Non-pharmacologic prevention of sudden cardiac death

Non-pharmacologic therapy has revolutionized the management of arrhythmias and prevention of sudden cardiac death (SCD). Of particular importance is the introduction of radiofrequent catheter ablation (RFCA) and implantable cardioverter-defibrillator (ICD). RFCA is effective and useful in the treatment and prevention of SCD, especially in supraventricular tachyarrhythmias related to dual or accessory atrioventricular pathways. There are some limitations in using this method in the prevention of SCD in ventricular tachyarrhythmias. RFCA is very successful, particularly in the treatment of bundle branch reentrant ventricular tachycardia and ventricular tachycardia in patients without structural heart disease. RFCA can be used as a palliative treatment of incessant or frequent VT before and after ICD implantation. Antibradycardia pacing decreases SCD not only by the removal of serious bradyarrhythmias but also by prevention of the occurrence of malignant ventricular tachyarrhythmias induced by bradyarrhythmia. Antitachycardia pacing is used in the prevention of SCD only as a part of ICD device. Implantation of an antitachycardia pacemaker as an isolated permanent treatment of tachycardias is currently almost not used. This method was replaced by RFCA in supraventricular tachyarrhythmias and by ICD in ventricular tachyarrhythmias. ICD is a very perspective non-pharmacologic approach to SCD prevention, particularly as transvenous leads were introduced and device construction was simplified. ICD is indicated especially in patients with spontaneous sustained hemodynamically significant ventricular tachycardia/ventricular fibrillation and when antiarrhythmic drug treatment, RFCA or antitachycardia surgery are ineffective, intolerated, contraindicated or cannot be performed. ICD as the treatment of first choice instead of antiarrhythmic drugs as well as prophylactic ICD implantation in asymptomatic patients at high risk is a subject of discussion. ICD decreases the incidence of SCD significantly. However, the decrease in overall mortality was not verified. Antitachycardia surgery is less frequently used after RFCA, and ICD have been introduced. At present, this therapy is reserved only for the cases of failure of RFCA or the impossibility to use RFCA and ICD. Surgical therapy can be combined also with concommitant surgical correction of associated structural heart disease. Sympathectomy is used in prevention of malignant ventricular tachyarrhythmias and SCD in patients with congenital long Q-T syndrome. Selective left cardiac sympathetic denervation significantly reduces the risk of SCD in these patients but does not remove it completely. Heart transplantation is the last alternative of non-pharmacologic prevention of SCD. It is indicated in cases when all pharmacologic and non-pharmacologic approaches have been exhausted. Heart transplantation is the only effective modality for the improvement of long-term prognosis in patients with malignant ventricular tachyarrhythmias and advanced chronic heart failure.     

Dispersion of the Q-T interval after myocardial infarct

Non-homogenity of ventricular myocardial repolarization is a substrate for the reentry mechanism of ventricular arrhythmias. It is manifestant by dispersion of Q-T and Q-Tc intervals on the standard ECG curve. The authors studied the possibility of using the dispersity of Q-T and Q-Tc intervals in clinical practice. They evaluated the dispersion of these intervals within the set of 21 patients after myocardial infarction with sustained ventricular tachycardia, and compared it with the dispersion within the control set of 17 patients after myocardial infarction without an arrhythmic episode. By means of comparison, they have discovered that: 1) the dispersion of Q-T and Q-Tc intervals is significantly higher in patients with ventricular tachycardia: Q-T (mean +/- SE) 82.8 +/- 7.8 msec vs 42.2 +/- 4.8 msec, Q-Tc 93.0 +/- 10.2 msec vs 47.1 +/- 4.8 msec, p > 0.001, 2) the dispersion of Q-Tc when higher than 60 msec is an optimum discrimination value for the prognosis of sudden arrhythmic death after myocardial infarction (sensitivity 81%, specificity 76%) and 3) the dispersion of Q-T and Q-Tc intervals has no relation to the function of the left ventricle. Therefore the authors consider the dispersion of Q-T and Q-Tc intervals as being a useful marker of malignant ventricular arrhythmia which could be included into the algorithm of assessment of the risk of sudden arrhythmic death after myocardial infarction.     

The role of the atrium and optimal values of AV intervals in sequentially paced patients

In 1995, 2249 dual chamber pacemakers were implanted in the Czech Republic. These pacemakers make it possible to set an optimal AV delay between the atrial and ventricular impulse. Although the optimization of the AV interval has its well defined physiologic advantages, it does not seem to be necessary in otherwise healthy individuals with a good atrial and ventricular function. In these patients the default value, usually about 170 ms, is acceptable. However, AV interval optimization--i.e. finding the interval at which the atrial contribution to ventricular filling is maximal--should be done in all patients with left ventricular dysfunction, indicated for pacing because of bradyarrhthmia. In this subset of patients, even a small improvement in ventricular filling is believed to be clinically useful. Moreover, it has been documented, that in some types of ventricular dysfunction the so-called "primary optimization" (i.e. optimization of the AV interval in patients, in whom the pacemaker is not indicated for bradyarrhthmia but for ventricular dysfunction that might be improved by AV interval optimization) may be clinically useful. It is the case in patients with hypertrophic obstructive cardiomyopathy, dilated cardiomyopathy with presystolic regurgitation and AV interval prolongation, and perhaps even in some patients with impairment of ventricular systolic function and substantial prolongation of the AV interval. Despite all that, optimization of the AV interval is not routinely performed because even the best available optimization procedures (stroke volume measurements at different AV intervals by aortic Doppler echography) is observer dependent, time-consuming and costly.     

Neuropsychological function in adults with attention-deficit hyperactivity disorder

Pacemaker therapy in patients with atrial fibrillation means the best current pacemaker therapy for patients with bradycardias with the aim to avoid the onset of atrial fibrillation and to establish DDD pacing despite of a history of atrial tachyarrhythmias. The newer application of pacing is the suppression of atrial arrhythmias in patients with medical refractory atrial tachyarrhythmias. Patients with slow ventricular rates and permanent atrial fibrillation should receive a VVI-pacemaker, if the bradycardias causes syncope, dizziness or a decrease of their exercise tolerance. In case of chronotropic incompetence the pacemaker should provide rate responsive pacing. Patients with sick sinus syndrome should receive an atrial (AAI) or dual-chamber (DDD) pacemaker, because patients with these in contrast to VVI-pacemakers develop less often atrial fibrillation and subsequent complications such as atrial thromboembolism. A dual-chamber or VDD-pacemaker--the latter connected to a VDD-single-lead--is indicated in patients with advanced AV-block. Atrial fibrillation occurs in 3 to 6% of the patients with no history of arrythmia and is, if pacemakers have no automatic mode switch, an often reason to program the devices to the VVI-pacing mode. Nowadays, most DDD(R)-pacemakers provide an automatic mode switch: During an atrial tachycardia the pacemaker switches to a VVI/VVIR mode and restores the initial DDD(R)-pacing mode with termination of the arrhythmia. In respect to the newer applications, one approach to prevent atrial tachyarrhythmias is permanent atrial pacing. As lower pacing rates of 80 to 90 ppm are usually needed and many patients hardly tolerate these pacing rates, new algorithms are under clinical investigation. Another approach is the simultaneous depolarization of the right and left atrium. Biatrial pacing is performed with one lead in the high right atrium and another lead in the coronary sinus. Another solution is bifocal atrial pacing with leads placed in the high right atrium and in the coronary sinus ostium. One effect of the new pacing techniques is to shorten interatrial conduction times. Therefore, biatrial pacing has become a therapy to prevent atrial arrhythmias deriving from delayed interatrial conduction times. As atrial reentry circuits seem to be important in atrial fibrillation, multisite atrial pacing is also performed in patients with medical refractory paroxysmal atrial fibrillation. Preliminary results suggest a more effective prevention of atrial fibrillation; nevertheless, these techniques should be still restricted to patients enrolled in clinical studies.     

Circannual variation of malignant ventricular tachyarrhythmias in patients with implantable cardioverter-defibrillators and either coronary artery disease or idiopathic dilated cardiomyopathy

We studied the possible relation between the frequency of ventricular tachyarrhythmic events and thermal stress in patients with an implantable cardioverter-defibrillator (ICD) living in a locally limited area under homogeneous climatic conditions. The frequency of tachyarrhythmic events was correlated with the thermal stress level according to the "Klima Michel Model," a complete thermophysiologic model that calculates "felt-temperature" values on the basis of the outdoor temperature and further meteorologic data. During a mean follow-up time of 40 +/- 17 months (range 4 to 72), 761 ventricular tachyarrhythmic events occurred in 50 of 138 consecutive ICD recipients. Analysis of the monthly felt-temperature levels and the mean circannual variation of the registered ventricular arrhythmias suggested that very cold and very hot conditions may be associated with an increased frequency of ventricular tachyarrhythmias. This finding was confirmed by calculation of the sum of tachyarrhythmias on all 2,039 days of the follow-up period divided into 5-degree-step felt-temperature classes. Thus, thermal stress may be 1 factor triggering the occurrence of ventricular tachyarrhythmias in patients with cardiac disease and suppressed cardiac function. Part of the increase in cardiac mortality under above-average hot and cold atmospheric conditions may be attributed to ventricular arrhythmic events.     

Recurrent polymorphic ventricular tachycardia complicating radiofrequency catheter ablation of the atrioventricular junction

Recurrent ventricular tachycardia and ventricular fibrillation were observed immediately after RF ablation of the AV junction in a 64-year-old man. This arrhythmia was preceded by ventricular bigeminy and a long-short sequence. It was not associated with prolongation of the QT interval compared to baseline, and recurred 3 months later despite ventricular pacing at 90 beats/min. This is the first reported case of sustained ventricular arrhythmia complicating RF AV junction ablation despite rapid ventricular pacing, and recurring 3 months after discharge. It may explain the rare cases of sudden death complicating this procedure.     

Frequency-dependent effects of propafenone decrease with duration of ventricular tachycardia in isolated guinea pig hearts

Na+ channel blockers terminate tachyarrhythmias primarily by rate-dependent effects. The purpose of this study was to investigate the use-dependent effects of propafenone in isolated guinea pig and rabbit hearts perfused by the method of Langendorff. In the presence of propafenone (0.3 microM) during ventricular pacing, an abrupt decrease of the pacing cycle length (220 ms to 120 ms) slowed the intraventricular conduction with a transient peak QRS prolongation of 33.8 +/- 2.0% after 5.7 +/- 0.5 s (P < 0.01) which subsequently decreased to a steady state of 14.0 +/- 2.5% after 38.0 +/- 5.5 s (mean +/- S.E.M.; n = 10; P < 0.01). The ventricular effective refractory period was significantly prolonged if evaluated by a train of 10 basic stimuli (S1) (interstimulus interval: 120 ms) followed by a premature stimulus (S2). However, when the train of basic stimuli was increased the effective refractory period diminished progressively. An initial increase in total activation time vanished with continued rapid ventricular stimulation. These effects may be explained by a shortening of the action potential during high rates resulting in a decreased binding of propafenone to Na+ channels.     

Probucol-induced QT prolongation and syncope

We report a patient who experienced a reversible prolongation of the QT interval and episodes of syncope while receiving probucol. A 64-year-old woman experienced syncopal attacks 8 and 11 weeks after beginning probucol treatment (500 mg twice daily). The pre-treatment ECG showed a slight prolongation of the corrected QT interval (QTc) (0.46 sec). Her QTc increased to 0.62 sec 12 weeks after beginning probucol treatment and decreased to about the baseline value (0.48 sec) 6 weeks after treatment was discontinued. Probucol is known to prolong the QT interval. A long QT interval has been linked to an increased risk of ventricular arrhythmias, syncope or sudden death. However, clinical reports which causally relate probucol treatment to syncope are very rare. Although an ECG during the episodes of syncope was not available, this patient's syncope might be due to ventricular tachyarrhythmia associated with probucol-induced QT prolongation. This case emphasizes the need for careful evaluation of the QT interval before and during probucol treatment.     

Depressed renal and vascular nitric oxide synthase expression in cyclosporine-induced hypertension

With the longer life expectancy of the population, calcific aortic stenosis has become a common cardiac problem in the elderly. When patients with moderate to severe aortic stenosis become symptomatic, the prognosis is usually poor in absence of valve replacement and sudden death is a feared complication. It has been hypothesized that malignant ventricular arrhythmias could be responsible for the high incidence of sudden death in symptomatic patients with aortic stenosis. The purpose of this review is to analyze the prevalence, the electrophysiologic mechanisms, and the possible role of ventricular arrhythmias in the development of symptoms and in the outcome of adult subjects with aortic stenosis.     

Noise detection during bradycardia pacing with a hybrid nonthoracotomy implantable cardioverter defibrillator system: incidence and clinical significance

The purpose of this study was to prospectively evaluate the incidence of noise detection during bradycardia pacing by an FDA approved hybrid nonthoracotomy ICD system. An illustrative case report which prompted this investigation is provided. Backup bradycardia pacing by tiered therapy cardioverter defibrillators has been useful in preventing postshock bradycardia and occasionally for chronic rate support in bradycardic patients. Unexplained "noise" detected by real-time telemetry has been previously described during bradycardia pacing by a device utilizing automatic gain control for sensing. Eighteen patients were prospectively evaluated for noise detection during ventricular pacing by the ICD. Real-time telemetry was analyzed with each patient: (1) supine, (2) supine with deep inspiration/expiration, (3) supine during Valsalva, and (4) during a change in position from supine to sitting. Analysis of pacing threshold and lead impedance was made in each patient. Eleven of 18 patients had noise detected on real-time telemetry during bradycardia pacing. In 10 patients this was noted during deep inspiration/expiration, in 2 during Valsalva maneuver, and in 5 with position change. There was no evidence in any patient of lead malfunction nor any difference in pacing threshold or lead impedance between patients with noise detected versus those without it. Noise detection by an approved hybrid ICD system is common and may be due to the automatic gain control which maximizes sensitivity during bradycardia pacing. This may lead to clinically significant events, with both suppression of bradycardia pacing and triggering of tachycardia therapy in the absence of ventricular tachyarrhythmias in pacemaker-dependent patients.     

Severe digoxin intoxication in a 15-year-old girl treated with Fab antidigoxin

The precise aetiology of sudden death in patients receiving neuroleptic medication is uncertain, but cardiac arrhythmias are a possible cause. We investigated the link between neuroleptic medication and electrocardiographic changes predictive of malignant cardiac arrhythmias. Electrocardiographs were performed on 111 patients receiving neuroleptic medication and on 42 unmedicated controls. Prolonged QTc intervals were more common in the patient sample, but QTc dispersion was not significantly increased. QTc interval prolongation was more likely in patients on doses above 2000 mg chlorpromazine equivalents daily (odds ratio 4.28, P < 0.02). Neuroleptic medication, especially at high doses, is associated with ECG changes that may herald more serious cardiac problems.     

The origin of ventricular arrhythmias 24 hours following experimental anterior septal coronary artery occlusion

The anterior septal coronary artery was acutely ligated in 16 open-chest anesthetized dogs to produce an infarct of the septal myocardium. Twenty-four hours following occlusion complete epicardial mapping and extensive plunge electrode recording techniques were used to localize the sites of origin and patterns of activation of the ventricular tachyarrhythmias that developed during recovery. The earliest electrical activity for 13 individual rhythms was recorded from surviving septal subendocardial Purkinje fibers at the margins of the infarct, in the right or left ventricle, directly underlying the sites of earliest epicardial breakthrough. The sites of origin were verified by demonstrating unchanged activation sequences during pacing through the electrode sites which recorded the earliest activity. None of the arrhythmias arose from the His bundle or bundle branches despite the fact that these tissues course directly through the necrotic septum. The data presented supports the hypothesis that ventricular arrhythmias occuring in the 24-36 hour post acute infarction period may originate in the surviving subendocardial Purkinje system. Our experimental model shows that in cases in which a malignant rhythm arises from a focus, whether it is due to enhanced automaticity or local re-entry, epicardial mapping alone may not identify the source of the arrhythmias. Extensive endocardial mapping may provide a more rational basis for surgical interventions designed to abolish these arrhythmias.     

Arrhythmias associated with acute myocardial infarction and thrombolysis

Ninety percent of patients with acute myocardial infarction have some cardiac rhythm abnormality, and approximately twenty-five percent have cardiac conduction disturbance within 24 hours following infarct onset. Almost any rhythm disturbance can be associated with acute myocardial infarction, including bradyarrhythmias, supraventricular tachyarrhythmias, ventricular arrhythmias, and atrioventricular block. With the advent of thrombolytic therapy, it was found that some rhythm disturbances in patients with acute myocardial infarction may be related to successful coronary artery reperfusion. This article addresses the role and treatment of arrhythmias and conduction disturbances that complicate the course of patients with acute infarction and thrombolysis.     

Pediatric use of intravenous amiodarone: efficacy and safety in critically ill patients from a multicenter protocol

OBJECTIVE: The purpose of this study was to analyze the efficacy and safety of intravenous amiodarone in young patients with critical, drug-resistant arrhythmias. BACKGROUND: Intravenous amiodarone has been investigated in adults since the early 1980s. Experience with the drug in young patients is limited. A larger pediatric study group was necessary to provide responsible guidelines for the drug's use before its market release. METHODS: Eight centers obtained institutional approval of a standardized protocol. Other centers were approved on a compassionate use basis after contacting the primary investigator (J.C.P). RESULTS: Forty patients were enrolled. Standard management in all failed. Many patients had early postoperative tachyarrhythmias (25 of 40), with early successful treatment in 21 (84%) of 25. Twelve patients had ventricular tachyarrhythmias: seven had successful therapy, and six died, none related to the drug. Eleven patients had atrial tachyarrhythmias: 10 of 11 had immediate success, but 3 later died. Fourteen patients had junctional ectopic tachycardia, which was treated with success (sinus rhythm or slowing, allowing pacing) in 13 of 14, with no deaths. Three other patients had supraventricular tachycardias, with success in two and no deaths. The average loading dose was 6.3 mg/kg body weight, and 50% of patients required a continuous infusion. Four patients had mild hypotension during the amiodarone bolus. One postoperative patient experienced bradycardia requiring temporary pacing. There were no proarrhythmic effects. Deaths (9 [23%] of 40) were not attributed to amiodarone. CONCLUSIONS: Intravenous amiodarone is safe and effective in most young patients with critical tachyarrhythmia. Intravenous amiodarone can be lifesaving, particularly for postoperative junctional ectopic tachycardia, when standard therapy is ineffective.     

Clinical and electrophysiological observations in a case of Romano-Ward syndrome

Syncope associated with atypical ventricular tachycardia of the "torsades de pointes" type was observed in a 16 year-old girl with hereditary QT prolongation. The arrhythmia occurred only during maximal prolongation of the QTc to 0.77 sec, which had possibly been aggravated by exercise and hypokalaemia. Electrophysiological studies were performed when the QTc was 0.59 sec. Incremental as well as premature ventricular pacing with single or double premature ventricular beats did not initiate ventricular arrhythmias, but revealed AV nodal and bundle branch reentry. It is postulated that these types of macroreentry are involved in the twisting of the QRS complexes in the surface ECG in torsades de pointes.     

Effect of flecainide on atrial and ventricular refractoriness and conduction in patients with normal left ventricle. Implications for possible antiarrhythmic and proarrhythmic mechanisms

We studied the effects of intravenous flecainide (2 mg.kg-1) on atrial and ventricular refractoriness and conduction during sinus rhythm, induced atrial fibrillation and atrial pacing at rates of 100, 120 and 150 ppm, in 14 patients with normal left ventricle. Flecainide caused a significant increase in QRS duration during sinus rhythm (mean +/- SD: 87.2 +/- 8.4 ms vs 102.8 +/- 9.1 ms, P < 0.001), atrial fibrillation (87.8 +/- 10.0 ms vs 108.8 +/- 13.7 ms, P < 0.001) and at all paced rates. The duration of the atrial electrogram was significantly increased during sinus rhythm (54.9 +/- 13.2 ms vs 64.8 +/- 16.6 ms, P = 0.003) and at all pacing rates. The PA interval was also significantly prolonged, as was the pacing stimulus-to-atrial-electrogram interval at all pacing rates. There was increased QRS duration and atrial electrogram prolongation at higher pacing rates. Atrial refractoriness was prolonged during sinus rhythm (216.4 +/- 28.2 vs 228.6 +/- 36.1, P = 0.02), but not during atrial pacing at any rate. The QT interval, but not the JT interval or ventricular refractoriness, was significantly prolonged during sinus rhythm and at all pacing rates. Flecainide slows atrial conduction in a use dependent manner and increases atrial refractoriness during sinus rhythm but not during faster atrial pacing, thus not displaying a use-dependent effect. QRS duration is prolonged in a use-dependent manner without a commensurate increase in ventricular refractoriness. In the presence of rapidly conducted atrial fibrillation, which was not found to be slowed by flecainide, this effect may constitute a proarrhythmic mechanism even in patients with no apparent myocardial abnormality.     

Effect of para-aminobenzoic acid on the development of rat embryos when applied to pregnant females

BACKGROUND: Epicardial pacing wires are routinely used for the diagnosis and treatment of bradyarrhythmias after cardiac surgery. The frequency of arrhythmias during removal of the wires is unknown, and methods of removal vary among institutions. OBJECTIVES: To describe the frequency of ventricular arrhythmias during removal of epicardial pacing wires from the right ventricle, to determine variables that are predictive of ventricular arrhythmias during wire removal, and to describe patients' perceptions of wire removal. METHODS: A convenience sample of 145 patients who had undergone cardiac surgery was studied during the course of 1 year. Electrocardiographic and vital signs were recorded throughout wire removal. Patients' records were reviewed for variables that could predict the occurrence of arrhythmias during wire removal: laboratory values, history of arrhythmias, medications, medical history, postoperative course, and pain reported by the patient. RESULTS: Sixty-six percent of patients had one premature ventricular contraction or more while the ventricular wires were being removed. Seven percent of patients had nonsustained ventricular tachycardia during wire removal. Patients who had repeat cardiac surgery had significantly more nonsustained ventricular tachycardia than did all other patients (P < .01). Only a history of heart failure (P < .02) was a significant predictor of premature ventricular contractions during wire removal. On a scale of 0 (no pain) to 10 (worst pain), the mean rating of pain intensity reported by patients was 2.39 (SD = 2.77). CONCLUSION: Patients may be at risk for ventricular arrhythmias during removal of epicardial pacing wires. Findings support the need for electrocardiographic monitoring while pacing wires are being removed.     

Block of potassium currents in guinea pig ventricular myocytes and lengthening of cardiac repolarization in man by the histamine H1 receptor antagonist diphenhydramine

Treatment with second generation histamine H1 receptor antagonists has been associated with lengthening of the Q-T interval and proarrhythmia. Similarly, lengthening of the Q-T interval has been reported in patients after overdosing with diphenhydramine (DPH), a first generation agent. Therefore, our study was designed 1) to assess effects of DPH on cardiac repolarization and 2) to characterize effects of the drug on major voltage-dependent cardiac K+ currents. First, we noticed that oral administration of DPH at usual dosages to healthy volunteers or to patients (prior to angioplasty) was associated with prolongation of the Q-Tc interval. Although this effect was modest in most individuals, Q-Tc was increased more than 20 ms in 7 of 20 patients. Second, we noticed that exposure of isolated guinea pig hearts to DPH 10(-5) M caused a lengthening of monophasic action potential duration. This effect was potentiated by the combined perfusion of other K+ channel blockers such as indapamide. Finally, experiments performed with the patch-clamp technique demonstrated unequivocal block of the rapid component of the delayed rectifier (IKr) by DPH; however, IC50 determined for block of IKr (3 x 10(-5) M) is approximately 40-fold greater than plasma concentrations of the drug measured at usual dosages (7 x 10(-7) M). Consequently, in agreement with the long-term clinical use of the drug, prolongation of cardiac repolarization should be minimal in most patients at usual dosages but may be observed with overdosing. Nevertheless, caution remains since excessive lengthening of cardiac repolarization may occur after administration of DPH with other drugs due to 1) concomitant block of other ionic currents or 2) pharmacokinetic interactions leading to toxic concentrations of DPH.     

Cardiac arrhythmia associated with malignant neuroleptic syndrome: description of 2 clinical cases

Malignant neuroleptic syndrome (alteration of consciousness, muscle rigidity and hyperthermia) is a potentially lethal condition, due also to its life-threatening complications. In particular, hypokinetic and hyperkinetic arrhythmias can be rare and severe early manifestations of this illness, and they deserve a careful approach because of their drug-refractoriness. Arrhythmias associated with the malignant neuroleptic syndrome depend on various mechanisms: neurotransmitter receptor blockades typical of neuroleptic drugs, clustered lipid droplets among the cardiac myofibrils and possible electrolytic disorder due to diaphoresis. The two cases described here presented hypokinetic and hyperkinetic (supraventricular and ventricular) arrhythmias. The arrhythmias, which failed to respond to antiarrhythmic drugs, were temporarily suppressed by DC shock, over-drive pacing and correction of electrolytic imbalance. In case 1, prolonged bromocriptine treatment was required. Complete wash-out of the causative agents resulted in lasting regression of arrhythmias. In conclusion, a correct treatment and a favourable outcome of this syndrome can be achieved only through early diagnosis.     

Therapy of ventricular tachyarrhythmia with implantable cardioverters/defibrillators--mortality and complications using epicardial electrodes

Technical improvements of third generation implantable cardioverter defibrillators (ICD) like antitachycardia pacing modalities lead to an extended use of ICDs, not only in patients with aborted sudden cardiac death, but also in patients with hemodynamically tolerable ventricular tachycardia. In addition, anticipated results of current prospective studies might indicate the prophylactic use of ICDs in patients with high risk for sudden cardiac death, but without documented ventricular tachyarrhythmias. This report reviews mortality and complications associated with the ICDs with epicardial defibrillation leads. Mortality is separated in cardiac death, sudden cardiac, arrhythmogenic "not so sudden" cardiac death, and overall mortality. Pulmonary complications and infections are related to the underlying disease and the surgical procedure. Device- and lead-related complications, high defibrillation thresholds, pacemaker interactions, inappropriate shocks, arrhythmic effects, syncope, and psychosocial problems are reported, respectively.