Efficacy and safety of ibutilide fumarate for the conversion of atrial arrhythmias after cardiac surgery.

BACKGROUND: Atrial arrhythmias occur commonly after cardiac surgery and are a cause of significant morbidity and increased hospital costs, yet there is no well-studied treatment strategy to deal with them expeditiously. The purpose of this study was to determine the efficacy and safety of ibutilide fumarate, an approved drug for the rapid conversion of atrial fibrillation and flutter, in patients after cardiac surgery. METHODS AND RESULTS: Patients with atrial fibrillation or flutter occurring 1 to 7 days after surgery and lasting 1 hour to 3 days were randomized to receive two 10-minute blinded infusions of placebo or 0.25, 0.5, or 1.0 mg of ibutilide fumarate. Treatment was considered successful if sinus rhythm was restored for any period of time by hour 1.5. A total of 302 patients were randomized, 201 with fibrillation and 101 with flutter. Treatment with ibutilide resulted in significantly higher conversion rates than placebo, and efficacy was dose related (placebo 15%; ibutilide 0.25 mg 40%, 0.5 mg 47%, and 1.0 mg 57%). Conversion rates at all doses were higher for atrial flutter than for atrial fibrillation. Mean time to conversion decreased as the dose was increased. Polymorphic ventricular tachycardia was the most serious adverse effect and occurred in 1.8% of the ibutilide-treated patients compared with 1.2% of patients who received placebo. CONCLUSIONS: Ibutilide is a useful and safe treatment alternative for the atrial arrhythmias that occur after cardiac surgery.

Successful implantation of cardioverter-defibrillator systems in patients with elevated defibrillation thresholds.

OBJECTIVES: . The purpose of this study was to conduct a retrospective analysis of 16 patients with high initial defibrillation thresholds in whom a three-electrode system was used to lower defibrillation thresholds and permit implantation of a cardioverter-defibrillator system. BACKGROUND: Patients with high defibrillation thresholds (> 25 J) are uncommon but may be problematic to physicians implanting cardioverter-defibrillator systems. Most conventional systems use two defibrillating electrodes, most commonly two epicardial patches. When defibrillation thresholds remain elevated despite extensive testing of a two-electrode system, a third electrode can be incorporated and tested. However, few published data exist on the use of a three-electrode system in patients with high defibrillation thresholds. METHODS: After failure to achieve satisfactory defibrillation thresholds < 25 J with a two-patch electrode system, a third electrode was incorporated and tested. In all cases, two electrodes were joined to form a common cathode or anode, while a single electrode was used as the opposite polarity electrode. Various three-electrode configurations were then tested. RESULTS: In all 16 patients, satisfactory defibrillation thresholds were achieved and a cardioverter-defibrillator was implanted (95% confidence interval [CI] = 0% to 21%). The mean final defibrillation threshold using the revised three-electrode system was 19.5 +/- 3.7 J (p < 0.0001). A mean of 6 +/- 3 electrode configurations/patient were tested before the final configuration was selected. A total of nine different electrode configurations were used in the 16 study patients; the most common of these incorporated left and right ventricular patches as combined cathode and a superior vena cava coil (n = 5) or right atrial patch electrode (n = 3) as single anode. CONCLUSION: Patients with high initial defibrillation thresholds can generally undergo successful cardioverter-defibrillator implantation with a three-electrode system if enough electrode configurations are tested after a third electrode is incorporated.

Determinants of successful nonthoracotomy cardioverter-defibrillator implantation: experience in 101 patients using two different lead systems.

OBJECTIVES: This study was conducted to identify the determinants of successful nonthoracotomy cardioverter-defibrillator implantation. BACKGROUND: Until recently, either median sternotomy or thoracotomy was necessary to implant the electrodes used for internal cardioverter-defibrillator systems. A number of manufacturers have developed nonthoracotomy lead systems comprising two transvenous coil electrodes and a subcutaneous patch electrode. At present, the factors associated with the success or failure of a nonthoracotomy approach are unknown. METHODS: A total of 101 consecutive patients requiring a cardioverter-defibrillator underwent an initial nonthoracotomy approach. Factors associated with successful nonthoracotomy implantation were prospectively determined. RESULTS: A nonthoracotomy system was implanted in 72 (71%) of 101 patients. Twenty-nine patients (29%) required thoracotomy. Univariate predictors of successful nonthoracotomy implantation included smaller cardiac size (p < 0.0001), smaller cardiothoracic ratio (p < 0.0002), QRS duration < 120 ms (p = 0.003), female gender (p = 0.006), ventricular fibrillation as the presenting arrhythmia (p = 0.03) and smaller echocardiographic left ventricular size (p = 0.04). Multivariate predictors included smaller cardiac size (p < 0.002) and female gender (p < 0.007). Total actuarial survival over a mean (+/- SD) follow-up interval of 12 +/- 7 months was 91 +/- 0.03% and was not different in the thoracotomy and nonthoracotomy groups. CONCLUSIONS: A nonthoracotomy cardioverter-defibrillator system can be implanted in a majority of patients. Smaller cardiac size and female gender are associated with a high probability of successful implantation.

Three-year outcome of a nonthoracotomy approach to cardioverter-defibrillator implantation in 189 consecutive patients.

To date, no long-term clinical data have been published in patients undergoing a nonthoracotomy approach to cardioverter-defibrillator system implantation. In the present report, 189 consecutive patients prospectively underwent a standardized approach to cardioverter-defibrillator system implantation in which the nonthoracotomy configurations were tested first. If satisfactory defibrillation thresholds were not obtained, thoracotomy was performed during the same intraoperative session. A nonthoracotomy system was successfully implanted in 149 of 189 patients (79%), with a higher success rate (90%) observed in patients who had more recent implantations. The overall rate of complications associated with these systems was low (11%). Over a mean follow-up of 12.5 +/- 9.3 months, 17 patients (9%) died. Three-year total, cardiac, and sudden death-free actuarial survival for all patients was 83 +/- 11%, 88 +/- 7%, and 94 +/- 2%, respectively. Three-year sudden death-free actuarial survival was higher in the nonthoracotomy than in the thoracotomy patients (97 +/- 2% vs 87 +/- 6%, p = 0.047), although total survival was similar (77 +/- 11% vs 83 +/- 7%, p = 0.77). These data suggest that a majority of patients (> 80%) requiring a cardioverter-defibrillator system can undergo implantation using a nonthoracotomy approach. Patients receiving nonthoracotomy systems have 3-year outcomes comparable to those implanted via thoracotomy. If these results are maintained, a nonthoracotomy approach will supplant thoracotomy-implanted systems as the preferred method because of the simpler implant procedure and lower overall cost involved.

Long-term infection rates associated with the pectoral versus abdominal approach to cardioverter- defibrillator implants.

Infection is an uncommon (0% to 6.7%) but serious complication after implantable cardioverter-defibrillator (ICD) implantation. All ICD primary implants, replacements, or revisions performed at the Massachusetts General Hospital between April 1983 and May 1999 were reviewed. A total of 21 ICD-related infections (1.2%) were identified among 1,700 procedures affecting 1.8% of the 1,170 patients who underwent a primary implant, a generator change, or a revision of their systems. The mean follow-up time was 35 +/- 33 months. Of the 959 patients with long-term follow-up, 19 of the 584 patients (3.2%) with abdominal and 2 of the 375 patients (0.5%) with pectoral systems developed ICD-related infections (p = 0.03). There was no significant difference between the infection rate among the 959 primary ICD implants and the 447 replacements or system revisions. Only 5 of the patients (24%) had systemic signs of infection, including fever (T>100.5) and elevated white blood count >12,000. Cultures from the wound revealed staphylococcal species in 16 patients (76%). Nineteen patients were treated with removal of the entire ICD system in addition to intravenous antibiotics for 2 to 4 weeks. A decrease in the incidence of ICD-related infection has occurred since the advent of transvenous pectoral systems. The main organism responsible for ICD infection is Staphylococcus. The mainstay of ICD infection management consists of complete removal of the entire implanted system.

Experience with an implantable tiered therapy device incorporating antitachycardia pacing and cardioverter/defibrillator therapy.

The implantable cardioverter-defibrillator provides an alternative therapy for medically refractory ventricular tachyarrhythmias in patients who are not candidates for ventricular operations or in whom these operations have failed. Currently, however, available devices have limitations. In this report we describe our experience with a programmable, tiered therapy device with anti-ventricular tachyarrhythmia pacing and VVI pacing capabilities (Cadence V-100, Ventritex Inc., Sunnyvale, Calif.). This device offers certain advantages compared with conventional implantable cardioverter-defibrillators: (1) tiered, anti-ventricular tachyarrhythmia therapy incorporating programmable, rate-adaptive burst pacing in addition to energy-programmable cardioversion/defibrillation, (2) biphasic cardioversion/defibrillation waveforms, resulting in lower defibrillation thresholds, (3) the ability to abort therapy for nonsustained ventricular tachyarrhythmias, (4) electrogram storage of detected events for later retrieval and analysis, (5) noninvasive, device-generated programmed stimulation for system testing, and (6) backup VVI pacing capability. Forty patients (aged 14 to 79 years) with ventricular tachyarrhythmias refractory to medical therapy received this device. The mean left ventricular ejection fraction was 33% +/- 16%. Preoperative electrophysiologic testing revealed inducible monomorphic ventricular tachyarrhythmia responsive to rapid ventricular pacing in 36 patients (90%). An extrapericardial two-patch configuration was used with either epicardial screw-in or bipolar endocardial sensing/pacing wires. No operative mortality and no device-related infection occurred. During a follow-up period of 16 +/- 7 months (range 3 to 30 months), 38 patients remained active with the implanted device; one patient died of congestive heart failure 4 months after implantation, and the system was explanted in one patient who underwent cardiac transplantation. In 33 patients a total of 1815 ventricular tachyarrhythmias were detected that resulted in therapy. Rate-adaptive burst pacing was used as the initial therapy in 1470 episodes and was successful in 1352 instances (92%). Pacing-induced ventricular tachyarrhythmia acceleration occurred in 4% of episodes. The remaining ventricular tachyarrhythmia episodes were treated with cardioversion. In 18 patients (45%) cardioversion therapy was aborted after spontaneous termination of ventricular tachyarrhythmia.(ABSTRACT TRUNCATED AT 400 WORDS)

Calcium-induced ventricular contraction during cardioplegic arrest.

Cardiac arrest induced by hyperkalemic perfusion is generally considered to represent a state of complete electromechanical arrest. However, high-energy phosphate concentrations and ventricular function decrease with increasing cardioplegic calcium concentrations, possibly because of elevated resting muscle tone produced by calcium influx. We examined isolated rat hearts containing an isovolumic intraventricular balloon for the presence of contractile activity during the administration at 10 degrees C of a cardioplegic solution containing potassium, 20 mEq/L. Significant left ventricular pressure was developed (35.6% +/- 4.3% of prearrest systolic pressure) during administration of a solution containing a calcium concentration of 1.0 mmol/L and far less (9.7% +/- 1.6% of prearrest systolic pressure) with a calcium-free cardioplegic solution. The muscle contraction diminished with repeated doses, was increased by increasing cardioplegic calcium content, and was inhibited by magnesium. Adenosine triphosphate and creatine phosphate concentrations were 9.0 +/- 1.4 and 7.0 +/- 0.9 nmol/mg dry weight immediately after infusion of 15 ml of a hypoxic cardioplegic solution containing calcium, versus 13.3 +/- 1.3 (p less than 0.02) and 31.9 +/- 3.5 nmol/mg dry weight (p less than 0.0001) after a hypoxic acalcemic solution was given. When repeated doses of a hypoxic cardioplegic solution containing calcium in a concentration of 1.0 mmol/L were given at 15 minute intervals at 10 degrees C, ischemic contracture (a sustained development of ventricular pressure, mean 51% +/- 4% of prearrest systolic pressure) resulted within 1 hour. Coronary vascular resistance was increased during the muscle contractions induced by calcium-containing solutions, markedly so during contracture. Calcium-related mechanical activity was also observed during hypothermic cardioplegic arrest in five of six isolated isovolumic canine hearts. We conclude that hearts remain potentially active mechanically during cold hyperkalemic arrest and undergo energetically wasteful contraction when stimulated with calcium-containing hyperkalemic cardioplegic solutions.

Optimal myocardial preservation with an acalcemic crystalloid cardioplegic solution.

The effect of the calcium and oxygen contents of a hyperkalemic glucose-containing cardioplegic solution on myocardial preservation was examined in the isolated working rat heart. The cardioplegic solution was delivered at 4 degrees C every 15 minutes during 2 hours of arrest, maintaining a myocardial temperature of 8 degrees +/- 2 degrees C. Hearts were reperfused in the Langendorff mode for 15 minutes and then resumed the working mode for a further 30 minutes. Groups of hearts were given the oxygenated cardioplegic solution containing an ionized calcium concentration of 0, 0.25, 0.75, or 1.25 mmol/L or the same solution nitrogenated to reduce the oxygen content and containing 0 or 0.75 mmol ionized calcium per liter. The myocardial adenosine triphosphate concentrations at the end of arrest in these six groups of hearts were 15.6 +/- 1.2, 9.5 +/- 0.5, 8.2 +/- 1.1, 4.9 +/- 1.8, 10.1 +/- 2.0, and 1.6 +/- 0.4 nmol/mg dry weight, respectively. At 5 minutes of working reperfusion, the percentages of prearrest aortic flow were 80 +/- 2, 62 +/- 4, 33 +/- 6, 37 +/- 5, 48 +/- 7 and 46 +/- 8, respectively. The differences among the groups in adenosine triphosphate concentrations and in functional recovery diminished during reperfusion. In hearts given the hypoxic calcium-containing solution, there was a marked increase in coronary vascular resistance during the administration of successive doses of cardioplegic solution, which was rapidly reversible upon reperfusion. These data indicate that hearts given the acalcemic oxygenated solution had better adenosine triphosphate preservation during arrest and better functional recovery than hearts in any other group. Addition of calcium to the oxygenated cardioplegic solution decreased adenosine triphosphate preservation and functional recovery. Oxygenation of the acalcemic solution increased adenosine triphosphate preservation and functional recovery. The lowest adenosine triphosphate levels at end arrest were observed in hearts given the hypoxic calcium-containing solution. In the setting of hypothermia and multidose administration, the addition of calcium to a cardioplegic solution resulted in increased energy depletion during arrest and depressed recovery.

Intraaortic balloon pumping for cardiac support: trends in practice and outcome, 1968 to 1995.

OBJECTIVES: A total of 4756 cases of intraaortic balloon pump support have been recorded at the Massachusetts General Hospital since the first clinical insertion for cardiogenic shock in 1968. This report describes the patterns of intraaortic balloon use and associated outcomes over this time period. METHODS: A retrospective record review was conducted. RESULTS: Balloon use has increased to more than 300 cases a year at present. The practice of balloon placement for control of ischemia (2453 cases, 11.9% mortality) has become more frequent, whereas support for hemodynamic decompensation (congestive heart failure, hypotension, cardiogenic shock) has been relatively constant (1760 cases, 38.2% mortality). Mean patient age has increased from 54 to 66 years, and mortality has fallen from 41% to 20%. Sixty-five percent (3097/4756) of the total patient population receiving balloon support underwent cardiac surgery. Placement before the operation (2038 patients) was associated with a lower mortality (13.6%) than intraoperative (771 patients, 35.7% mortality) or postoperative use (276 patients, 35.9% mortality). Independent predictors of death with balloon pump support were insertion in the operating room or intensive care unit, transthoracic insertion, age, procedure other than angioplasty or coronary artery bypass, and insertion for cardiogenic shock. Independent predictors of death with intraoperative balloon insertion were age, mitral valve replacement, prolonged cardiopulmonary bypass, urgent or emergency operation, preoperative renal dysfunction, complex ventricular ectopy, right ventricular failure, and emergency reinstitution of cardiopulmonary bypass. CONCLUSIONS: Balloons are being used more frequently for control of ischemia in more patients who are elderly with lower mortality. An institutional bias toward preoperative use of the balloon pump appears to be associated with improved outcomes.

The treatment of patients with infected implantable cardioverter-defibrillator systems.

OBJECTIVE: The purpose of this study was to evaluate the treatment of patients with infected implantable cardioverter-defibrillator systems. METHODS: Retrospective analysis was done of the cases of 21 patients treated for implantable cardioverter-defibrillator infection during an 11-year period. RESULTS: Of 723 cardioverter-defibrillator implantations (550 primary implants, 173 replacements), nine (1.2%) were complicated by early postoperative device-related infections. Late infections developed in two patients 19 and 22 months, respectively, after implantation. Ten other patients were transferred to our institution for treatment of cardioverter-defibrillator infection. The time from implantation to overt infection was 2.2 +/- 1.3 months, excluding the two late infections. The responsible organisms were Staphylococcus aureus (9), Staphylococcus epidermidis (6), Streptococcus hemolyticus (1), gram-negative bacteria (3), Candida albicans (1), and Corynebacterium (1). All patients were treated with intravenous antibiotic drugs. Total system removal was done in 15 patients and partial removal in 2; in 4, the cardioverter-defibrillator system was not explanted. There were no perioperative deaths. A new implantable cardioverter-defibrillator system was reimplanted in 7 patients after 2 to 6 weeks of antibiotic therapy. Ten patients were treated without reimplantation (2 arrhythmia operation, 8 antiarrhythmic drugs). Four patients (3 patients without explantation and 1 with partial system removal) were treated with maintenance long-term antibiotic therapy. During a mean follow-up of 21 +/- 2.8 months, no patient had clinical recurrence of infection. One patient treated with antiarrhythmic drugs without system reimplantation died suddenly. CONCLUSIONS: Infections that involve implantable cardioverter-defibrillator systems can be safely managed by removing the entire system with reimplantation after intravenous antibiotic therapy. In selected patients in whom the risk for system explantation is high and anticipated life expectancy is short, long-term antibiotic therapy to suppress low-virulence infections may represent an acceptable alternative.

Bronchopulmonary carcinoid tumors associated with Cushing's syndrome: a more aggressive variant of typical carcinoid.

OBJECTIVES: Our objectives were to delineate the clinicopathologic characteristics of adrenocorticotropin-secreting bronchopulmonary carcinoid tumors causing Cushing's syndrome and to derive from these findings a rational approach to diagnosis and surgical management of this unusual condition. METHODS: We conducted a retrospective, chart-review analysis of seven consecutive patients treated at the Massachusetts General Hospital over a 16-year period. RESULTS: The patients uniformly had symptoms of marked hypercortisolism, and the underlying lung lesions remained clinically occult for a mean of 24 months. Standard endocrine testing was misleading in 83% of patients, reinforcing the need for an alternative diagnostic strategy based on petrosal sinus catheterization and computed tomography of the chest. Although 72% of the tumors were typical carcinoids by standard criteria, 57% demonstrated microscopic evidence of local invasiveness, and 43% were associated with mediastinal lymph node metastases. Eighty-six percent of patients have been cured by pulmonary resection a mean of 59 months after the operation, but 50% of these required a second operation for resection of involved lymph nodes after an initial relapse. CONCLUSIONS: These data suggest that adrenocorticotropin-secreting bronchopulmonary carcinoid tumors represent a distinct, more aggressive subtype of the usual, typical carcinoid. The high rate of lymphatic and local spread demands a surgical approach consisting of anatomic resection and routine mediastinal lymph node dissection.

The effects of calcium and magnesium in hyperkalemic cardioplegic solutions on myocardial preservation.

Sustained left ventricular pressure development during each infusion of a cold calcium-containing hyperkalemic cardioplegic solution has been observed in rat hearts. The present study was undertaken to relate such contraction (i.e., increase in resting pressure) to myocardial preservation and to the calcium and magnesium contents of a crystalloid hyperkalemic cardioplegic solution. Isolated perfused rat hearts with a left ventricular isovolumic balloon were arrested at 8 degrees C by the fully oxygenated cardioplegic solution infused every 15 minutes for 2 hours. Cardioplegic solutions containing ionized calcium in concentrations of 0, 0.1, or 1.2 mmol/L were each studied with (groups 2, 4, and 6) and without (groups 1, 3, and 5) the addition of magnesium (16 mmol/L). Hearts arrested by the cardioplegic solution with no calcium or magnesium (group 1) developed a pressure (averaged over the second to eighth infusion and expressed as percent prearrest left ventricular pressure) of 6.0% +/- 0.4% during cardioplegic infusions. This solution maintained end-arrest myocardial adenosine triphosphate (13.1 +/- 1.0 nmol/mg dry weight) and phosphocreatine (21.7 +/- 2.8 nmol/mg dry weight) contents near the prearrest contents and preserved left ventricular function at 95% +/- 3% of prearrest developed left ventricular pressure at 15 minutes of reperfusion at 37 degrees C. Calcium (groups 3 and 5) increased pressure development during cardioplegic infusions (10.4% +/- 0.5% and 15.1% +/- 0.9%), depleted adenosine triphosphate (7.2 +/- 1.0 and 7.4 +/- 0.9) and phosphocreatine (13.3 +/- 1.8 and 10.7 +/- 1.5), and depressed left ventricular functional recovery (71% +/- 1% and 73% +/- 3%). Magnesium alone (group 2) decreased pressure development during cardioplegic infusions (3.0% +/- 0.3%), maintained adenosine triphosphate (15.6 +/- 0.9), augmented phosphocreatine (38.3 +/- 1.2), and preserved left ventricular function (99% +/- 4%). Magnesium added to calcium (groups 4 and 6) prevented the calcium-induced increased pressure development during cardioplegic infusions (4.0% +/- 0.5% and 6.7% +/- 0.6%), maintained adenosine triphosphate (13.6 +/- 1.4 and 14.9 +/- 0.7), augmented phosphocreatine (31.3 +/- 1.6 and 32.2 +/- 2.4), and ameliorated the depression of functional recovery (82% +/- 2% and 86% +/- 2%). These data suggest that left ventricular pressure development during arrest contributed to calcium-induced energy depletion and impairment of functional recovery and that these deleterious effects were inhibited by magnesium. The inhibitory effects of magnesium on left ventricular pressure development were rapidly reversed on reperfusion. The data support the addition

Operation for recurrent ventricular tachycardia. Predictors of short- and long-term efficacy.

The success of ventricular operation in ablating drug-refractory ventricular tachycardia secondary to ischemic heart disease varies with surgical technique, the presence of certain identified risk factors, and patient selection biases. Forty-eight patients with drug-refractory ventricular tachycardia secondary to ischemic heart disease underwent directed ventricular operation. All patients had previous myocardial infarction, and 46 of 48 patients had a left-ventricular aneurysm. Mapping was done in 81% of patients. Patients underwent a combination of subendocardial resection, aneurysmectomy, and cryoablation. The operative mortality rate was 8%. Age greater than 65 years was the only risk factor for operative mortality. Forty-one patients underwent postoperative programmed electrical stimulation. In 26 patients (63%) tachycardia was noninducible, whereas it was inducible in 15 patients (37%). Stepwise logistic regression identified septal and inferior focus location as the most significant predictors of outcome. Septal focus location was a significant (p = 0.008) predictor of surgical success whereas inferior focus location was a significant (p = 0.015) predictor of surgical failure. Other identified independent risk factors for surgical failure were (1) use of cardioplegia, (2) lack of a completed intraoperative endocardial map, and (3) decreased ejection fraction. This generated model to predict success or failure had a sensitivity of 93.3% and a specificity of 92.4%. The success of ventricular operation is affected by the presence of certain risk factors. In the management of those patients at high risk for failure, other surgical options such as the placement of implantable cardioverter-defibrillator electrode patches at the time of ventricular operation or the alternative placement of a palliative implantable cardioverter-defibrillator should be considered.

Ischemic intervals during warm blood cardioplegia in the canine heart evaluated by phosphorus 31-magnetic resonance spectroscopy.

OBJECTIVE: Warm blood cardioplegia requires interruption by ischemic intervals to aid visualization. We evaluated the safety of repeated interruption of warm blood cardioplegia by normothermic ischemic periods of varying durations. METHODS: In three groups of isolated cross-perfused canine hearts, left ventricular function was measured before and for 2 hours of recovery after arrest, which comprised four 15-minute periods of cardioplegia alternating with three ischemic intervals of 15, 20, or 30 minutes (I15, I20, and I30). Metabolism was continuously measured by phosphorus 31-magnetic resonance spectroscopy. RESULTS: Adenosine triphosphate level fell progressively as ischemia was prolonged; after recovery, adenosine triphosphate was 99% +/- 6%, 90% +/- 1% (p = 0.0004 vs control), and 68% +/- 3% (p = 0.0002) of control levels in I15, I20, and I30, respectively. Intracellular acidosis with ischemia was most marked in I30. After recovery, left ventricular maximal systolic elastance at constant heart rate and coronary perfusion pressure was maintained in I15 but fell to 85% +/- 3% in I20, (p = 0.003) and to 65% +/- 6% (p = 0.003) of control values in I30, while relaxation (tau) was prolonged only in I30 (p = 0.007). CONCLUSIONS: Hearts recover fully after three 15-minutes periods of ischemia during warm blood cardioplegia, but deterioration, significant with 20-minute periods, is profound when the ischemic periods are lengthened to 30 minutes. This suggests that in the clinical setting warm cardioplegia can be safely interrupted for short intervals, but longer interruptions require caution.

Warm heart surgery in patients with cold autoimmune disorders.

Continuous warm antegrade delivery of cardioplegia while maintaining systemic normothermia is a new method of performing coronary artery bypass grafting. It can be used to avoid the detrimental effects of hypothermia in patients with cold autoimmune disease.

Left ventricular hamartoma associated with ventricular tachycardia.

Cardiac hamartomas are a rare type of benign tumor affecting the heart. We describe a 33-year-old patient who presented with a wide complex tachycardia. Diagnostic imaging revealed a mass in the patient's left ventricular wall, near the apex of the heart. The mass was surgically resected and appeared benign. Its pathology was that of a hamartoma of mature cardiac myocytes. Postoperative electrophysiology evaluation showed no inducible focus and the patient remains alive and asymptomatic after 2 years of follow-up.

The temperature dependence of cardioplegic distribution in the canine heart.

BACKGROUND: Cold cardioplegic arrest can produce cooling contracture and suboptimal myocardial protection. This study examines whether cooling contracture is associated with maldistribution of cardioplegic solution, particularly subendocardial hypoperfusion, which may impair recovery. METHODS: Canine hearts were arrested by antegrade cold and warm blood cardioplegia in random order. Cardioplegic distribution was measured using radiolabeled microspheres before and just after induction of each period of arrest. RESULTS: With cold cardioplegia, perfusion of left ventricular subepicardial and midwall regions decreased. Subendocardial to subepicardial perfusion ratios increased significantly in the left ventricle as a whole, the anterior and posterior regions of the left ventricular free wall, and the interventricular septum. With warm arrest, transmural flow distribution was not significantly altered from preceding prearrest values. At constant coronary flow, coronary perfusion pressure was initially similar after induction of arrest at both temperatures, but it rose subsequently during warm cardioplegia. CONCLUSIONS: The data suggest that during normothermic arrest, vasomotor tone regulates cardioplegic distribution, and hyperkalemic vasoconstriction is of slow onset. In the absence of beating and with vasomotion inhibited by hypothermia, cardioplegic distribution during cold arrest appears to be primarily dependent on vascular anatomy. There was no evidence of subendocardial underperfusion during cooling contracture.

Cardioplegia and ischemia in the canine heart evaluated by 31P magnetic resonance spectroscopy.

BACKGROUND: Warm continuous blood cardioplegia provides excellent protection, but must be interrupted by ischemic intervals to aid visualization. We hypothesized that (1) as ischemia is prolonged, the reduced metabolic rate offered by cooling gives the advantage to hypothermic cardioplegia; and (2) prior cardioplegia mitigates the deleterious effects of normothermic ischemia. METHODS: Isolated cross-perfused canine hearts underwent cardioplegic arrest followed by 45 minutes of global ischemia at 10 degrees C or 37 degrees C, or 45 minutes of normothermic ischemia without prior cardioplegia. Left ventricular function was measured at baseline and during 2 hours of recovery. Metabolism was continuously evaluated by phosphorus-31 magnetic resonance spectroscopy. RESULTS: Adenosine triphosphate was 71% +/- 4%, 71% +/- 7%, and 38% +/- 5% of baseline at 30 minutes, and 71% +/- 4%, 48% +/- 5%, and 39% +/- 6% at 42 minutes of ischemia in the cold ischemia, warm ischemia, and normothermic ischemia without prior cardioplegia groups, respectively. Left ventricular systolic function, left ventricular relaxation, and high-energy phosphate levels recovered fully after cold cardioplegia and ischemia. Prior cardioplegia delayed the decline in intracellular pH during normothermic ischemia initially by 9 minutes, and better preserved left ventricular relaxation during recovery, but did not ameliorate the severe postischemic impairment of left ventricular systolic function, marked adenosine triphosphate depletion, and creatine phosphate increase. Left ventricular distensibility decreased in all groups. CONCLUSIONS: When cardioplegia is followed by prolonged ischemia, better protection is provided by hypothermia than by normothermia. Prior cardioplegia confers little advantage on recovery after prolonged normothermic ischemia but delays initial ischemic metabolic deterioration, which would contribute to the safety of brief interruptions of warm cardioplegia.

Reoperative coronary grafting: changing patient profiles, operative indications, techniques, and results.

To assess the changing trends in patient profiles, operative indications and techniques, and their impact on the results of reoperative myocardial revascularization, we reviewed the records of 750 consecutive patients who had an isolated first reoperation for coronary artery disease at the Massachusetts General Hospital from 1977 to 1992. The patients were chronologically grouped into three equal cohorts of 250 patients. Our assessment over time revealed a significantly (p < 0.03) increased incidence of the following: older age, peripheral vascular disease, grafts at the first revascularization, longer operative interval, interval infarctions and angioplasties, and congestive heart failure and unstable angina requiring greater use of preoperative intraaortic balloon pumping. At catheterization significantly more left main coronary disease, lower ejection fractions, and more patent but diseased grafts were found. The reoperations were significantly done more urgently, with more grafts placed and a greater use of mammary artery grafting. Despite these increased risks over time, median postoperative hospital stay was significantly shortened (p < 0.001), though hospital mortality (5.3%) and perioperative myocardial infarction (6.3%) did not change significantly. Significant multivariate predictors of hospital death were nonelective operation, perioperative myocardial infarction, prior myocardial infarction, and mammary artery grafting at the initial operation.

Mitral valve reconstruction versus replacement for degenerative or ischemic mitral regurgitation.

Between January 1985 and June 1992, 263 consecutive patients had mitral valve reconstruction (133 patients) or replacement (130 patients) for degenerative or ischemic mitral regurgitation. The two groups were similar in sex, age, prior infarctions or cardiac operations, hypertension, angina, and functional class. Both groups were similar in mean ejection fraction, pulmonary artery pressure, cardiac index, and incidence of coronary artery disease. More reconstruction than replacement patients had ischemic etiology (22 [16%] versus 12 [9%]; p = not significant), and fewer reconstruction patients had ruptured anterior leaflet chordae (9 [7%] versus 39 [30%]; p < 0.01). More reconstruction than replacement patients had concomitant cardiac procedures (67 [50%] versus 59 [45%]; p = not significant). Hospital death occurred in 4 reconstruction patients (3%) and 15 (12%) replacement patients (p < 0.01). Median postoperative stay was shorter in reconstruction patients (10 versus 12 days; p = 0.02). Late valve-related death occurred in 3 reconstruction patients (2%) and 8 (6%) replacement patients (p = 0.08). Six-year actuarial freedom from thromboembolism was 92% for the reconstruction group and 85% for the replacement group (p = 0.12). Freedom from all valve-related morbidity and mortality was 85% for the reconstruction patients and 73% for the replacement patients (p = 0.03). Significant multivariate predictors of hospital death were age, mitral valve replacement, functional class, congestive heart failure, no posterior chordal rupture, and nonelective operation. Mitral valve reconstruction, when technically feasible, is the procedure of choice for degenerative or ischemic mitral regurgitation because of significantly lower hospital mortality and late valve-related events.