The implanted defibrillator: relation of defibrillating lead configuration and clinical variables to defibrillation threshold.

Forty-two defibrillating lead systems for the automatic implantable defibrillator were implanted and tested in 41 patients. Two basic lead configurations were used: 1) spring-patch, consisting of a transvenous superior vena cava spring electrode as the anode and an apical or left lateral ventricular patch electrode (either small [13.9 cm2] or large [27.9 cm2]) as the cathode; and 2) patch-patch, consisting of an anterior right ventricular patch as the anode and a posterior left ventricular patch as the cathode. Of the 42 lead systems, 10 were spring-patch and 32 were patch-patch combinations. The defibrillation threshold for the patch-patch combinations (9.8 +/- 6.5 J, mean +/- standard deviation) was significantly (p less than 0.01) lower than that for the spring-patch combinations (19.1 +/- 10.3 J). Subgroup analysis revealed the lowest defibrillation thresholds for patch-patch combinations with at least one large patch. Total surface area of defibrillating leads was strongly negatively correlated with the defibrillation threshold (p less than 0.005). Analysis of the relation of clinical variables to defibrillation threshold revealed that only amiodarone therapy was independently associated with a significantly (p less than 0.05) higher defibrillation threshold. Thus, surface area of the defibrillating leads is a critical determinant of the defibrillation threshold for the implanted defibrillator. Patch-patch lead systems with at least one large patch may provide an increased safety margin for defibrillation. Conversely, amiodarone therapy is associated with higher defibrillation thresholds and may decrease the margin of safety.

Hemodynamic and hormonal abnormalities in canine aortic coarctation at rest and during exercise.

This study was designed to determine the hemodynamic and hormonal consequences of aortic coarctation at rest and during treadmill exercise. Twelve normal adult dogs served as controls. In eight dogs coarctation was created within 1 week of birth by banding the aorta just proximal to the ductus ligament, thereby fixing luminal diameter at 1 to 2 mm. Studies were performed 18 months after operation. Vascular pressures were monitored proximal and distal to the coarctation, cardiac output and regional blood flow were evaluated with radioactive microspheres and blood samples were collected for determination of hormone levels and blood gases. At rest, systolic pressure in the proximal aorta was 130 +/- 12 mm Hg (mean +/- SD) in the control group and 167 +/- 16 mm Hg in dogs with coarctation (p less than 0.01). During exercise at a level that doubled heart rate and cardiac index, mean aortic pressure increased by 11 and 31% (p less than 0.01) in the control and the coarctation group, respectively. Mean distal aortic pressure increased by 8% during exercise in control dogs but decreased by 29% in dogs with coarctation. Exercise decreased flow to the kidneys and the large intestine in the coarctation group. Plasma norepinephrine concentrations were greater in the coarctation group than in control dogs at rest; during exercise, plasma norepinephrine, epinephrine and renin activity increased in both groups, but to a greater degree in the group with coarctation. These results confirm an abnormality in renal and gut perfusion in experimental coarctation and suggest that this may be related to a decline in perfusion pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Infected left atrial myxoma with bacteremia simulating infective endocarditis.

A 58-year-old man had intermittent fever of eight months' duration following a dental extraction. There were no abnormal cardiac auscultatory findings. Multiple blood cultures yielded Streptococcus mutans. Treatment for infective endocarditis was initiated; however, an echocardiogram suggested the presence of a left atrial myxoma. The diagnosis was confirmed by angiography and the infected tumor was removed successfully. Differentiating features between left atrial myxoma and mitral valve endocarditis may not be obvious clinically, and bacteremia does not preclude atrial myxoma as a diagnostic possibility. We therefore suggest that all cases of infective endocarditis be evaluated by echocardiography to elucidate lesions such as large vegetations or left atrial myxoma, both of which may require urgent operative intervention.

Mitral valve prolapse requiring surgery. Clinical and pathologic study.

The clinical, hemodynamic, surgical, and pathologic findings in 30 patients who required mitral valvular surgery and who had a preoperative diagnosis of mitral valve prolapse were reviewed. The mean age of the patients was 59.5 years; 28 patients were over 45 years of age and 10 were over 60 years. Surprisingly, 20 were males. A long history of systolic murmur was common, whereas symptoms of heart failure were of abrupt onset. At the time of surgery, a local holosystolic murmur typical of mitral regurgitation was present, although a mid- to late systolic click was not heard in any of the patients. Electrocardiographic abnormalities were present in all patients, with 13 patients demonstrating atrial fibrillation. Only four patients had a normal heart size radiographically. Echocardiography confirmed the radiographic findings, in that 27 patients demonstrated left atrial and ventricular enlargement. All 29 patients undergoing cardiac catheterization and angiography demonstrated a prolapsing mitral valve with severe regurgitation. Surgical and pathologic examination revealed findings characteristic of a myxomatous valve in all patients, with 19 also demonstrating ruptured chordae tendineae. This study demonstrates that heart failure requiring valvular surgery occurs in a subset of patients with mitral valve prolapse. In this subset, males predominate and most are over 50 years of age. These patients may be asymptomatic for many years, demonstrating mild to moderate mitral valvular regurgitation, before heart failure develops.

Aspirin or dipyridamole individually prevent lipid accumulation in primate vein bypass grafts.

Although platelet inhibition with both aspirin and dipyridamole is widely prescribed for patients with coronary artery bypass grafts, data are lacking to prove that combined drug therapy has greater efficacy in preserving graft integrity than either drug given independently. Thus, the ability of combined vs single drug therapy to reduce cholesterol and apolipoprotein-B accumulation were compared in autologous cephalic veins grafted into femoral arteries of 23 stump-tailed macaque monkeys. Ten monkeys were studied in 2 phases. They were treated with aspirin (80 mg/day) during 1 phase and with dipyridamole (50 mg/day) during the other phase. Five monkeys received aspirin plus dipyridamole in combination and 8 received no medication and served as controls. When grafts were removed 3 months after insertion cholesterol and apolipoprotein-B concentrations in grafts were similar for groups treated with aspirin, with dipyridamole, and with the drugs combined, and in each of the treated groups these concentrations were significantly reduced compared with grafts from untreated control monkeys. Cholesterol and apolipoprotein-B concentrations in grafts from the treated groups were similar to concentrations in normal ungrafted veins, whereas cholesterol and apolipoprotein-B levels in grafts from control monkeys were significantly greater than those in ungrafted veins (250% and 925% of normal, respectively). Our findings reaffirm the ameliorative effect of anti-platelet drugs in reducing the accumulation of lipid in vein bypass grafts and indicate that the efficacy of aspirin or dipyridamole given individually equals that of the combination of these drugs in this subhuman primate model. The relation of the lipid-lowering effect of these agents to their antithrombotic effect is uncertain.

Intra-aortic balloon counterpulsation for cardiac support during noncardiac operations.

Major noncardiac surgery is a serious hazard to patients with advanced coronary disease. Perioperative infarction is common, and preliminary coronary bypass is often unwarranted. We suggest that the use of the intra-aortic balloon pump (IABP) for perioperative support of such patients makes perioperative infarction unlikely and permits otherwise hazardous operations. Three patients with advanced coronary disease (unstable angina in two) had major thoracotomies for lung masses without cardiac complications. This management plan has wider implications for other noncardiac surgical problems in such patients, particularly for mandatory operations wuch as relieving intestinal obstructions.

Trans--pulmonary artery repair of ventricular septal defect associated with congenitally corrected transposition of the great arteries.

This report documents successful trans-pulmonary artery repair of ventricular septal defect (VSD) in 2 patients with congenitally corrected transposition of the great arteries, one patient having associated subpulmonic stenosis. In selected cases, the method of repair that is described offers significant advantages over techniques employing transventricular or transatrial access to the VSD.

An improved method of topical cardiac hypothermia.

Current methods of myocardial protection usually employ together with topical hypothermia by pericardial lavage. Pericardial lavage is inconvenient, inconsistent, and noisy: it wastes blood: it cannot cool the right ventricle effectively. We use a new myocardial protection jacket to cool the heart during operation other than simple coronary bypass procedures. Myocardial temperatures are maintained at 7 degrees to 14 degrees C indefinitely without reinfusion of cardioplegia solution. The jacket is a more convenient and much more effective method of obtaining profound topical hypothermia.

Age-related changes in the ability of hypothermia and cardioplegia to protect ischemic rabbit myocardium.

Hypothermia combined with pharmacologic cardioplegia protects the globally ischemic adult heart, but this benefit may not extend to children; poor postischemic recovery of function and increased mortality may result when this method of myocardial protection is used in children. The relative susceptibilities to ischemia-induced injury modified by hypothermia alone and by hypothermia plus cardioplegia were assessed in isolated perfused immature (7- to 10-day-old) and mature (6- to 24-month-old) rabbit hearts. Hearts were perfused aerobically with Krebs-Henseleit buffer in the working mode for 30 minutes, and aortic flow was recorded. This was followed by 3 minutes of hypothermic (14 degrees C) coronary perfusion with either Krebs or St. Thomas' Hospital cardioplegic solution No. 2, followed by hypothermic (14 degrees C) global ischemia (mature hearts 2 and 4 hours; immature hearts 2, 4, and 6 hours). Hearts were reperfused for 15 minutes in the Langendorff mode and 30 minutes in the working mode, and recovery of postischemic function was measured. Hypothermia alone provided excellent protection of the ischemic immature rabbit heart, with recovery of aortic flow after 2 and 4 hours of ischemia at 97% +/- 3% and 93% +/- 4% (mean +/- standard deviation) of the preischemic value. Mature hearts protected with hypothermia alone recovered only minimally, with 22% +/- 16% recovery of preischemic aortic flow after 2 hours; none were able to generate flow at 4 hours. St. Thomas' Hospital solution No. 2 improved postischemic recovery of aortic flow after 2 hours of ischemia in mature hearts from 22% +/- 16% to 65% +/- 6% (p less than 0.05), but actually decreased postischemic aortic flow in immature hearts from 97% +/- 3% to 86% +/- 10% (p less than 0.05). To investigate any dose-dependency of this effect, we subjected hearts from both age groups to reperfusion with either Krebs solution or St. Thomas' Hospital solution No. 2 for 3 minutes every 30 minutes throughout a 2-hour period of ischemia. Reexposure to Krebs solution during ischemia did not affect postischemic function in either age group. Reexposure of immature hearts to St. Thomas' Hospital solution No. 2 caused a decremental loss of postischemic function in contrast to incremental protection with multidose cardioplegia in the mature heart. We conclude that immature rabbit hearts are significantly more tolerant of ischemic injury than mature rabbit hearts and that, unexpectedly, St. Thomas' Hospital solution No. 2 damages immature rabbit hearts.

Mitral valve replacement in idiopathic hypereosinophilic syndrome.

Idiopathic hypereosinophilic syndrome is a rare systemic disease that can cause one form of endocardial fibrosis. Endocardial fibrous tissue with overlying thrombus formation in idiopathic hypereosinophilic syndrome leads to a restrictive cardiomyopathy that may produce mitral and/or tricuspid regurgitation. This report describes a patient with idiopathic hypereosinophilic syndrome who underwent mitral valve replacement and successful steroid therapy for an usually localized form of endocardial fibrosis.

Is protection of ischemic neonatal myocardium by cardioplegia species dependent?

Hypothermia combined with pharmacologic cardioplegia protects the globally ischemic adult heart, but this benefit may not extend to children, resulting in poor postischemic recovery of function and increased mortality. The relative susceptibilities to ischemia modified by hypothermia alone and by hypothermia plus cardioplegia were assessed in isolated perfused neonatal (3- to 4-day-old) rabbit and pig hearts. Hearts were perfused aerobically with Krebs buffer solution in the working mode for 30 minutes and aortic flow was recorded. This was followed by 3 minutes of hypothermic (14 degrees C) coronary perfusion with either Krebs or St. Thomas' Hospital cardioplegic solution No. 2 followed by hypothermic (14 degrees C) global ischemia (rabbits 2, 4, and 6 hours; pigs 2 and 4 hours). Hearts were reperfused for 15 minutes in the Langendorff mode and 30 minutes in the working mode, and recovery of postischemic aortic flow was measured. Hypothermia alone provided excellent protection of the ischemic neonatal rabbit heart, with recovery of aortic flow after 2 and 4 hours of ischemia at 91% +/- 4% and 87% +/- 5% (mean +/- standard deviation) of its preischemic value. Recovery after 6 hours of ischemia was depressed to 58% +/- 9% of its preischemic value. Ischemic neonatal pig hearts protected with hypothermia alone recovered 94% +/- 3% of preischemic aortic flow after 2 hours; none was able to generate flow after 4 hours. St. Thomas' Hospital solution No. 2 decreased postischemic aortic flow after 4 hours of ischemia in rabbit hearts from 87% +/- 5% to 70% +/- 7% (p less than 0.05, hypothermia alone versus hypothermia plus cardioplegia) but improved postischemic recovery of aortic flow in pig hearts after 4 hours of ischemia from 0 to 73% +/- 13% (p less than 0.0001, hypothermia alone versus hypothermia plus cardioplegia). This effect was dose related in both species. We conclude that the neonatal pig heart is more susceptible to ischemia modified by hypothermia alone than the neonatal rabbit and that St. Thomas' Hospital solution No. 2 improves postischemic recovery of function in the neonatal pig but decreases it in the neonatal rabbit. This species-dependent protection of the neonatal heart may be related to differences in the extent of myocardial maturity at the time of study.

Effects of postischemic left ventricular pressure-volume unloading on contractile recovery and myocardial blood flow in the regionally stunned canine heart.

OBJECTIVE: Myocardial stunning remains a clinical problem without definitive therapy. This study tested the hypothesis that mechanical therapy with a ventricular assist device would accelerate recovery of contractility in stunned myocardium by increasing the postischemic myocardial blood flow. METHODS: Regional stunning was induced in dogs (25 kg) by 15 minutes of coronary occlusion and 180 minutes of reperfusion. One group (ventricular assist device; n = 10) was reperfused in conjunction with left ventricular unloading with a centrifugal-pump ventricular assist device. A second group (control; n = 8) underwent unmodified reperfusion. Hemodynamic and regional function data were acquired in all dogs with the heart in the working state before and during ischemia and after 180 minutes of reperfusion. Regional myocardial blood flow was measured at these same intervals and after 30 minutes of reperfusion, at which time the left ventricle was mechanically unloaded in animals with a ventricular assist device. RESULTS: Regional stunning was observed in all animals, but cardiogenic shock developed in none of them. After 180 minutes of reperfusion, animals with a ventricular assist device had greater systolic shortening in the risk segment than did control animals (11.5% +/- 2.8% vs 1.1% +/- 1.3%; P <.05) and had no differences in either the slope or x-axis intercept of regional preload recruitable stroke work relations compared with preischemic values. Differences in contractile recovery did not correlate, however, with postischemic myocardial blood flow. Hyperperfusion mediated by the ventricular assist device was not observed in either stunned or remote segments. CONCLUSIONS: Mechanical left ventricular unloading attenuates regional myocardial stunning within 3 hours in normotensive dogs, independent of effects on myocardial blood flow. The mechanism underlying this effect remains undefined, but these data support expanded use of mechanical therapy for stunned myocardium in clinical settings.

Depressed postoperative cardiac performance. Prevention by adequate myocardial protection during cardiopulmonary bypass.

Depressed postoperative myocardial performance (low output syndrome) requiring inotropic drugs or balloon counterpulsation is due to subendocardial ischemic damage. Before July, 1972, we needed inotropic drugs in 30 to 52 per cent of 189 patients undergoing coronary revascularization or aortic or mitral valve replacement in whom we used ischemic arrest, profound topical hypothermia, and ventricular fibrillation. The mortality rate ranged from 10 to 17 per cent. Our experimental studies show that morbidity and death in such cases are caused by ischemic injury to the heart resulting from inadequate myocardial protection during bypass. Based on these experimental studies, we have, since July, 1972, employed the following principles clinically: (1) Maintain beating empty heart whenever possible; (2) maintain adequate coronary perfusion pressure (less than 80 mm. Hg); (3) avoid extreme hemodilution; (4) avoid ventricular fibrillation; (5) avoid prolonged hypothermic arrest, limiting ischemic periods to less than 15 minutes; (6) repay myocardial ischemic oxygen debt with total (vented) bypass; and (7) optimize DPTI/TTI (supply/demand ratio) pre- and postoperatively. These principles were followed in 189 consecutive operations, and postoperative inotropic drugs were needed in only 12. The principles were violated in 4 of the 12 patients (6 per cent), and 5 others had identifiable causes of myocardial depression; low output syndrome was unexplained in only 3 patients (1.7 per cent).

Management of long-standing cardiocutaneous fistulas after resection of left ventricular aneurysms.

Cardiocutaneous fistulas arising from pledgets used in the closure of resected left ventricular aneurysms are rare but have serious implications. The case histories of four patients, each managed in a somewhat different manner, are presented. From this experience we recommend an aggressive approach to remove the infected pledgets once scar formation is complete and before erosion of the pledgets into the left ventricular cavity can occur.

Delayed infection of the automatic implantable cardioverter-defibrillator. Current recognition and management.

Three cases of delayed infection of automatic implantable cardioverter-defibrillator devices without systemic manifestations are reported. Computed tomographic scan of the heart revealed fluid deep to the patch in each case. Sonication of explanted automatic implantable cardioverter-defibrillator patches facilitated the recovery of adherent microorganisms in one case. Management of this previously unrecognized problem is outlined.

Low-dose aspirin protects against lipid accumulation in primate vein bypass grafts.

Platelet inhibition with high-dose aspirin combined with dipyridamole reduces lipid accumulation and improves early patency of coronary artery bypass grafts. However, recent evidence suggests that platelet inhibition can be achieved with substantially lower aspirin doses than have been conventionally prescribed. To evaluate whether low-dose aspirin protects against lipid accumulation in bypass grafts, we studied 15 stump-tailed macaque monkeys in which autologous cephalic veins were grafted into the femoral arteries. A control group received no treatment, a second group was treated with a low, single daily dose of aspirin (12 mg), and a third group was given a higher dosage of aspirin (80 mg/day) combined with dipyridamole (50 mg/day) divided into two daily doses. A special diet was fed that resulted in plasma cholesterol levels (224 +/- 50 mg/dl, mean +/- standard deviation) and plasma lipoprotein distributions that mimic the profile in humans. Cholesterol concentration in grafts removed 3 months after insertion was 0.47 +/- 0.12 mg/100 mg tissue in the control group; it was reduced to 0.23 +/- 0.04 mg/100 mg (p less than 0.001) by low-dose aspirin and to 0.17 +/- 0.05 mg/100 mg (p less than 0.001) by combined aspirin and dipyridamole therapy. Graft apolipoprotein B concentration was 66 +/- 19 micrograms/100 mg in control group; it was reduced to 40 +/- 8 micrograms/100 mg (p less than 0.05) by low-dose aspirin and to 23 +/- 7 micrograms/100 mg (p less than 0.001) with the combination treatment. There were no differences between groups in either cholesterol concentration (0.09 +/- 0.02 mg/100 mg) or apolipoprotein B concentration (10 +/- 3 micrograms/100 mg) in normal ungrafted vein. Platelet function tests demonstrated platelet aggregation in all control monkeys, in none of the combined therapy group, and in two of five monkeys receiving low-dose aspirin. This study indicates that low-dose aspirin is protective against graft lipid accumulation in monkeys. The mechanism of this antilipid effect and its relation to any antithrombotic effect remain to be elucidated.

The effect of ambient temperature on papaverine-induced relaxations in canine saphenous veins.

This study was designed to measure the effect of ambient temperature (25 degrees C) on papaverine-induced relaxations in canine saphenous veins. Segments of vein were suspended in water-jacketed tissue baths at 37 degrees C, and isometric tension was recorded. After equilibration, veins were preconstricted by a median effective dose of norepinephrine 2 x 10(-6) mol/L at either 25 degrees C or 37 degrees C. Consequent dose-dependent relaxations showed that papaverine (10(-7) to 10(-3) mol/L was three times more potent as a dilator at 37 degrees C than at 25 degrees C, with half-maximal relaxations occurring at 2.2 x 10(-5) mol/L and 6.4 x 10(-5) mol/L, respectively. A 10(-4) mol/L dose of papaverine completely relaxed veins at 37 degrees C, whereas veins at 25 degrees C never fully relaxed even at ten times the standard concentration. In addition, the time for half-maximal relaxation with a 10(-4) mol/L dose of papaverine averaged 40 minutes at 25 degrees C compared with 22 minutes at 37 degrees C; this is indicative of a reduced relaxation rate at the lower temperature. These data show that papaverine is a slower and less potent dilator of canine saphenous veins at 25 degrees C than at 37 degrees C. This may have implications for the use of papaverine in the operating room, where it is usually applied at ambient temperature to reduce vasospasm of the saphenous vein during coronary artery bypass procedures.

Optimal lead positioning for postoperative atrial pacing.

Temporary atrial pacing leads have uncontested utility for diagnosis and treatment of postoperative supraventricular arrhythmias. Sensing and capture thresholds may be inconsistent, however. We evaluated intraoperative atrial sensing amplitude and capture thresholds in 25 patients after coronary bypass using six bipolar and four unipolar lead combinations based on four lead positions: A, atrial appendage; B, 1 cm above the presumed sinoatrial node at the atrial-superior-vena caval junction; C, interatrial groove at the right superior pulmonary vein; and D, caudal inferolateral free wall. Unipolar lead B and bipolar lead B-D had the best voltage pacing threshold and system resistance (p less than 0.05). The lowest current was also observed with unipolar lead B and bipolar lead B-D, but the difference was not significant (p greater than 0.05). P-wave amplitude was not significantly different for any lead combination. Location C, in unipolar or bipolar combinations, frequently paced the phrenic nerve. These data provide new guidelines for establishment of postoperative temporary atrial pacing leads.

Constrictive pericarditis associated with patch electrodes of the automatic implantable cardioverter-defibrillator.

A case of constrictive pericarditis intimately involving patch electrodes of the automatic implantable cardioverter-defibrillator is described. Typical clinical and hemodynamic findings for constrictive pericarditis were noted 15 months after lead installation. Additionally, chest x-ray examination revealed a severe crumpling deformity of the patch electrodes. Thoracotomy was performed and revealed marked fibrous reaction surrounding both surfaces of each patch electrode. Histologic examination revealed fibrous tissue with multinucleated giant cells, consistent with a foreign body reaction. The patient had complete resolution of signs and symptoms of constrictive pericarditis after removal of the patch electrodes and pericardial stripping. Constrictive pericarditis from implanted patch electrodes appears to be an uncommon complication of the automatic implantable cardioverter-defibrillator and should be considered in patients with one or more patch electrodes and other signs of constrictive pericarditis.

Stratified application of the automatic implantable cardioverter defibrillator.

Since June 1983 we have developed a stratified regimen for staged implantation of the automatic implantable cardioverter defibrillator system. The protocol for management in patients who have fully recovered from sudden cardiac death is initiated with the use of standard electrophysiologic evaluation. Treatment in order of application has consisted of drugs followed by implantation of the device for patients with drug-refractory arrhythmias in whom direct cardiac surgical intervention for anatomic substrates for sudden death are absent. In surgical candidates, combinations of coronary revascularization and ablative therapy have been used to mitigrate the potential for lethal arrhythmia. Sensing and defibrillator lead systems have been placed at corrective operations to be followed later by implantation of the cardioverter defibrillator generator for either inducible or spontaneous tachyarrhythmia. This staged application has been effective in markedly reducing actual sudden cardiac death while at the same time saving on unnecessary device implantation. Morbidity of lead implantation alone remains a concern, particularly for infective complications. Additional follow-up is required to assess the validity of this approach.