Induced Sustained Ventricular Tachycardia in Nonischemic Dilated Cardiomyopathy: Dependence on Clinical Presentation and Response to Antiarrhythmic Agents

Thirty-one patients with nonischemic dilated cardiomyopathy either idiopathic or due to regurgitant valvular disease were studied in the cardiac electrophysiology lab. The indications for study were sustained ventricular tachycardia (VT) in 26, ventricular fibrillation (VF) in 11, and syncope of unknown etiology in 4. Sustained VT was reproducibly induced in 17 patients, including 12 with a history of sustained VT, 2 with VF and 3 with syncope. Of 15 patients undergoing serial antiarrhythmic drug studies, sustained VT was rendered noninducible or nonsustained in 23. Three had recurrent arrhythmic events while on therapy predicted to be effective. One of 2 patients discharged on a regimen predicted to be ineffective had a recurrence of sustained VT that resulted in cardiac arrest. Of 14 patients in whom sustained VT could not he reproducibly induced, 2 subsequently had spontaneous occurrences of sustained VT, and 2 experienced aborted sudden death. These results suggest the following; (1) the induction of sustained VT in the setting of nonischemic dilated cardiomyopathy is dependent on the clinical presentation; (2) antiarrhythmic drugs frequently render sustained VT noninducible or nonsustained; (3) antiarrhythmic drug suppression of inducible sustained VT predicts long-term prevention of spontaneous recurrences; and (4) noninducibility of sustained VT in the baseline state does not predict freedom from subsequent episodes of VT or sudden death.     

A Comparison of Ventricular Arrhythmias Induced with Programmed Stimulation Versus Alternating Current

In patients undergoing implantation and testing of the implantable cardio-verter defibrillator (ICD), alternating current (AC) may be used to induce ventricular tachyarrhythmias in a prompt, safe, and efficient manner. These arrhythmias have been previously reported to be similar to those induced during programmed electrical stimulation (PES). We compared the ventricular tachyarrhythmias induced by both methods in 14 patients: 8 male, 6 female; mean age 61 years; coronary disease in 10, cardiomyopathy in 4; mean ejection fraction 31%. The presenting arrhythmia was nonsustained ventricuiar tachycardia (VT) in four, sustained monomorphic ventricular tachycardia (SMVT) in five, ventricular fibrillation (VF) in four, and unknown in one patient with syncope. PES (single, double, triple extrastimuli; burst pacing) and AC (1–2 sec application) stimulation via right ventricular endocardial electrode catheter was performed off antiarrhythmic drugs in the nonsedated state. PES induced SMVT in nine, polymorphic VT in two, and VF in three. AC induced VF in all patients. Although AC can reliably induce ventricular tachyarrhythmias during de/ibrillation threshold and ICD testing, there is poor correlation to PES induced tachyarrhythmias.     

Heart failure

Survival of patients with heart failure has improved over the past decade due to advances in medical therapy. However, sudden cardiac death continues to cause 35 to 65% of death. Ventricular arrhythmias are important causes of sudden cardiac death in patients with heart failure. The risks of antiarrhythmic drugs are increased in patients with heart failure. Therefore, in the absence of a clear indication, antiarrhythmic drug therapy should be avoided. A number of recent randomized trials have provided evidence that beta-adrenergic blockers, angiotensin-converting enzyme(ACE) inhibitors and angiotensin II receptor blockers(ARB) significantly reduces the risk of sudden death in patients with chronic congestive heart failure. For patients who have a history of sustained ventricular tachycardia(VT) or ventricular fibrillation(VF) amiodarone or an implantable cardioverter defibrillator(ICD) should be considered, and these therapy may benefit some high risk patients who have nonsustained VT.     

Long-Term Outcome Following Programmed Electrical Stimulation in Patients with High-Grade Ventricular Ectopy

To determine if programmed electrical stimulation (PES) could be utilized to identify patients with high-grade ventricular ectopy at low- or high-risk for sudden cardiac death, we performed PES in 40 patients with high-grade ventricular ectopy refractory to conventional antiarrhythmic agents. Twenty-one patients had a previous myocardial infarction, five had cardiomyopathy, six had hypertension, three had valvular heart disease and five had no known structural heart disease. The mean age was 50 years (range, 18 to 76). During programmed ventricular stimulation, eight patients had inducible sustained (more than 30 seconds) monomorphic ventricular tachycardia (Group I) but in 32 patients sustained ventricular tachycardia was not inducible (Group II). None of the five patients without structural heart disease were inducible while seven out of 21 (33%) patients with previous myocardial infarction had inducible ventricular tachycardia (VT). Antiarrhythmic therapy was instituted in patients with inducible VT; patients without inducible VT did not receive antiarrhythmic agents. In Group I, seven of the eight patients are alive (mean follow-up, 16 months) and in Group II, 28 of the 32 patients are alive (mean follow-up, 17 months). None of the five deaths were sudden. We conclude that in the absence of antiarrhythmic therapy, the incidence of sudden cardiac death is very low in patients with high-grade ventricular ectopy who do not have inducible monomorphic ventricular tachycardia during programmed ventricular stimulation.     

Amiodarone in the Management of Patients with Ventricular Tachycardia and Ventricular Fibrillation

Fifty-eight patients with symptomatic ventricular tachycardia (VT) or ventricular fibrillation (VF) were treated with amiodarone. All had clinical episodes of VT/VF or inducible VT during electropharmacologic testing despite treatment with maximumtolerated doses of conventional antiarrhythmic agents. Chronic treatment with amiodarone was begun at a dose of 800–1000 mg per day. Thirty-two patients were also treated with a previously ineffective conventional agent. Thirty patients underwent programmed ventricular stimulation after 2.6 ± 1.7 months (mean ± S. D.) of treatment with amiodarone at a mean daily dose of 588 ± 155 mg. VT was induced in 25 patients (sustained in 20, nonsustained in five). Seventeen patients had a recurrence of VT or VF after 0.5–9 months of treatment with amiodarone (fatal in seven, non-fatal in 10). Forty-one patients (71%) had no recurrence of symptomatic VT or VF while being treated with amiodarone (mean follow-up period, 17.1 ± 12.4 months). Among the 25 patients who had inducible VT with programmed ventricular stimulation while being treated with amiodarone, 19 patients (76%) have had no recurrence of symptomatic VT or VF overa follow-up period of 21.5 ± 7.3 months. Ambulatory electrocardiographic recordings obtained after one week of treatment with amiodarone were not helpful in predicting clinical response. Twenty-two patients (38%) developed ataxia and/or an intention tremor which improved with a decrease in the amiodarone dose. Amiodarone, either by itself or in combination with conventional antiarrhythmic drugs, has a significant therapeutic effect in high risk patients with refractory VT. The finding of inducible VT during electropharmacologic testing in patients taking amiodarone does not preclude a favorable clinical response. Neurologic toxicity is common in patients treated with 600–800 mg per day of amiodarone.     

Malignant Ventricular Arrhythmias in Patients with Mitral Valve Prolapse and Mild Mitral Regurgitation

Mitral valve prolapse (MVP) is a common disorder that, in general, has a good prognosis. Rare occasions of sudden death have been reported in patients with MVP and it is presumed that the basis of sudden death is arrhythmic. We report seven patients with moderate to severe MVP and malignant ventricular arrhythmias. All patients had trivial to mild mitral regurgitation and normal left ventricular function. Three patients presented with syncope, two with out-of-hospital cardiac arrest, and three with recurrent palpitations and presyncope. In a mean follow-up period of 2.5 years (range 6 months to 5 years), two patients died suddenly despite successful control of their nonsustained ventricular tachycardia (VT) with sotalol as shown by ambulatory monitoring. Two patients, who had sustained VT despite antiarrhythmic drug therapy, had mitral valve surgery, however, monomorphic VT could be induced in both even after surgery. The arrhythmias in the remaining three patients are controlled on antiarrhythmic drugs. We conclude that a selected subset of patients with MVP, malignant ventricular arrhythmias, and miid mitral regurgitation are at risk of sudden death. Syncope, inferolateral repolarization changes, complex ventricular ectopy, and a markedly myxomatous valve may be pointers to higher risk of sudden death and mitral valve surgery may not provide control of ventricular arrhythmias.     

The Value of Electrophysiology Study and Prophylactic Implantation of Cardioverter Defibrillator in Patients with Hypertrophic Cardiomyopathy

Fifty-three consecutive patients with hypertrophic cardiomyopathy (HCM) and no history of sudden death underwent electrophysiology (EP) study. Sustained polymorphic ventricular tachycardia (VT) or ventricular fibrillation (VF) was induced in 19 patients (35%). Patients with prior syncope or near syncope had a higher incidence of VT/VF inducibility. An implantable cardioverter defibrillator (ICD) was placed in 14 of the 19 patients. Of the remaining 5 patients with inducible VT/VF, three refused ICD implantation, while two underwent septal myectomy and VT/VF was no longer inducible afier the operation. None of the patients received antiarrhythmic drugs. During a mean follow-up period of 47 ± 31 (2–117) months, no events occurred in the 34 patients with negative EP study. Three events occurred among the 19 patients with inducible VT/VF. One patient died suddenly, one developed wide complex tachycardia which required resuscitation, and one patient received an appropriate ICD shock. In conclusion, sustained polymorphic VT/VF was inducible in about one-third of patients with HCM. Noninducibility of VT/VF appeared to predict a favorable prognosis. Although the overall event rate was low in patients with inducible VT/VF, prophylactic ICD implantation in patients with multiple risk factors may be appropriate.     

Sustained polymorphic arrhythmias induced by programmed ventricular stimulation have prognostic value in patients receiving defibrillators

BACKGROUND: Patients with ischemic cardiomyopathy (ICM) who have monomorphic ventricular tachycardia (VT) induced by programmed ventricular stimulation (PVS) are at increased risk of sudden cardiac death (SCD). Among a primary prevention population, the prognostic significance of induced polymorphic ventricular arrhythmias is unknown. METHODS: A total of 105 consecutive patients who received an implantable cardioverter-defibrillator (ICD) for primary prevention of SCD in the setting of ICM and non-sustained VT were retrospectively evaluated. Seventy-five patients (group I) had induction of monomorphic VT and 30 patients (group II) had a sustained ventricular arrhythmia other than monomorphic VT (ventricular flutter, ventricular fibrillation, and polymorphic VT) induced during PVS. RESULTS: Baseline characteristics were similar between group I and group II except for ejection fraction (25% vs. 31%, P = 0.0001) and QRS duration (123 milliseconds vs. 109 milliseconds, P = 0.04). Sixteen of 75 (21.3%) patients in group I and 6 of 30 (20%) patients in group II received appropriate ICD therapy (P = 0.88). Survival free from ICD therapy was similar between groups (P = 0.54). There was a trend toward increased all-cause mortality among patients in group I by Kaplan-Meier analysis (P = 0.08). However, when adjusted for age, EF, and QRS duration mortality was similar (P = 0.45). CONCLUSIONS: There is no difference in rates of appropriate ICD discharge or mortality between patients dichotomized by type of rhythm induced during PVS. These results suggest that patients in this population who have inducible VF or sustained polymorphic VT have similar rates of subsequent clinical ventricular tachyarrhythmias as those with inducible monomorphic VT.     

Inappropriate shock delivery by implantable defibrillators with dual chamber pacing during nonsustained ventricular tachycardia in patients with heart block

Transvenous implantable cardioverter defibrillators (ICDs) have improved the management of patients with ventricular tachycardia/ventricular fibrillation (VT/VF). Many patients with sustained VT/VF have bradyarrhythmias and nonsustained VT. Shock delivery due to nonsustained VT would be an undesirable feature. Abortive shock capability (noncommitted shocks) is a feature available in devices to prevent delivery of shocks for nonsustained VT. Recently, the availability of dual chamber pacing capability has improved the efficacy of ICDs by obviating the need of separate pacemaker implantation in patients with VT/VF and concomitant bradyarrhythmias. However, interaction between bradyarrhythmias and VT/VF has not been described and has important clinical implications. We report a case in which a patient with complete atrioventricular (AV) block and ventricular arrhythmias received an inappropriate shock following spontaneous termination of nonsustained VT, showing an important shortcoming of devices with these features.     

Effects of Coronary Artery Bypass Grafting on Ventricular Arrhythmias: Results with Electrophysiological Testing and Long-Term Follow-Up

Myocardial revascularization was performed in 56 patients with coronary artery disease who presented with ventricular tachycardia (VT) (n = 39) or ventricular fibrillation (n = 17). There were 46 men and 10 women, aged 65 ± 10 years. Three vessel (n = 42) or left main disease (n = 4) was present in 82%. Left ventricular ejection fraction averaged 36%± 11%. Electrophysioiogical studies were performed preoperatively in all patients; 50 (89%) had inducible ventricular arrhythmias. Sustained monomorphic VT was induced in 40 patients (cycle length 284 ± 61 msec). Reproducible symptomatic nonsustained VT was induced in four patients and ventricular fibrillation in six patients, while six patients had no inducible arrhythmia. Preoperatively the patients with inducible VT failed 3.3 ± 1.2 drug trials during electrophysiological studies. In addition to coronary bypass, 22 patients also received an automatic implantable cardioverter defibrillator (ICD), 26 patients received prophylactic ICD patches, and 1 patient had resection of a false aneurysm. There were no perioperative deaths. Postoperative electrophysiological studies were performed in all 56 surgical survivors. Ventricular tachyarrhythmia could not be induced in the six patients who had no inducible VT preoperatively and in 13 of 40 (33%) with preoperatively inducible sustained VT or in 19 of 50 (38%) patients with any previously inducible ventricular arrhythmia, thus a totaJ of 25 patients (45%) had no inducible VT postoperatively. Of the remaining, 11 patients were treated with antiarrhythmic drugs alone, 11 had already received an ICD (combined with drugs in 7), and another 9 received the ICD postoperatively (combined with drugs in 4). At a mean foJJow-up of 28 ± 21 months there were 11 deaths (20%): 2 sudden, 5 nonsudden cardiac, and 4 noncardiac deaths. There were 16 nonfatal VT recurrences (29%): 14 among patients with persistently inducible arrhythmias, and onJy 2 among those with no inducible arrhythmia postoperatively (P = 0.004); 13 occurred in patients with an ICD (P = 0.01). Thus among these patients with malignant ventricular arrhythmias who underwent revascuJarization, 45% had no inducible arrhythmia postoperatively with 33% of those with preoperatively inducible sustained VT apparently rendered noninducible by revascularization, while the majority (70%) remained free of major arrhythmic events during long-term follow-up. We conclude that myocardial revascularization alone can result in no ventricular arrhythmia induction in selected patients with VT inducible prior to surgery. Long-term follow-up of such patients indicates a low sudden death and arrhythmia recurrence rate. Furthermore, in patients with persistently inducible ventricular tachyarrhythmias after coronary revascuJarization, the sudden death rate is low despite a high frequency of nonfatal arrhythmia recurrence when antiarrhythmic medications are guided by programmed stimulation or an ICD is used.     

Predictive Characteristics of Holter-Based Postinfarction Risk Stratifiers Appear Superior to Electrophysiological Testing

Prevalent low-frequency (PLF) oscillation of heart rate and turbulence slope (TS) are both powerful postmyocardial infarction (MI) risk factors. Abnormal composite risk stratifier (CRS) was defined as abnormal PLF or abnormal TS when PLF was not analyzable. We compared the predictive power of CRS with the previously published predictive value of conventional electrophysiological (EP) testing based on the presence of nonsustained ventricular tachycardia (NSVT) and inducibility of sustained ventricular tachycardia/fibrillation (VT/VF) during programmed ventricular stimulation (PVS). PLF and TS were calculated from baseline Holter recordings in the placebo population of European Amiodarone Infarction Myocardial Infarction Trial (EMIAT trial) (n = 633; LVEF ≤ 40%; 87 deaths; 22-month follow-up). Previously established cut-off values of PLF ≥ 0.1 Hz and TS ≤ 2.5 ms/RR were used. The clinical characteristics of the EMIAT population were similar to those of the Multicenter Unsustained Tachycardia Trial (MUSTT trial). Therefore, we compared the predictive power of CRS and conventional PVS using the values of 35% VT/VF inducibility during PVS in NSVT patients, and a 33% and 50% increase in all-cause and arrhythmic mortality, respectively, associated with VT/VF inducibility in MUSTT. Projecting the predictive power of PVS in MUSTT into the EMIAT population yielded a sensitivity of 13.8% and 14.0% and positive predictive value (PPV) of 27.9% and 14.0% for all-cause and arrhythmic mortality, respectively, whereas an abnormal CRS was associated with sensitivities of 46.0% and 46.5% and PPV of 37.4% and 18.7%. Compared with the noninvasive Holter-based CRS, invasive PVS appears inferior in the identification of high-risk post-MI patients with left ventricular dysfunction.     

Management of Nonsustained Ventricular Tachycardia Guided By Electrophysiological Testing

Two hundred eighty patients with spontaneous nonsusfained ventricular tachycardia were treated based on the results of electrophysiological testing. Seventy-nine patients had no evidence of structural heart disease, 134 had coronary artery disease, 43 had idiopathic dilated cardiomyopathy, and 24 patients had miscellaneous types of heart disease. Sustained monomorphic ventricular tachycardia was induced during electrophysiological testing in the drug free state in 52 of 280 patients (19%). Ventricular tachycardia was induced more frequently in patients with coronary artery disease (32%) than in any of the other groups (P < 0.001). The patients with inducible sustained monomorphic ventricular tachycardia underwent a mean of 1.9 ± 1.3 drug trials. Twenty-five patients had the induction of ventricular tachycardia suppressed by pharmacological therapy and were treated with the drug judged to be effective during electropharmacological testing. Twenty-seven patients continued to have inducible sustained monomorphic ventricular tachycardia despite antiarrhythmic therapy and were discharged on the drug that made induced ventricular tachycardia best tolerated. Forty-five of 280 patients (16.1%) died during a mean follow-up period of 19.6 ± 14.4 months, There were 15 sudden cardiac deaths, 21 nonsudden cardiac deaths, 6 noncardiac deaths, and 3 deaths that could not be classified. Sudden cardiac death mortality was lowest in the patients without structural heart disease (0% at 2 years), intermediate in the patients with coronary artery disease and miscellaneous heart disease (4% al 2 years), and highest in the patients with idiopathic dilated cardiomyopathy (13% at 2 years; P < 0.01 for pairwise comparisons). No patient treated with a drug that had suppressed the induction of sustained ventricular tachycardia died suddenly during the follow-up period whereas four of 27 patients who were discharged on “ineffective antiarrhythmic drugs” and 11 of 228 patients without inducible sustained ventricular tachycardia experienced sudden cardiac death during the follow-up period. By multivariate analysis, ejection fraction and inducible ventricular tachycardia during the predischarge eiectrophysiological test were independent predictors of sudden cardiac death. In conclusion, in patients with spontaneous nonsustained ventricular tachycardia: (1) Arrhythmia inducibility varies depending on the underlying heart disease. Ventricular tachycardia is most often inducible in patients with coronary artery disease and least often in patients without structural heart disease; (2) With the exception of patients with idiopathic dilated cardiomyopathy, management of patients with nonsustained ventricular tachycardia guided by electrophysiological testing appears to result in a low incidence of sudden cardiac death although effects on total mortality are less impressive; and (3) Patients with idiopathic dilated cardiomyopathy and patients with other heart diseases who continue to have inducible ventricular tachycardia despite antiarrhythmic drug therapy are at substantial risk of sudden cardiac death.     

Electrophysiologic studies of patients with hypertrophic cardiomyopathy presenting with syncope of undetermined etiology

Patients with hypertrophic cardiomyopathy (HC) have a high risk of sudden death. The best clinical predictors of sudden death from HC are young age, strong family history of sudden death, ventricular tachycardia (VT), and progression of symptoms such as syncope. We performed 24-hour Holter monitoring and electrophysiologic studies (EPS) on 26 patients with HC, some with the obstructive form of the disease and some with syncope, in order to predict their vulnerability to syncope and to potentially malignant arrhythmias. Holter monitoring demonstrated supraventricular tachycardia (SVT) in 9/26 patients whereas atrial programmed electrical stimulation induced SVT in 17/26 patients. Of the 17 patients, nine had symptomatic hypotension with SVT while lying supine. Holter monitoring demonstrated nonsustained VT in 7/26 patients whereas ventricular programmed electrical stimulation induced VT or ventricular fibrillation (VF) in 6/26 patients. The patient who had the longest run of nonsustained VT on Holter had VF induced by ventricular programmed electrical stimulation. He was cardioverted to normal sinus rhythm with no untoward effects. We found that atrial programmed electrical stimulation induced SVT with hypotension best predicted a history of syncope in these patients. Although one patient required direct current cardioversion, EPS was conducted safely in all patients. Further long-term studies are needed to demonstrate the value of clinical decisions based upon EPS in patients with HC.     

Noninvasive Arrhythmia Risk Stratification in Idiopathic Dilated Cardiomyopathy: Design and First Results of the Marburg Cardiomyopathy Study

The Marburg Cardiomyopathy Study (MACAS) is a prospective, observational study designed to determine the value of the following potential noninvasive arrhythmia risk predictors in at least 200 patients with idiopathic dilated Cardiomyopathy (IDC) over a 5-year follow-up period: NYHA-class, left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter, left bundle branch block and atrial fibrillation on ECG, QT/JT dispersion on 12-lead ECG, signal-averaged ECG, ventricular arrhythmias and heart rate variability (HRV) on 24-hour Hotter ECG, baroreflex sensitivity, and microvolt T wave alternans during exercise. This article describes the findings among the first 159 patients with IDCs enrolled in MACAS until May 1998 (40 women, 119 men;age:49 ± 12 years; LVEF: 32 ± 10%). Twenty-nine patients (18%) had atrial fibrillation and 130 patients (82%) were in sinus rhythm. Patients with sinus rhythm were further stratified according to LVEF < 30% (n = 54) versus LVEF ≥ 50% (n = 76). Compared to patients with LVEF ≥ 30%, patients with LVEF < 30% more often had left bundle branch block (43% vs 25%, P < 0.05), nonsustained VT (44% vs 22%, P < 0.05), decreased HRV (SDNN: 95 ± 39 vs 128 ± 42 ms, P < 0.01), decreased baroreflex sensitivity (5.6 ± 4 vs 8.3 ± 6 ms/mmHg, P < 0.01), and T wave alternans (59% vs 37%, P < 0.05). The prognostic significance of these findings will be determined by multivariate Cox analysis at the end of a 5-year follow-up. Primary endpoints in MACAS are overall mortality and arrhythmic events (i.e., sustained VT or VF, or sudden cardiac death).     

Nonsustained, asymptomatic ventricular tachycardia in patients with coronary artery disease: prognosis and incidence of sudden death of patients who are noninducible by electrophysiological testing

The objective of this study was to determine the long-term prognosis and the sudden death risk for patients with coronary artery disease and spontaneous nonsustained ventricular tachycardia who are not inducible by electrophysiological testing. Patients with coronary artery disease (CAD) who have spontaneous or inducible sustained ventricular tachycardia (VT) by electrophysiological testing are at increased risk of dying suddenly, and noninducibility is often considered as a favorable prognostic factor in their risk assessment. We studied 120 consecutive patients with CAD and nonsustained VT during Holter monitoring and followed the patients who were noninducible (n = 93) for 3.5 +/- 1.6 years. None of these patients received antiarrhythmic therapy except beta-blockade. Overall mortality and the sudden death risk was assessed by the Kaplan-Meier estimation. Predictors for overall mortality and sudden death were determined by multivariate analysis. During follow-up, 23 of the 93 patients died, including 13 suddenly. Overall mortality was 9% after 1 year, 16% after 2 years, and 21% after 3 years, respectively. The incidence of sudden death was 1% after 1 year, 8% after 2 years, and 13% after 3 years, respectively. Patients with a LVEF < or = 0.35 had an increased overall mortality risk with 15% after 1 year, 29% after 2 years, and 34% after 3 years (P = 0.012) and a risk of dying suddenly of 4% after 1 year, 12% after 2 years, and 18% after 3 years (P = NS), respectively. LVEF was the only independent predictor for overall mortality. In conclusion, patients with coronary artery disease and nonsustained ventricular tachycardia who are not inducible by electrophysiological testing have a moderate long-term overall mortality risk. The risk of dying suddenly in this patient group is small but not negligible, especially in patients with impaired LVEF.     

Failure of Third-Generation Implantable Cardioverter Defibrillators to Abort Shock Therapy for onsustained Ventricular Tachycardia Due to Shortcomings of the VF Confirmation Algorithm

Unnecessary shocks by ICDs for rhythms other than sustained VT or VF have been described as the most frequent adverse event in ICD patients. To avoid unnecessary shocks for self-terminating arrhythmias, the third-generation Jewel PCD defibrillators 7202, 7219, and 7220 Plus use a specially designed VF confirmation algorithm after charge end. The purpose of this study was to determine the ability of this VF confirmation algorithm to recognize nonsustained VT, and to analyze the reasons for failure of the PCD device to abort shock therapy for nonsustained VT despite use of this VF confirmation algorithm. Analysis of stored electrograms of electrical events triggering high voltage capacitor charging in the programmed VF zone of the device showed 36 spontaneous episodes of nonsustained VT (227 ± 21 beats/mm) during 18 ± 7 months follow-up in 15 patients who had a Jewel PCD implanted at our hospital. Intracardiac electrogram recordings and simultaneously retrieved marker channels demonstrated that the ICD shock was appropriately aborted according to the VF confirmation algorithm in 24 (67%) of 36 episodes of nonsustained VT. Twelve episodes (33%) of nonsustained VT, however, were followed by a spontaneous ICD shock in 6 (40%) of the 15 study patients. The only reason for all 12 shocks for nonsustained VT was the inability of the device to recognize the absence of VT after charge end due to shortcomings of the VF confirmation algorithm: 11 of the 12 shocks for nonsustained VT were triggered by the occurrence of paced beats during the VF confirmation period and 1 shock for nonsustained VT was triggered by the occurrence of 2 premature beats after charge end. Thus, better VF confirmation algorithms need to be incorporated in future PCD devices to avoid unnecessary shocks for nonsustained VT.     

Efficacy and Safety of Low Doses of Beta-Blocker Agents Combined with Amiodarone in Refractory Ventricular Tachycardia

Twenty patients aged 55 ± 16 years with 40 chronic ventricular tachycardias (VT) refractory to 4.6 ± 1.9 antiarrhythmic drugs, used alone or in combination, were managed by low doses of beta-blocker agents combined with oral amiodarone (Am), either after loading (1.2 g for 7 days, n: 5) or reloading (1.2 g for 4 days, n: 15) of Am. All patients proved refractory to Am alone. Seven VT were also refractory to endocardial catheter fulguration in six patients. Thirteen patients had coronary artery disease, three had arrhythmogenic right ventricular dysplasia, two had dilated cardiomyopathy, one had valvular disease, and one had no structural heart disease. Ten patients had an EF <30%. Ten patients were in NYHA functional class three. VT was permanent in three patients, daily in three, weekly in seven, paroxysmal in seven. In 11 patients, VT occurred both at day and night. In 11 patients, decrease of the sinus cycle preceeded VT. Oral administration of a daily low dose of a beta blocker agent (acebutolol 100 mg, betaxolol 5–10 mg, metoprolol 50 mg, nadolol 20–40 mg, pindolol 2.5 mg, propanolol 30 mg, sotalol 80–160 mg, terta-tolol 2.5 mg) combined with 400 mg/day of Am suppressed VT episodes in all patients. None presented heart failure or collapse. The mean reduction of the heart rate was 15% (65 to 55/min). At discharge, exercise ECG (n: 14) induced non sustained VT in two patients. At programmed electrical stimulation (PES) (n: 15), VT was no longer inducible in 4 patients, was slower, well-tolerated in nine patients, and remained inducible at the same rate in only two patients. Chronic treatment prevents recurrence of VT in 19 patients during a follow-up of 14 ± 9 months (range 2 to 33). Conclusions: (1) beta blockers agents and Am have strong synergistic effects; (2) antiarrhythmic treatment with low doses of beta blockers could be managed by PES; (3) at the doses used in (his study, all beta blockers presented the same safety; (4) combination of low doses of beta blockers agents with chronic Am therapy inhibit VT.     

Long-Term Follow-Up of Patients with Nonischemic Dilated Cardiomyopathy and Ventricular Tachyarrhythmias Treated with Implantable Cardioverter Defibrillators

We analyzed our 10-year cumulative experience of 40 consecutive patients with idiopathic dilated Cardiomyopathy and associated ventricular tachyarrhythmias, treated with implantable Cardioverter defibrillators. Dilated Cardiomyopathy was defined as left ventricular ejection fraction (EF) ≤50% with no defineable etiology. Patient characteristics included: 24 male, mean age 52 years, mean EF = 33%, New York Heart Association Class I–III, presenting syndrome—cardiac arrest (n = 28), syncope/near syncope (n = 12). At 2.5 years mean follow-up, there were 16 deaths: one operative, three sudden, two incessant ventricular tachycardia/ventricular fibrillation (VT/VF), six heart failure, and four noncardiac. The actuarial mortality at 1 and 4 years was 0% and 14% for sudden death, 11% and 34% for cardiac death. The projected mortality was 52% and 78% for same time intervals (P < 0.01). No useful baseline variable predicted who would or would not receive an ICD shock in follow-up. ICD therapy appears effective in reducing sudden death mortality in this high risk population.     

Results of Electrophysiological Testing and Long-Term Follow-Up in Patients Sustaining Cardiac Arrest Only While Receiving Type IA Antiarrhythmic Agents

Therapeutic management of patients sustaining a cardiac arrest while receiving antiarrhythmic agents can be difficult since the role of the drug in possibly facilitating the arrhythmia is often difficult to define. To determine if the response to programmed stimulation could give insight into which patients may have experienced a drug-induced cardiac arrest, we studied 29 patients (61 +/- 9 years) with no prior history of sustained ventricular tachyarrhythmias (VT) who suffered a cardiac arrest only while receiving type Ia antiarrhythmic agents. Patients with documented myocardial infarction, acute ischemia, electrolyte abnormalities, or torsade de pointes were excluded from the study. Twenty-four patients had coronary artery disease with prior myocardial infarction (ejection fraction 28% +/- 9%) and five patients had idiopathic dilated cardiomyopathy (ejection fraction 31% +/- 6%). During baseline electrophysiological testing, 19 patients (66%) had inducible sustained ventricular arrhythmias: uniform VT, n = 14 (group I), polymorphic VT or ventricular fibrillation, n = 5 (group II). Ten patients (group III) had no inducible sustained ventricular arrhythmias. To determine if rechallenge with a type Ia agent could facilitate induction of a sustained ventricular arrhythmia in group III, eight patients underwent ten electrophysiological studies during therapy with either procainamide or quinidine. Only two patients developed sustained VT in response to programmed stimulation. Patients in groups I and II received therapy guided by electrophysiological testing, including antiarrhythmic agents alone (n = 8), subendocardial resection (n = 4), or an implantable cardioverter defibrillator (n = 7). Patients in group III received antiarrhythmic agents empirically (n = 3), or for treatment of atrial tachyarrhythmias (n = 2) or nonsustained VT (n = 1). In addition, four patients in group III received an implantable cardioverter defibrillator. During a mean follow-up of 28 +/- 27 months (range: 1 day-84 months) 13 patients died suddenly or received a defibrillator shock preceded by syncope or presyncope: group I: n = 5; group II: n = 2; group III: n = 6. In conclusion: (1) most patients sustaining a cardiac arrest only in the presence of type Ia antiarrhythmic agents have inducible sustained VT in the absence of antiarrhythmic agents, and (2) the risk of recurrent VT persists in patients without inducible sustained arrhythmias in the drug-free state, regardless of whether they manifest inducible arrhythmias after rechallenge with a type Ia agent.     

Ventricular tachyarrhythmias in patients receiving an implantable cardioverter-defibrillator for primary versus secondary prophylaxis indications

Introduction: Data on the mechanisms of sudden cardiac death are limited and may be biased by delays in rhythm recording and selection bias in survivors. As a result, the relative contributions of monomorphic ventricular tachycardia (VT) (cycle length [CL] > 260 ms), monomorphic fast VT (FVT) (CL ≤ 260 ms), and polymorphic VT (PMVT)/ventricular fibrillation (VF) have not been well characterized nor compared in patients with and without prior arrhythmic events. Methods: A retrospective cohort study of implantable cardioverter‐defibrillator (ICD) recipients with primary or secondary implant indications was used to evaluate intracardiac electrograms (EGMs) for the first spontaneous VT/VF resulting in appropriate ICD therapy. EGMs were categorized into VT, FVT, and PMVT/VF based on CL and morphologic criteria. Results: Of 616 implants, 145 patients (58 [40%] primary indications) received appropriate ICD therapy for VT/VF over mean follow‐up of 3.8 ± 3.2 years. Primary implants had more diabetes (28% vs 12%; P = 0.02) and less antiarrhythmic use (15% vs 33%; P = 0.02). In those patients with spontaneous arrhythmia, PMVT/VF occurred in 20.7% of primary versus 21.8% of secondary implants, FVT in 19.0% versus 21.8%, and VT in 60.3% versus 56.4%, respectively (P = 0.88). Spontaneous VT CL was similar regardless of implant indication (284 ± 56 [primary] vs 286 ± 67 ms [secondary]; P = 0.92). Conclusions: Monomorphic VT is the most common cause of appropriate ICD therapy regardless of implant indication. These results provide insight into the mechanisms of sudden cardiac death and have implications for the use of interventions designed to limit ICD shocks. (PACE 2011; 34:571–576)