mycotic aneurysms involving the aortic annulus permits aggressive debridement of the abscess cavity and affords closure of the orifice without tension. The prosthetic valve can be seated at the level of the native annulus, thus avoiding complicated reconstructive procedures of the aortic root and coronary arteries. This technique is an effective alternative in selected cases of mycotic aneurysms involving the aortic annulus.

Several investigators have demonstrated acute, reversible shifts in the position of the diastolic, left ventricular pressure-volume curve (1,2,3 4,5,6). Upward shifts tend to be associated with conditions that increase the load against which the heart ejects or conditions which decrease the capacity of the heart to meet that load. Downward shifts have followed administration of the pharmacologic vasodilators nitroglycerin or nitroprusside and are presumably associated with a more advantageous relation of the contractile capacity of the heart to the load presented by the circulation.

During a 31 month period, 1,433 consecutive patients undergoing cardiac procedures were screened for carotid bruit. A total of 94 patients with carotid bruit were identified who had ultrasonic carotid duplex scans. Nine patients had a history of transient ischemic attack, carotid bruit, and reduction in internal carotid artery diameter by ≥50% according to ultrasonic carotid duplex scanning. All nine patients underwent carotid angiography followed by thromboendarterectomy prior to or simultaneous with cardiopulmonary bypass. There was one neurological complication leading to death in this subset. Sixteen patients with asymptomatic carotid bruit had ultrasonic carotid duplex scanning revealing an internal carotid artery lesion of ≥50% but did not undergo arteriography or thromboendarterectomy prior to the cardiac procedure. Perfusion pressure was maintained at ≥70 mm Hg during bypass. There were no focal neurological events in this subset. Sixty-six patients with internal carotid artery stenosis of