Endoscopic robot-assisted extended thymectomy by subxiphoid approach with sternal lifting: feasibility in the pig.

BACKGROUND: In the search for novel approaches to thoracoscopic thymectomy we assessed the feasibility of a subxiphoid approach using computer-enhanced instruments and sternal lifting. METHODS: In 12 pigs, after lifting of the sternum, ports were placed subxiphoid (stereoscope) and in the left and right fourth intercostal space (instruments). Using computer-enhanced instruments, dissection of the thymus and anterior mediastinal fat pads was started at the diaphragm and continued cephalad. RESULTS: After setup of the robot system (23 +/- 6 min, mean +/- SD), the thymus, including both superior horns, and fat pads in the anterior mediastinum and cardiophrenic angles were dissected (109 +/- 23 min), with excellent view of the phrenic nerves. Visual inspection after sternotomy after the procedure showed all thymic and fatty tissue was removed. CONCLUSIONS: In the pig, endoscopic extended thymectomy can be safely performed by subxiphoid access using computer-enhanced instruments, sternal lifting, and three ports total.

The development of spectral EEG changes during short periods of circulatory arrest.

The EEG was monitored in 56 patients during implantation of an internal cardioverter defibrillator. The purpose of this study was to determine the main EEG frequency ranges that represent ischemic changes during short periods of circulatory arrest. The EEG was recorded with a 16-channel common reference montage (Cz). After onset of circulatory arrest, the log spectral changes of three-epoch moving averages were calculated relative to the baseline spectrum. For factor analysis, 17 EEG periods were selected that showed changes progressing to an isoelectrical period. Topographic differences and the time course of quantitative EEG (qEEG) changes were studied in all 56 patients. For each patient the EEG period with the longest duration of circulatory arrest was chosen. Factor analysis revealed four factors that represented the spectral EEG changes occurring during circulatory arrest and recovery. The frequency intervals of these factors were 0 to 0.5 Hz, 1.5 to 3 Hz, 7.5 to 9.5 Hz, and 15 to 20 Hz for all channels. Only minor topographic differences were found in the power of the spectral changes; the sequence of events was similar for all electrode positions. The first EEG change after circulatory arrest was an initial increase in alpha power and a decrease in beta power. On average, after approximately 15 seconds alpha power started to decrease, beta power decreased further, delta-1 power started to increase, and delta-2 power started to decrease. After approximately 25 seconds, the delta-1 power increase appeared to plateau or to decrease. A circulatory arrest longer than approximately 30 seconds resulted in an isoelectrical EEG. After restoration of the circulation, there was a fast transient increase in delta-1 and delta-2 power, followed by a decrease to baseline. alpha and beta power showed a more gradual increase in power toward baseline and were the last to restore after 60 to 90 seconds. In general, the spectral changes in the alpha and beta frequency ranges were most pronounced and consistent. In conclusion, to detect intraoperative cerebral ischemia, monitoring of changes in the four frequency ranges found is preferable to monitoring changes in the classically defined frequency bands. Furthermore, these results stress the importance of the alpha and beta ranges in detecting cerebral ischemia.

Sequential map-guided endocardial resection for ventricular tachycardia improves outcome.

OBJECTIVE: Surgery for ventricular tachycardias late after myocardial infarction is frequently associated with high mortality including sudden death, and arrhythmia recurrences. We examined our results of sequential map-guided endocardial resection at normothermia in patients with ventricular tachyarrhythmias late after myocardial infarction to assess the efficacy of this technique as well as the early and long-term outcome. METHODS: From 1995 to 1999, 22 patients underwent normothermic sequential map-guided endocardial resection for ventricular tachyarrhythmias late after myocardial infarction. Mean age was 61.2+/-6.5 years and left ventricular ejection fraction 32.5+/-8.7%. Adjunctive procedures included endoventricular patch repair of left ventricular aneurysm in 21 patients, coronary artery bypass grafting in 15 patients, and mitral valve replacement in one patient. Inducibility of ventricular tachycardia was evaluated postoperatively and patients were treated with sotalol or defibrillator implantation. RESULTS: The intraoperative number of inducible different ventricular tachycardia morphologies was 4.0+/-2.7. More than one mapping-resection sequence was needed in ten patients. In only one patient, sustained ventricular tachycardia was induced postoperatively, sotalol was not tolerated and a defibrillator was implanted. Five patients with inducible non-sustained ventricular tachycardia became non-inducible while on sotalol. There was one operative death (4.5%). During a median follow-up of 26 (1--62) months, there were neither cardiac deaths nor ventricular tachycardia recurrences. Two patients died from non-cardiac causes. Cumulative probability of survival at 5 years was 0.83+/-0.09. CONCLUSIONS: Sequential map-guided endocardial resection at normothermia was associated with low operative mortality and low postoperative inducibility of sustained ventricular tachycardia. The selected therapeutic approach resulted in freedom of arrhythmia recurrence and cardiac mortality including sudden death, during long-term follow-up.

Biventricular pacing in end-stage heart failure improves functional capacity and left ventricular function.

BACKGROUND: Asynchronous patterns of contraction and relaxation may contribute to hemodynamic and functional impairment in heart failure. In 1993, we introduced biventricular pacing as a novel method to treat heart failure by synchronous stimulation of the right and left ventricles after an appropriate atrioventricular delay. The objectives of this study were to assess the early and long-term effects of this therapy on functional capacity and left ventricular function in patients with severe heart failure and left bundle branch block. METHODS AND RESULTS: Twelve patients with end-stage congestive heart failure, sinus rhythm and complete left bundle branch block were treated with biventricular stimulation at optimized atrioventricular delay. The NYHA functional class and maximal bicycle exercise capacity were assessed. Systolic and diastolic left ventricular function were studied with echocardiography and radionuclide angiography. Data was collected at various intervals during 1-year follow-up. Cumulative survival [95% CI] was 66.7% [40.0,93.4] at 1 year and 50 % [21.8, 78.2] at 2 and 3 years. Median NYHA class improved from class IV to class II at 1 year (p=0.008). After 6 weeks an increase in exercise capacity occurred, which was sustained. A less restrictive left ventricular filling pattern, an increase in dP/dt and left ventricular ejection fraction, and a decrease in mitral regurgitation were observed early and long-term. CONCLUSIONS: Biventricular pacing at optimized atrioventricular delay results in improvement in functional capacity, which is associated with improved systolic and diastolic left ventricular function, and a decrease in mitral regurgitation during short- and long-term follow-up.

Staging of lymph nodes with FDG dual-headed PET in patients with non-small-cell lung cancer.

Accurate assessment of mediastinal lymph node involvement in patients with non-small-cell lung cancer (NSCLC) is necessary to select patients for direct surgical treatment. The aims of the present study were to assess the feasibility of staging NSCLC with FDG using a dual-headed positron emission tomographic (PET) camera and to compare this non-invasive technique with computed tomography (CT) and lymph node sampling, since both modalities are currently used for staging NSCLC. Thirty-three patients (29 men and 4 women, mean age 60 years) with newly diagnosed NSCLC were studied. In all patients, CT, FDG dual-headed PET and mediastinoscopy were performed within 4 weeks. The results of mediastinoscopy were used to select patients for thoracotomy. For both the assessment of individual lymph node involvement and the patient-based classification, the results of FDG dual-headed PET and CT were compared using the McNemar test. Thirty-one of 187 lymph nodes studied contained tumour metastases. FDG dual-headed PET showed a significantly higher sensitivity (P < 0.001) and specificity (P < 0.001) than CT. FDG dual-headed PET and CT correctly staged 27 and 20 patients, respectively. Due to the significantly higher negative predictive value of FDG dual-headed PET versus CT (P = 0.012), it was a better non-invasive diagnostic tool for selecting patients for surgery. In seven of eight patients, additional intrapulmonary sites of increased uptake were found, which revealed malignancy on histological examination. CT was false-negative in three of these patients. In one patients, increased FDG uptake was caused by an infection. In conclusion, it is possible to stage mediastinal lymph nodes in patients with NSCLC using a dual-headed PET camera. The high negative predictive value of FDG dual-headed PET suggests that mediastinoscopy may be omitted in patients with NSCLC.

Changes in cerebral oxygen uptake and cerebral electrical activity during defibrillation threshold testing.

UNLABELLED: During cardioverter-defibrillator implantation, repeated episodes of ventricular fibrillation (VF) are induced. Insufficient recovery of oxygen metabolism may cause neurological sequelae. In this prospective clinical study, we monitored the electroencephalogram (EEG), middle cerebral artery blood flow velocity (Vmca), and jugular bulb oxygen saturation and estimated cerebral oxygen uptake. Results were analyzed for tests requiring a single shock (Group 1) and tests requiring multiple shocks for defibrillation (Group 2). Immediately after the induction of VF, the mean arterial blood pressure (MAP) decreased to < 30 mm Hg, and the Vmca decreased to 0 cm/s. The EEG showed ischemic changes consisting of a decrease of fast, and an increase of slow, activity, progressively declining to isoelectricity within 11 +/- 2 s. After defibrillation, the MAP recovered rapidly regardless of the arrest duration (3 +/- 2 s). The EEG recovered within 17 +/- 9 and 22 +/- 12 s, respectively, for Groups 1 and 2 (P < 0.05) and did not reveal ischemic changes until induction of a subsequent arrest. In Group 1, the cerebral oxygen uptake increased to 191% +/- 31% of baseline values and returned to baseline in 16 +/- 7 s, whereas in Group 2, it increased to 229% +/- 38% (P < 0.05), followed by a significant decrease to less than baseline (85% +/- 18%; P < 0.005), and returned to baseline simultaneously with the Vmca. We conclude that, although restoration to normal of the EEG and cerebral oxygen uptake coincide in short arrests, EEG recovery underestimates metabolic recovery after tests requiring multiple shocks. IMPLICATIONS: Short test intervals have been mentioned as a cause of neurological sequelae after cardioverter-defibrillator implantation. This study demonstrates that although all systemic hemodynamic variables and the electrocardiogram may have returned to normal, cerebral oxygen uptake may still be depressed for a considerable time, especially after tests requiring two or more shocks.

Neuromonitoring in defibrillation threshold testing. A comparison between EEG, near-infrared spectroscopy and jugular bulb oximetry.

OBJECTIVES: The aim was to study the physiological effects of induced ventricular fibrillation and subsequent circulatory arrest for defibrillation threshold testing on the brain using the EEG, jugular bulb oxymetry and near-infrared spectroscopy. METHODS: Thirteen patients undergoing surgery for implantable cardioverter-defibrillator implantation or replacement under general anesthesia were included. We continuously monitored the jugular bulb oxygen saturation (SjO2), regional oxygen saturation (rSO2) and the EEG. RESULTS: 59 episodes of circulatory arrest were studied. In all cases the rSO2 fell instantly while the EEG changed within 12 +/- 4 seconds after induction. The EEG indicated ischemic changes, ranging from occurrence of rhythmic delta activity to cessation of all electrical activity. On successful defibrillation the rSO2 increased to values in excess of pre-arrest levels and restored towards baseline; the SjO2 initially fell followed by a similar overshoot. Recovery times increased in proportion to arrest duration. CONCLUSION: Short lasting episodes of circulatory arrest have serious, but transient effects on brain function. The rSO2 is an effective non-invasive tool for monitoring cerebral oxygenation during DFT-testing.

Mitral valve prolapse and ventricular arrhythmias: observations in a patient with a 20-year history.

INTRODUCTION: Ventricular arrhythmias are a common feature in patients with mitral valve prolapse. In an attempt to determine the origin and underlying electrophysiologic mechanism, we describe a patient with ventricular fibrillation, exercise-induced ventricular tachycardia (VT), and, at the time of diagnosis, prolapse of the posterior mitral valve leaflet without mitral regurgitation. METHODS AND RESULTS: Treatment with beta-blockade and diphenylhydantoin prevented the occurrence of malignant ventricular arrhythmias for more than 17 years. Discontinuation of the therapy resulted in an immediate reappearance of the VT, which, despite the marked enlargement of the left ventricle (secondary to development of severe mitral valve regurgitation), had a strikingly similar morphology. For hemodynamic reasons, the patient was finally selected for valve replacement. Detailed pre-, peri-, and postoperative studies were performed, including administration of flunarizine, body surface mapping, construction of perioperative epicardial and endocardial maps, and studies of the excised muscles in vitro. CONCLUSIONS: Delayed afterdepolarization-induced triggered activity is the mechanism of VT in this mitral valve prolapse patient. The trigger is provided by isolated ventricular premature complexes elicited by a different electrophysiologic mechanism, possibly reentry, which is related to stretch and presumably to fibrosis of the papillary muscles.

Prediction of surgical strategy in mitral valve regurgitation based on echocardiography. Interuniversity Cardiology Institute of The Netherlands.

The purpose of this prospective multicenter study of 350 consecutive patients who were accepted for mitral valve surgery because of severe regurgitation, was to assess the value of preoperative transthoracic and transesophageal echocardiography in predicting the surgical strategy in severe mitral regurgitation: repair or replacement. The cardiologist predicted the surgical strategy on the basis of the echocardiographic examination, according to predefined guidelines for repair and replacement. The predicted strategy and motivation thereof were compared with the surgical findings and procedure that was performed. Agreement on the basis of transthoracic echocardiography was reached in 86% of the repair patients and on the basis of transesophageal echocardiography in 89%. Agreement on the basis of transthoracic echocardiography was reached in 74% of the replacement patients and on the basis of transesophageal echocardiography in 75%. This study underlines the potential role of echocardiography in predicting the surgical procedure to be applied, provided that both surgeon and cardiologist use the same nomenclature and that the guidelines for replacement/repair are adhered to. Both transthoracic and transesophageal echocardiography appear to be equally accurate in predicting the optimal surgical procedure in this respect.

The effect of inhaled thiorphan on allergen-induced airway responses in asthmatic subjects.

BACKGROUND: Neuropeptides are likely to be implicated in the pathophysiology of allergen-induced airway responses. However, upon release in the airways, neuropeptides are potentially inactivated by neutral endopeptidase (NEP). OBJECTIVE: We hypothesized that NEP-inhibition by inhaled thiorphan (TH) would increase allergen-induced early (EAR) and late (LAR) asthmatic responses, and allergen-induced airway hyperresponsiveness to histamine in asthmatic subjects in vivo. The dose and dosing intervals of TH were derived from previous pharmacokinetic and dose-finding studies. METHODS: Nine non-smoking, atopic, asthmatic men with dual asthmatic responses to inhaled house-dust mite extract participated in a double-blind, placebo-controlled, cross-over study. During each study period PC20 histamine was measured 24 h before, and 3 and 24 h post-allergen. TH (1.25 mg/mL, 0.5 mL) or placebo (P) were aerosolized pre-allergen, and three times at 2 h intervals post-allergen (total dose of TH: 2.5 mg). Forced expiratory volume in one second (FEV1) was recorded and expressed as percentage fall from baseline. The EAR (0-3 h) and the LAR (3-8 h) were defined as maximum percentage fall from the pre-allergen baseline and as corresponding areas under the time-response curves (AUC). RESULTS: As compared with P, TH failed to induce an acute effect on FEV1 at any of the timepoints (P > 0.08). There was no significant difference between P and TH in the EAR and the LAR: neither in terms of maximum percentage fall from baseline (mean +/- SEM: EAR: 22.3 +/- 4.7% (P) and 20.4 +/- 4.1% (TH), P = 0.75; LAR: 25.2 +/- 4.7% (P) and 26.4 +/- 5.8% (TH), P = 0.77) nor in terms of AUC (P = 0.76). Correspondingly, the changes in PC20 histamine were not different between the two treatments (P > 0.40). CONCLUSION: We conclude that four adequate doses of the inhaled NEP-inhibitor, thiorphan, failed to potentiate allergen-induced airway responses in asthma. These results suggest that either neuropeptides do not play a predominant role in allergen-induced airway responses, or that allergen challenge induces NEP-dysfunction in humans in vivo.

The impact of repeated short episodes of circulatory arrest on cerebral function. Reassuring electroencephalographic (EEG) findings during defibrillation threshold testing at defibrillator implantation.

The impact of circulatory arrest on EEG features during defibrillation threshold testing for implantation of a cardioverter defibrillator has been disputed. Cumulation of cerebral ischemic effects during threshold testing has been observed, and consequently the advice was given to avoid short intervals between tests and to limit the test number. This study investigated the duration of EEG signs of cerebral ischemia as well as the occurrence of cumulation. EEGs were recorded during standardized general anesthesia. Subsequent tests were performed after recovery of EEG, electrocardiogram, systemic arterial blood pressure, and heart rate. In 36 consecutive survivors of out-of-hospital cardiac arrest 286 episodes of induced circulatory arrest were analyzed. Ischemic EEG changes were present in all episodes of circulatory arrest, consisting of slowing, progressing to absence of activity. The relation between the onset time or recovery time and the test number and test interval was studied. A highly significant correlation between circulatory arrest and recovery time was found (P < 0.001). A significant negative correlation existed between test number and recovery time (P < 0.05). Test interval was not related with either onset or recovery time. We conclude that repeated threshold tests which are monitored by assessment of EEG and hemodynamics are not associated with cumulative EEG changes as a result of ischemia. Our results do not support the advice that the number of tests should be limited.

Cost-effectiveness of implantable defibrillator as first-choice therapy versus electrophysiologically guided, tiered strategy in postinfarct sudden death survivors. A randomized study.

BACKGROUND: Rising costs of health care, partly as a result of costly therapeutic innovations, are of concern to both the medical profession and healthcare authorities. The implantable cardioverter-defibrillator (ICD) is still not remunerated by Dutch healthcare insurers. The aim of this study was to evaluate the cost-effectiveness of early implantation of the ICD in postinfarct sudden death survivors. METHODS AND RESULTS: Sixty consecutive postinfarct survivors of cardiac arrest caused by ventricular tachycardia or fibrillation were randomly assigned either ICD as first choice (n = 29) or a tiered therapy starting with antiarrhythmic drugs and guided by electrophysiological (EP) testing (n = 31). Median follow-up was 729 days (range, 3 to 1675 days). Fifteen patients died, 4 in the early ICD group and 11 in the EP-guided strategy group (P = .07). For quantitative assessment, the cost-effectiveness ratio was calculated for both groups and expressed as median total costs per patient per day alive. Because effectiveness aspects other than mortality are not incorporated in this ratio, other factors related to quality of life were used as qualitative measures of cost-effectiveness. The cost-effectiveness ratios were $63 and $94 for the early ICD and EP-guided strategy groups, respectively, per patient per day alive. This amounts to a net cost-effectiveness of $11,315 per patient per year alive saved by early ICD implantation. Costs in the early ICD group were higher only during the first 3 months of follow-up, but as a result of the high proportion of therapy changes, including arrhythmia surgery and late ICD implantation, costs in the EP-guided strategy group became higher after that. Patients discharged with antiarrhythmic drugs as sole therapy had the lowest total costs. This subset, however, showed extremely high mortality, resulting in a poor cost-effectiveness ratio ($196 per day). Invasive therapies and hospitalization were the major contributors to costs. If quality-of-life measures are taken into account, the cost-effectiveness of early ICD implantation was even more favorable. Recurrent cardiac arrest and cardiac transplantation occurred in the EP-guided strategy group only, whereas exercise tolerance, total hospitalization duration, number of invasive procedures, and antiarrhythmic therapy changes were significantly in favor of early ICD implantation. CONCLUSIONS: In terms of cost-effectiveness, early ICD implantation is superior to the EP-guided therapeutic strategy in postinfarct sudden death survivors.

Randomized study of implantable defibrillator as first-choice therapy versus conventional strategy in postinfarct sudden death survivors.

BACKGROUND: In retrospective studies of sudden cardiac death survivors, the implantable cardioverter-defibrillator (ICD) compares favorably with medical and surgical therapy. Thus, use of the conventional strategy of starting treatment with antiarrhythmic drugs (AD), at least in certain patient categories, may be questionable. The goal of this study was to analyze the effectiveness of ICD implantation as first-choice therapy versus the conventional therapeutic strategy of starting with AD. METHODS AND RESULTS: Sixty consecutive survivors of cardiac arrest caused by old myocardial infarction were randomly assigned early ICD implantation (n = 29) or conventional therapy (n = 31). Baseline characteristics were similar in the two groups. Therapy in each patient was always guided by ECG monitoring, exercise testing, and programmed electrical stimulation (PES). Primary end points (main outcome events, including death, recurrent cardiac arrest, and cardiac transplantation), number of invasive procedures and antiarrhythmic therapy changes, and duration of hospitalization were compared. Median follow-up was 24 months (mean, 27 months). In the early ICD group, 4 patients (14%) died, all of cardiac causes. In the conventional group, 20 patients failed AD and subsequently underwent map-guided ventricular tachycardia (VT) surgery (6 patients) or ICD implantation (14 patients). Of the 6 VT surgery patients, 1 died, 1 had cardiac transplantation, and 1 had an ICD implantation because of persistent inducibility despite the addition of AD. Of the 11 patients who remained on AD as sole therapy, 2 died in the hospital before they could be retested by PES, leaving 9, judged adequately protected by AD alone. Of those, 5 died, and 1 survived recurrent cardiac arrest followed by ICD implantation. In total, 16 conventionally treated patients ended up with late ICD implantation, 3 of whom died. Thus, total mortality in the conventional group was 11 patients (35%): 4 died suddenly, 5 died of heart failure, and 2 died of noncardiac causes. Comparison of the main outcome events in both strategies showed a significant difference in favor of early ICD implantation (hazard ratio, 0.27; 95% CI, 0.09 to 0.85; P = .02). In addition, the early ICD group underwent fewer invasive procedures (median, 1 versus 3; P < .0001), had less therapy changes (P < .0001), and spent fewer days in hospital (median, 34 versus 49; P = .02). CONCLUSIONS: These data suggest that ICD implantation as first choice is preferable to the conventional approach in survivors of cardiac arrest caused by old myocardial infarction. Conventionally treated patients are likely to end up with an ICD, and those who remain on AD as sole therapy have a high risk of death regardless of efficacy assessment, including PES.

Abnormal automaticity as mechanism of atrial tachycardia in the human heart--electrophysiologic and histologic correlation: a case report.

INTRODUCTION: A 32-year-old woman was operated upon because of drug refractory atrial tachycardia. METHODS AND RESULTS: Electrophysiologic study was performed prior to operation. During surgery, epicardial mapping of the electrical activity of the left atrium was performed. The left atrial appendage was resected and studied in a tissue bath. Thereafter, histologic examination was performed. Polarity of the P wave in the surface ECG suggested that the tachycardia originated high in the left atrium. Epicardial mapping disclosed earliest activation in the apex of the left atrial appendage. Intracellular recordings from surgical specimen made at the site of origin, which was marked during surgery, revealed cells with phase 4 depolarization at cycle lengths ranging from 360 to 540 msec. Exit block prevented spread of activation from the spontaneously firing cells to surrounding tissue. Histology showed that spontaneous activity arose in an area with abnormal cells--characterized by an amorphous, pale eosinophilic staining cytoplasm and absence of nuclei--surrounded by normal myocytes. CONCLUSION: The observations indicate that the mechanism of the atrial tachycardia was based on abnormal automaticity in an area consisting of a conglomeration of normal and abnormal myocytes.

Unfavorable outcome in patients with primary electrical disease who survived an episode of ventricular fibrillation.

BACKGROUND: Prognosis in patients with ventricular tachyarrhythmia without structural heart disease (primary electrical disease) has been described as excellent. However, prognosis may be less favourable in the subgroup surviving an episode of ventricular fibrillation. METHODS AND RESULTS: We prospectively followed 19 consecutive patients (age, 13 to 66 years; mean age, 33 years) who had survived an episode of documented ventricular fibrillation. Structural heart disease, preexcitation, and long QT syndromes were excluded by thorough cardiologic evaluation. All patients underwent 24-hour Holter monitoring, exercise testing, and programmed electrical stimulation according to a standardized protocol. Holter monitoring revealed episodes of ventricular tachyarrhythmia in 5 patients. Exercise testing reproducibly provoked ventricular tachycardia in 2 patients. Baseline programmed electrical stimulation yielded inducibility of rapid ventricular tachyarrhythmia in 10 patients (53%) and noninducibility in 9 (47%). Nine patients were discharged on antiarrhythmic drug therapy. A defibrillator was implanted in 10 patients. During 43-month follow-up (range, 5 to 85 months; median, 41 months), major arrhythmic events recurred in 7 patients (37%). Four of these patients had noninducibility at baseline programmed electrical stimulation. Two patients on antiarrhythmic drugs had recurrent cardiac arrest: one died suddenly and the other was successfully resuscitated from ventricular fibrillation and subsequently underwent defibrillator implantation. In the other 5 patients, termination of (pre)syncopal episodes was associated with defibrillator shocks. Termination of ventricular fibrillation was documented by Holter recording in one of these patients. Specific markers predictive of a recurrent event could not be identified, although 6 of 7 patients with recurrent events had experienced at least one episode of cardiac arrest or (pre)syncope before the index episode. CONCLUSIONS: Patients with primary electrical disease presenting with ventricular fibrillation are at high risk of recurrence of major arrhythmic events during long-term follow-up. Noninducibility at baseline study does not predict an uneventful course. Also, early defibrillator implantation should be considered in these patients.

Extensive cryoablation of the left ventricular posterior papillary muscle and subjacent ventricular wall. Impact on mitral valve function and hemodynamics.

Ventricular tachycardias that originate from the inferior left ventricular wall may necessitate transmural ablation involving the posterior papillary muscle of the mitral valve. The effect on mitral valve function and hemodynamics of extensive cryoablation of the left ventricular posterior papillary muscle and subjacent ventricular wall was studied in 16 dogs. Two sham experiments were done. All dogs were studied preoperatively and postoperatively by pulsed Doppler and two-dimensional echocardiography. Left ventricular angiographic and hemodynamic studies were performed preoperatively in six treated dogs and two control dogs and in all dogs at the end of follow-up (1, 3, or 6 months). Postmortem studies were performed in all dogs. The cumulative probability of freedom from mitral regurgitation at 2 months was 0.43 +/- 0.14. Thereafter no new cases of mitral regurgitation could be demonstrated. The angiographic degree of mitral regurgitation was mild in five and moderate in two dogs and did not increase from 3 to 6 months. One dog with acute severe mitral regurgitation died early of heart failure. A significant increase in left ventricular end-diastolic and mean pulmonary capillary wedge pressure of 9.4 +/- 2.5 mm Hg and 6.4 +/- 2.6 mm Hg, respectively, was found in treated dogs at 3 months. These results suggest that extensive cryoablation of the left ventricular posterior papillary muscle and subjacent ventricular wall can be accomplished with an acceptable risk of mild to moderate mitral regurgitation, and without serious detrimental effect on left ventricular function. Retraction is probably the main mechanism of mitral regurgitation.

Effects of cryothermia during cold cardioplegia on epicardial and intramural coronary arteries.

Cryosurgery is playing an increasingly important role in the surgical treatment of various supraventricular and ventricular tachyarrhythmias. The short-term and long-term effects of cryogenic injury on epicardial and intramural coronary arteries were studied in 22 dogs. Transmural cryolesions encompassing a posterolateral branch of the circumflex coronary artery were produced in the inferior left ventricular wall during extracorporeal circulation and cold cardioplegic arrest. The mean epicardial cryolesion area +/- standard deviation was 10.4 +/- 1.8 cm2. The mean epicardial coronary artery diameter +/- standard deviation measured 1.2 +/- 0.4 mm. At 6 hours, no important structural changes were noted in any of 6 dogs. At 48 hours, 1 of 2 epicardial coronary arteries showed recent thrombus. At 1, 3, and 6 months, the epicardial coronary arteries were occluded due to thrombosis and intimal hyperplasia in 13 of 14 dogs. A limited degree of recanalization was observed. At all follow-up intervals, the intramural coronary arteries exhibited a histologic pattern similar to that of the epicardial coronary arteries. It is concluded that the exposure of major epicardial coronary arteries to cryoinjury during cold cardioplegic arrest should be avoided where possible.

Infections involving implanted cardioverter defibrillator devices.

Infection is one of the most serious complications in patients with an implanted cardioverter defibrillator. The diagnosis is facilitated by computed tomographic and radionuclide imaging. Infection may be caused by intraoperative contamination or hematogenous seeding. In view of the serious consequences, the emphasis should be on prevention of these events. Perioperative antibiotic prophylaxis is common practice but the utility of prophylactic antibiotic remote from surgery is questionable. Strict adherence to asepsis and a meticulous surgical technique are essential. Identification of risk factors in the individual patient allows a patient-tailored treatment policy that may add to infection prevention. If implant infection does occur, complete removal of the system is most successful.