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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

A consistently effective transvenous defibrillation system for use in automatic defibrillators could significantly alter the approach to patients at risk of sudden death. Transvenous defibrillation systems that use a right ventricular (RV) electrode only or an RV electrode in combination with a chest patch are relatively inefficient at applying current to the posterolateral left ventricle. An RV electrode combined with a coronary sinus (CS) electrode, however, may improve current distribution to the posterolateral left ventricle. The purpose of this investigation, therefore, was to evaluate the effectiveness and safety of a specially designed transvenous lead system with a CS electrode capable of current delivery to this relatively inaccessible region of the heart. In 20 survivors of cardiac arrest, we determined defibrillation efficacy immediately before defibrillator surgery for monophasic pulses delivered between an RV catheter electrode and a CS catheter electrode system and compared these findings with an RV catheter electrode-thoracic patch defibrillation system. Subsequently, we referenced the efficacy of both transvenous systems to an epicardial patch electrode system at the time of defibrillator implantation. The mean delivered-energy defibrillation threshold for the CS-RV electrode system was 17.5 +/- 7.9 J, which was substantially lower than the RV electrode-thoracic patch system (25.6 +/- 11.4 J, p = 0.0016 [46% more]). Defibrillation threshold voltage was 529 +/- 123 V for the CS-RV electrode system and 647 +/- 164 V (22% more) for the RV electrode-thoracic patch system (p = 0.0013).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

We obtained information from 677 cardiac surgeons in the United States on the type of practice, case load, and techniques currently used for coronary bypass operations. These surgeons collectively performed 93,000 bypass operations in 1979. Less than 25% of these procedures were done in university or federal hospitals; the majority were performed in the private sector by surgeons engaged in a single specialty group practice. The mean case load in 1979 was 137 operations per surgeon, and only 46 (6.8%) did fewer than 25 bypass operations during that year. These surgeons devote a relatively small percentage of their professional activity to other areas in thoracic surgery-the majority do not perform congenital heart surgery and two thirds devote less than 10% of their professional activity to general thoracic surgery. Compared with our previous national survey done in 1975, techniques used for bypass grafting have changed considerably over the past 5 years. An increasing number of surgeons conduct cardiopulmonary bypass with an arterial input line introduced into the ascending aorta and with a single cannula for venous drainage and do not routinely vent the left ventricle. Cold chemical cardioplegia has become the technique of choice (by 91% of surgeons) for myocardial protection, sequential bypass grafts are now widely employed, and 83.2% of surgeons perform all distal anastomoses during a single period of cardioplegic arrest.

We compared two methods of delivering single damped sine-wave defibrillator pulses to the coronary sinus orifice in 20 dogs. Ten dogs had "unipolar" (coronary sinus to precordial disc) and 10 had "bipolar" (coronary sinus proximal to coronary sinus distal electrode) discharges. Delivered voltage, current, and energy were recorded during each pulse. Electrophysiologic testing was done before and 4 weeks after the procedure. Histologic examination of the atrioventricular groove was done at 1 mm serial sections. For the unipolar configuration a 200 J defibrillator pulse resulted in a peak voltage of 3370 +/- 125 V, a peak current of 21 +/- 4 A, and a delivered energy of 253 +/- 29 J as compared with 3010 +/- 99 V, 70 +/- 4 A, and 144 +/- 18 J, respectively, for the bipolar configuration (p less than .001). Three dogs (two with bipolar, one with unipolar pulses) had gross coronary sinus rupture and died from acute pericardial tamponade. In addition, irrespective of electrode configuration, all dogs showed microscopic rupture of the coronary sinus internal elastic membrane. Transmural atrial scarring occurred in all 10 dogs that received a unipolar pulse but in only two dogs that received a bipolar pulse (p = .0004). Unlike the atrium, injury to the left ventricle was limited in both groups. Similarly, injury to the periannular myocardium was inconsistent and not transmural in either group. No significant electrophysiologic changes were observed. With the present technique, unipolar rather than bipolar catheter-mediated defibrillator pulses result in transmural atrial injury that might prevent accessory pathway conduction. Regardless of electrode configuration, high-energy defibrillator pulses consistently cause some degree of coronary sinus rupture, most likely related to a barotraumatic mechanism.

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.

The effect of electrode polarity on defibrillation thresholds in humans is unknown. This prospective, randomized evaluation of electrode polarity on defibrillation thresholds was performed in 21 survivors of ventricular fibrillation (VF) undergoing cardiac surgery. Defibrillation was always performed with 2 identical large rectangular, wire mesh electrodes positioned over the anterior wall of the right ventricle and the posterolateral wall of the left ventricle. The initial electrode polarity for the left ventricular (LV) electrode was chosen randomly for determination of the defibrillation threshold. Subsequently, electrode polarity was reversed. The defibrillation threshold was defined as the lowest pulse amplitude that would effectively terminate VF with a single discharge delivered 10 seconds after initiation of an episode of VF with alternating current. For each defibrillation pulse, voltage, current, resistance and delivered energy were recorded. Of the 21 patients, 15 (71%) had a lower defibrillation threshold when the LV electrode was positive, 2 patients (10%) had a lower defibrillation threshold when the LV electrode was negative and 4 patients (19%) had equal defibrillation thresholds (within 0.5 J) regardless of polarity. The mean leading edge defibrillation threshold voltage was 370 ± 88 volts when the LV electrode was negative and 320 ± 109 volts (14% less) when the LV electrode was positive (p = 0.014). Mean leading edge defibrillation threshold current was 9.3 ± 3.1 amps when the LV electrode was negative compared to 7.7 ± 3.1 amps (17% less) when the LV electrode was positive (p = 0.0033). There were no differences in resistance with the 2 configurations. The delivered energy defibrillation threshold was 10.1 ± 4.5 J when the LV electrode was negative and 7.8 ± 4.8 J (23% less) when the LV electrode was positive (p = 0.016). Thus, in most patients, the defibrillation threshold is lower when the LV electrode is positive.

Sixteen survivors of cardiac arrest underwent intraoperative comparison of the effectiveness of sequential-pulse and single-pulse defibrillation. Defibrillation was tested alternately with the single-pulse or sequential-pulse technique 10 seconds into an episode of ventricular fibrillation that was induced with alternating current. The sequential-pulse defibrillation technique using truncated exponential pulses was performed with a right ventricular endocardial catheter and a left ventricular epicardial patch electrode. The first pulse was delivered between the right ventricular apical and the superior vena caval electrode on the right ventricular endocardial catheter. The second pulse was delivered between the right ventricular apical electrode and the left ventricular patch electrode 0.2 ms after termination of the first pulse. Single-pulse defibrillation was performed with a standard intracardiac defibrillation system in which a single truncated exponential pulse was delivered across 2 epicardial patch electrodes positioned over the anterolateral right ventricle and the posterolateral left ventricle. During defibrillation threshold determination, voltage and current waveforms were recorded and integrated to determine delivered energy. Average defibrillation threshold leading-edge voltage for the sequential pulse technique was 496 +/- 140 V, compared with 365 +/- 157 V for the single-pulse technique (p less than 0.005). Defibrillation threshold leading-edge current for the sequential-pulse technique was 6.0 +/- 2.3 A, compared with 10.6 +/- 5.1 A for the single-pulse method (p less than 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)

In an effort to describe the immediate course of pulmonary hypertension following mitral valve replacement, we reviewed preoperative and postoperative data from 62 patients who underwent mitral valve replacement Patients were divided based on the absence (Group I) or presence (Group II) of severe preoperative pulmonary hypertension, defined as a mean pulmonary artery pressure ≥40 mm Hg. Group II patients were subdivided based on the absence (Group IIa) or presence (GroupIIb) of markedly elevated preoperative pulmonary vascular resistance indices, defined as a ≥700 dynes · sec · cm-5 · m2. Pulmonary artery wedge pressures fell promptly following mitral valve replacement in all groups, but the course of other hemodynamic parameters varied among groups. Cardiac index increased significantly among Group I and IIb patients but not among Group IIa patients. Group I patients did not have significant changes in mean pulmonary artery pressure and pulmonary vascular resistance index. Group IIa patients had substantial reductions in mean pulmonary artery pressure while pulmonary vascular resistance index remained near 400 dynes · sec · cm-5 · m2. Group IIb patients had substantial reductions in mean pulmonary artery pressure while pulmonary vascular resistance index fell significantly to about 400 dynes · sec · cm-5 · m2. Primary valvular lesion and pharmacologic support were insignificant variables. Data from these hemodynamic groups suggest that at least three mechanisms contribute to the pulmonary hypertension seen in mitral valve disease: passive transmission of elevated left atrial pressures, reactive pulmonary arteriolar vasoconstriction, and morphologic changes in the pulmonary vasculature. The first two mechanisms appear to be rapidly reversed following mitral valve replacement. While others have described the regression of pulmonary hypertension several months following mitral valve operations, data presented here suggest that changes in pulmonary artery pressures and pulmonary vascular resistance index may occur much earlier.

Nineteen patients with posterior accessory pathways and disabling, refractory arrhythmias, underwent catheter ablation using standard defibrillator pulses at energy settings of 150 to 400 J. Accessory pathway ablation was successful in 13 of 19 (68%). Effective catheter ablation correlated with local ventriculoatrial (VA) intervals determined from the coronary sinus catheter at the site of earliest retrograde atrial activation during orthodromic reciprocating tachycardia. In 12 of the 13 successfully ablated patients, the local VA interval was less than 80 ms. In 4 of the 6 unsuccessfully treated patients, the local VA interval was greater than or equal to 80 ms, p less than 0.01. Transient abnormalities noted with the procedure included sinus bradycardia (3 patients), atrioventricular block (5), accelerated junctional rhythm (3), ectopic atrial tachycardia (2), myocardial depression (1), "ischemic" appearing T-wave inversions (10) and hemodynamically insignificant small pericardial effusions (5) Creatine kinase-MB increased from 3 +/- 2 U/liter to 26 +/- 18 U/liter (p less than 0.001), 4 to 8 hours after ablation. In addition, electrical shorts occurring during the ablation procedure in 2 patients were identified and corrected only with oscilloscopic monitoring of voltage and current waveforms. Significant adverse sequelae were seen in 4 patients. Three patients required sternotomy for control of cardiac tamponade secondary to a ruptured coronary sinus and 1 patient had a small posterior left ventricular infarction related to spasm of a right coronary artery extension branch. Coronary sinus rupture correlated with the ratio of catheter diameter to coronary sinus diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular node reentry tachycardia is a common type of supraventricular tachycardia. Rarely is it incapacitating and refractory to drug therapy, but when it is, the only option in therapy until recently has been atrioventricular node ablation or antitachycardia pacemaker insertion. The purpose of this paper is to review the case histories of four patients in whom we have surgically abolished atrioventricular node reentrant tachycardia while intentionally preserving atrioventricular node conduction. All four patients had atrioventricular node reentrant tachycardia confirmed by electrophysiologic study as diagnosed by established criteria. One patient had a left posterior atrioventricular accessory pathway, in addition to atrioventricular node reentrant tachycardia. All patients underwent intraoperative epicardial and endocardial mapping. Direct surgical dissection of the atrioventricular node node was performed in all four patients during normothermic cardiopulmonary bypass. Early and late postoperative electrophysiologic studies were used to evaluate the success of the surgical dissection. None of the patients had any evidence of dual atrioventricular node pathways or spontaneous or inducible atrioventricular node reentrant tachycardia postoperatively. At last follow-up (15 weeks to 21 months postoperatively), all patients were free from arrhythmias and cardiac medications, all were in normal sinus rhythm, and all had a subjectively improved life-style. This technique of direct surgical dissection of the atrioventricular node during normothermic cardiopulmonary bypass has allowed for complete cure of atrioventricular node reentrant tachycardia, while maintaining normal atrioventricular node function in these four patients.

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.

Prostacyclin (PGI2) infusion was studied in patients during cardiopulmonary bypass for coronary artery bypass grafting to assess its capacity to protect platelet hemostatic function. Twelve patients received PGI2 at doses ranging from 20 to 70 ng/kg/min by continuous infusion directly into the bubble oxygenator. Nine control patients were also studied. Platelet counts were not different in the two groups; the platelet count at the completion of the operation was decreased by a mean of 29% in treated patients and 40% in control patients (p > 0.15). Bleeding times were uniformly greater than 30 minutes following 30 minutes on bypass in both groups (p > 0.5). Also there was no difference in the bleeding times between the treated and untreated groups in the immediate postbypass period (p > 0.05). In addition, no difference in transfusion requirements was observed between the treated and control groups. However, plasma levels of platelet factor 4 were lower in the treated patients (p

The risk of coronary arteriography is considerably increased in patients who have left main coronary artery stenosis (LMCAS). Among 1,060 patients undergoing coronary arteriography over a three-year period, 83 were found to have LMCAS and three of these patients died (3.6 percent) during or shortly after the arteriographic procedure. Bypass surgery, however, can now be carried out at a very low risk irrespective of the degree of coronary disease present--there was no hospital mortality in 74 patients with LMCAS undergoing bypass surgery at our institution during this period. In addition to careful attention to detail, techniques that can minimize the risk of both of these procedures in patients with LMCAS include invasive hemodynamic monitoring and various pharmacologic manipulations to prevent myocardial ischemia. In a small percentage of patients, rest angina may prove refractory to inhospital medical treatment, and intraaortic balloon pumping may be necessary to stabilize the conditions of these patients before proceeding with arteriography and myocardial revascularization.

In a series of 12 dogs, the electrophysiologic and histologic effects of a single damped sine-wave shock delivered via standard electrocatheters to the region of the coronary sinus orifice were investigated. Six dogs received 200 J and six received 360 J of stored energy. The shock was delivered to two consecutive proximal poles of a standard quadripolar catheter positioned at the coronary sinus orifice and connected to the positive output (anode) of a defibrillator. A disc electrode positioned on the anterior chest wall served as the cathode (negative pole). During the shock, voltage and current were recorded. Electrophysiologic testing was done before and 4 weeks after the shock. At 4 weeks, animals were killed and serial sections of the atrioventricular groove and conduction system were performed. No significant long-term change in atrioventricular conduction, spontaneous or induced atrial or ventricular arrhythmias was observed. However, transient atrioventricular block was seen in five and idioventricular rhythms in six animals in the short term. No persistent electrocardiographic changes were observed, and no sudden deaths occurred. Microscopically, transmural injury at the anulus proper or basilar ventricular epicardium was inconstant and infrequent. However, transmural atrial injury at the level of the coronary sinus was produced over a 10 +/- 5 mm length with the 200 J shock and a 21 +/- 6 mm length with the 360 J shock. Neither coronary artery injury nor damage to the conduction system was seen and cardiac tamponade did not occur. However, localized intramural atrial rupture of the coronary sinus wall (on the endocardial aspect only) was observed in each dog, consistent with barotrauma. With the present technique, atrial injury potentially capable of blocking the effects of accessory pathway conduction could be produced without other electrophysiologic alterations or complications. Injury to the anulus proper (and therefore to any accessory pathway per se) is probably unlikely. Barotrauma may play a significant role in the type of injury observed in this study.

This study evaluated the ability of 24 new standard tripolar and quadripolar U.S. Catheter Instruments catheters to withstand a single damped sinusoidal shock delivered by a standard defibrillator. The schema for energy delivery was meant to simulate possible clinical practices. Delivered peak voltage and current were measured during each shock. Each electrode was examined for pitting and changes in line resistance as a consequence of the shock. Electrode pitting occurred on all selected anodal poles. However, it also was found on “unsolicited” electrodes from 7 catheters, indicating that current had followed unanticipated routes. Electrode line resistance was unmeasurable in 6 of these 7 inappropriately pitted electrodes. Delivered peak voltage and postshock catheter dielectric strength depended on the manner of energy delivery. To simulate a posterior septal accessory pathway ablation procedure, a shock was delivered to 2 proximal (anodal) poles in 16 quadripolar catheters (8 received 200 J and 8 received 360 J). Delivered peak voltage was 3, 125 ± 362 V for the 200-J shock and 4,100 ± 160 V for the 360-J shock. Postshock catheter dielectric strength for the 200- and 360-J shock was 1,425 ± 826 V and 601 ± 707 V, respectively. This was significantly lower than peak delivered voltage (p To simulate His bundle or ventricular tachycardia focus ablation, 8 tripolar catheters each received a single 200-J shock to the tip electrode. This resulted in a delivered peak voltage of 2,900 ± 351 V, compared with a postshock dielectric strength of 1,325 ± 1,320 V (p It is concluded that standard catheters cannot control current flow adequately during a single high-energy shock because of inadequate dielectric strength. After the first shock an already inadequate dielectric strength deteriorates and increases the likelihood of current leakage with each subsequent shock.

A total of 116 patients undergoing coronary revascularization were randomized preoperatively in a double-blind manner to receive 80 mg daily of propranolol or placebo in the postoperative period. Preoperatively, all patients had been receiving at least 80 mg of propranolol a day to the time of the operation. In addition, all patients had a left ventricular ejection fraction of 0.4 or more, no history of supraventricular tachyarrhythmia (SVT), and no need of digitalis preparations or other antiarrhythmic drugs. All patients were monitored for 5 days and propranolol or placebo was started 24 hours postoperatively. SVT was documented with biatrial electrograms in all cases. Study groups were similar in postoperative creatine kinase MB levels and postoperative weight gain, but the placebo group tended to be older and have more grafts per patient. Seven patients randomized were dropped from the study, two with perioperative infarction, four with persistent ventricular arrhythmias necessitating quinidine or procainamide, and one with persistent postoperative hypotension (placebo). There were no significant differences in the incidence of postoperative SVT in these two groups: 13.2% in the propranolol group and 16.1% in the placebo group. We conclude that 80 mg daily of propranolol given postoperatively to patients undergoing coronary revascularization does not effectively reduce the incidence of SVT.

Seventy patients having aortocoronary vein bypass grafting surgery for angina pectoris underwent preoperative invasive exercise testing to symptom limits and again 6 to 14 months postoperatively. Cardiac output was measured using the direct Fick principle. Postoperatively at maximal exercise, there was a 3.11 liters/min (p less than 0.0001) increase in cardiac output in men (n = 61) and a 2.04 liters/min (p less than 0.01) increase in women (n = 9). Patients with complete revascularization showed a significantly greater improvement in cardiac output postoperatively than did those with incomplete revascularization (26 versus 6%, p less than 0.0001). The major reason for the increased maximal cardiac output was a marked increase in heart rate while stroke volume was maintained at the same preoperative level. These findings were true irrespective of preoperative use of beta-adrenergic blocking drugs.

The optimal approach to patients undergoing coronary bypass surgery for coronary artery disease with coexisting carotid disease is controversial. To determine the best approach to these patients, we screened carotid arteries in patients undergoing coronary artery bypass preoperatively with noninvasive ultrasonic duplex scanning. No correlation was noted between stroke and asymptomatic carotid disease in patients undergoing coronary revascularization. Prospective application of this finding in 2251 patients has yielded a very low incidence of perioperative stroke. We concluded that asymptomatic carotid arterial disease is not a significant risk to patients undergoing cardiopulmonary bypass and should be managed conservatively.

The occurrence of stroke associated with coronary artery bypass operations is approximately 2%. In an attempt to reduce this incidence some centers have proposed carotid thromboendarterectomy for symptomatic and asymptomatic carotid arterial disease in patients undergoing a coronary artery bypass operation. To obtain a better understanding of the incidence of carotid occlusive disease in candidates for the coronary bypass operation and to evaluate the practical use of a noninvasive method to screen patients preoperatively, we evaluated 102 patients preoperatively with an ultrasonic Duplex scanner; 24 studies were requested on the basis of either previous neurologic problems or the presence of a bruit and 78 patients were evaluated as part of a study protocol. In the unrequested group 6% (5/78) of the patients had a stenosis of 50% diameter reduction or more. In the requested group 54% (13/24) had a stenosis of 50% diameter reduction or more. In the postoperative phase one stroke and one transient ischemic attack were noted among the unrequested group and none in those suspected of having carotid disease on clinical grounds. Neither affected patient had a high-grade stenosis. There is little evidence to support the contention that noninvasive screening of patients free of symptoms or signs of carotid disease prior to coronary artery bypass operation is a valuable method of screening for patients who will sustain a focal neurologic event.

To assess the efficacy of surgical revascularization for postinfarction angina within 30 days of acute infarction, the clinical course of 103 patients treated surgically from January 1979 to July 1982 was reviewed. There were 84 men (82%) and 19 women (18%) with a mean age of 58 years (range 34 to 80). Group A (11 patients) underwent surgery within 24 hours of infarction, Group B (21 patients) within 7 days and Group C (71 patients) within 30 days. Eighty-four patients (82%) had subendocardial infarctions and 19 patients (18%) had transmural infarction. Transmural infarction was more common in patients in Group A (36%) than in those in either Group B (19%) or Group C (15%). There were two deaths, both in Group C (1.9%), within 30 days of surgery. The use of intraaortic balloon or inotropic support and the occurrence of major arrhythmias or perioperative infarction was noted in 30 patients (29%)(64% in Group A, 33% in Group B and 18% in Group C). The average time in the intensive care unit was 3.2 days, with an average total hospital stay after surgery of 8.3 days. Late follow-up (mean 15.4 months, range 1 to 39) is complete for 97 patients (97%). There were no late myocardial infarctions and 93 patients (96%) were essentially free of angina. The only late death (1.0%) was caused by septicemia from delayed sternal wound infection. This study suggests that myocardial revascularization within the first 30 days after myocardial infarction can be accomplished with an acceptable operative mortality in selected patients with postinfarction angina refractory to medical management.

The effect of initially ineffective defibrillation pulses on subsequent defibrillation success is not known. Therefore, the voltage, current and energy at the defibrillation threshold were compared with the defibrillation rescue pulse voltage, current and energy that terminated ventricular fibrillation when an ineffective pulse just below the defibrillation threshold had been used initially. This lower amplitude ineffective pulse was termed a “subdefibrillation threshold” pulse. The pulse that restored sinus rhythm after the subdefibrillation threshold pulse was delivered was termed the “subdefibrillation threshold rescue pulse.” This comparison was undertaken, intraoperatively, in 14 out-of-hospital cardiac arrest survivors using a sequential-pulse catheter-patch defibrillation system. Each of the 14 patients required higher voltage, current, delivered energy and stored energy for defibrillation with the subdefibrillation threshold rescue pulse than with the defibrillation threshold pulse. The defibrillation threshold voltage was 451 ± 127 volts compared with a subdefibrillation threshold rescue voltage of 585 ± 147 volts (p < 0.00002). The defibrillation threshold current was 5.5 ± 2.4 amps compared with a subdefibrillation threshold rescue current of 7.2 ± 2.7 amps (p < 0.00001). Delivered and stored energies were 10.9 ± 7.4 and 12.3 ± 7.2 J, respectively, for the defibrillation threshold pulse and were 17.6 ± 9.4 J (p < 0.00002) and 20.5 ± 9.3 J (p < 0.00005), respectively, for the sub-defibrillation threshold rescue pulse. It is concluded that the risk of requiring considerably higher energies than anticipated for defibrillation must be incurred, should defibrillation fail because of an initially insufficient defibrillation pulse. Such an occurrence might result in death should the energies necessary for defibrillation exceed the output limits of the implantable device.

Sixteen out-of-hospital survivors of ventricular fibrillation underwent a prospective, randomized, intraoperative comparison of sequential pulse and single pulse defibrillation with use of two distinct electrode systems and waveform shapes currently available for clinical use. Defibrillation was tested alternately with either the single pulse or the sequential pulse system 10 s into an episode of ventricular fibrillation. Sequential pulse defibrillation was performed with two 4 ms truncated exponential pulses of constant duration delivered to three equally spaced oval epicardial patch electrodes composed of concentric coils. The posterior left ventricular electrode served as the common cathode. The first anode was over the anterior right ventricle and the second anode was over the anterior left ventricle. Single pulse defibrillation was performed with the standard intracardiac defibrillation system with use of a single truncated exponential pulse with a fixed 65% tilt delivered across two rectangular, wire mesh epicardial patch electrodes positioned over the anterior right ventricle and posterolateral left ventricle. During defibrillation threshold determination, voltage and current waveforms were recorded and used to determine pulsing resistance and delivered and stored energy. Average defibrillation threshold leading edge voltage for the single pulse technique was 273 ± 101 V compared with 246 ± 67 V (11% less) for the sequential pulse technique (p = 0.136). Defibrillation threshold leading edge current for the single pulse technique was 6.7 ± 2.5 A compared with 5.2 ± 1.7 A (29% less) for the sequential pulse method (p = 0.005). The defibrillation threshold delivered energy was 5.6 ± 4.0 J for the single pulse technique and 3.5 ± 1.8 J (38% less) for the sequential pulse technique (p = 0.021). The defibrillation threshold stored energy for the single pulse technique was 6.3 ± 4.3 J compared with 4.0 ± 2.0 J (37% less) for the sequential pulse technique (p = 0.013). In survivors of cardiac arrest, the clinically available sequential pulse three electrode defibrillation system is at least as viable as the standard single pulse two electrode system for defibrillation of the heart. In some individuals, the sequential pulse system utilizes substantially lower current and energy to defibrillate than does the single pulse system.

Catheter mediated electrical ablation of posterior septal accessory pathways is appealing not only because of the opportunity to avoid a sternotomy but also because posterior septal accessory pathways are recognized as the most difficult type of accessory pathway to ablate surgically [1]. Previous work has documented that catheter mediated electrical ablation of posterior septal accessory pathways is, indeed, clinically feasible although with variable success [2–8]. The purpose of this chapter is to review our work investigating the histologic effects of single, damped sine wave defibrillator pulses on the canine proximal coronary sinus (CS) in order to gain insight into the factors leading to success or failure of the technique for posterior septal accessory pathway ablation in man [9–12].

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.

During a 30-month period, 51 patients underwent mitral valve replacement. There were 3 hospital deaths (5.9%), 2 of which were due to ventricular rupture. The 3 patients who died were among 13 patients in whom mitral valve replacement was combined with tricuspid or aortic valve operation or both. Postmortem findings in the 2 patients who died of ventricular rupture showed that the ventricular tears were located between the atrioventricular groove and the unresected papillary muscle stumps, in an area of ventricle formerly tethered by the posterior chordae tendineae. In the last 14 patients in the series, the posterior leaflet of the mitral valve and its chordae tendineae were left intact, and there was no mortality or prosthetic valve dysfunction. In patients with myxomatous or ischemic disease, the posterior leaflet was left completely intact. For patients with fibrocalcific rheumatic disease, we have developed a technique of partial excision and debridement of the posterior leaflet, preserving the intermediate and basal chordae tendineae attachments. With the techniques described, preservation of all or part of the posterior leaflet and its chordae tendineae does not appear to interfere with prosthetic valve function and, by reducing the risk of ventricular rupture, should enhance survival after mitral valve replacement.

The effect of ventricular fibrillation duration in humans on defibrillation efficacy as it pertains to the time of intervention of an automatic implantable defibrillator is unknown. If a difference in defibrillation efficacy exists in the early period after ventricular fibrillation onset, it may affect algorithms used by antiarrhythmic devices for arrhythmia detection and therapy. Therefore, a prospective, randomized evaluation was performed of the effect of ventricular fibrillation durations of 10 s and 20 s on defibrillation thresholds in 10 survivors of sudden cardiac arrest undergoing implantation of an automatic cardioverter defibrillator. The initial duration of ventricular fibrillation was chosen randomly. Subsequently, each patient served as his or her own control for the alternate duration of ventricular fibrillation to that chosen initially. The mean leading edge defibrillation threshold voltage was 411 ± 114 V when ventricular fibrillation persisted for 10 s and 419 ± 125 V when it persisted for 20 s (p = 0.73). The mean defibrillation threshold current was 11.4 ± 2.8 A when ventricular fibrillation persisted for 10 s and 11.4 ± 3.2 A when it persisted for 20 s (p = 0.97). The delivered energy defibrillation threshold was 11.5 ± 5.9 J when ventricular fibrillation persisted for 10 s and 12.0 ± 6.9 J when it persisted for 20 s (p = 0.67). These findings show that the defibrillation threshold does not change between 10 and 20 s of ventricular fibrillation in out-of-hospital survivors of cardiac arrest at the time of surgical implantation of an automatic defibrillator. The data may have influence on the programming of defibrillator detection algorithms.

Biphasic waveforms have been suggested as a superior waveform for ventricular defibrillation. To test this premise, a prospective randomized intraoperative evaluation of defibrillation efficacy of monophasic and biphasic waveform pulses was performed in 22 survivors of out of hospital ventricular fibrillation who were undergoing cardiac surgery for implantation of an automatic defibrillator.The initial waveform used in a patient for defibrillation testing, either monophasic or biphasic, was randomly selected. Subsequently, each patient served as his or her own control for defibrillation testing of the other waveform. The defibrillation threshold was defined as the lowest pulse amplitude that would effectively terminate ventricular fibrillation with a single discharge delivered 10 s after initiation of an episode of ventricular fibrillation induced with alternating current. Each defibrillation pulse was recorded oscilloscopically, and defibrillation pulse voltage, current, resistance and stored energy were measured.Fifteen (68%) of the 22 patients had a lower defibrillation threshold with the biphasic pulse, 3 (14%) had a lower threshold with the monophasic pulse and 4 (18%) had equal defibrillation thresholds (within 1.0 J) regardless of waveform. The mean leading edge defibrillation threshold voltage was 317 ± 105 V when the monophasic pulse was used and 267 ± 102 V (16% less) when the biphasic pulse was used (p = 0.008). Mean leading edge defibrillation threshold current was 7.9 ± 3.7 A when the monophasic pulse was used and 6.8 ± 3.8 A (14% less) when the biphasic pulse was used (p = 0.051). There were no differences in system resistance with the two waveforms: the leading edge resistance for the monophasic pulse was 45.3 ± 17.5 and 44.1 ± 14.4 ω for the biphasic pulse (p = 0.183). The stored energy defibrillation threshold was 8.5 ± 6.1 J when the monophasic pulse was used and 6.3 ± 5.2 J (26% less) when the biphasic pulse was used (p = 0.028). These findings show that in the majority of patients, biphasic pulse defibrillation is more efficient than monophasic pulse defibrillation.

Some of the reported problems with the use of the automatic implantable defibrillator (AID) include inappropriate discharge, 1–3 failure to defibrillate because of excessively high defibrillation thresholds 3–5 and failure to sense ventricular fibrillation (VF) in patients who also have pacemakers. 1,2 In this report, we describe another potential problem: the failure of an AID to sense VF because of variable bipolar epicardial electrogram amplitudes during VF.

Pericardial patching to enlarge the right ventricular outflow tract is often required in congenital cardiac surgery in lesions such as tetralogy of Fallot, pulmonary atresia, pulmonary stenosis, and pulmonary artery repair following removal of a palliative pulmonary artery band. A method of simplifying the attachment of the pericardial patch onto the right ventricular outflow tract is described.

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