Risk stratification and long-term therapy with amiodarone in patients with idiopathic dilated cardiomyopathy]

Patients with cardiomyopathy are known to suffer from a high prevalence of tachyarrhythmic complications and sudden cardiac death. In a prospective study, 30 patients (25 men, 5 women, mean age: 52 +/- 12 years) with dilated cardiomyopathy underwent 48-h-Holter monitoring and programmed electrical stimulation and, independent from the results of the diagnostic work-up, were then randomized either to amiodarone or to a conventional or no antiarrhythmic therapy. At baseline, frequent ventricular arrhythmias (> 30 ventricular premature beats/h) were observed in 15/30 patients (50%), 13 patients (43%) had repetitive ventricular arrhythmias, additionally. Four patients suffered spontaneous sustained tachyarrhythmias. During programmed electrical stimulation, sustained monomorphic ventricular tachycardia was induced in 3/3 patients with and in 1/25 patients (4%) without a history of sustained tachycardia. Sustained monomorphic ventricular tachycardia was induced with one to two extrastimuli; three extrastimuli only increased the incidence of inducible ventricular fibrillation (8 patients, 28%). During a mean follow-up of 28 +/- 6 months 10/30 patients (33%) died for cardiac reasons (sudden cardiac death: 4/10 patients). Cardiac death was most likely in patients with a left-ventricular ejection fraction < 35% (5/18 patients, 28% versus 1/12 patients with ejection fraction > 35%, 8%) and further increased in the presence of reduced exercise tolerance and frequent and repetitive ventricular arrhythmias (4/7 patients, 57%). In the amiodarone group 4/15 patients died (27%, sudden cardiac death: one patient), while in patients not treated by amiodarone 8/15 patients died (54%; sudden cardiac death: three patients). Amiodarone therapy was well tolerated in all but one patient.     

Malignant ventricular arrhythmias in the subacute and late phases of myocardial infarction. Clinical arrhythmological characteristics and prognostic value

The purposes of this study are as follows: 1) to describe the clinical and arrhythmological characteristics of 30 patients (23 male, 7 female, mean age: 61 years) who suffered from episodes of ventricular tachycardia and/or ventricular fibrillation between the 7th and the 90th day following acute myocardial infarction; 2) to evaluate the effectiveness of treatment with amiodarone also taking into account the results of electrophysiologic study; 3) to correlate our results with data from previous studies. The site of the acute myocardial infarction was anterior in 16 patients, inferior in 12, and anterior and inferior in 2. Twenty patients had early post-acute myocardial infarction complications (67%) such as cardiac failure (16), bundle branch blocks (9) and ventricular fibrillation in the first 48 hours (6). The mean ejection fraction was 33 +/- 8% and a left ventricular aneurysmatic evolution was observed in 13 patients (43%). The first episodes of spontaneous ventricular arrhythmias occurred after a mean interval of 32 +/- 24 days following acute myocardial infarction. These occurred in the form of ventricular fibrillation in 19 patients (63%) and of ventricular tachycardia in the other 11 (37%). The patients experienced 5.6 +/- 5 episodes of ventricular fibrillation or ventricular tachycardia. Of the 30 patients, 28 received amiodarone, 1 procainamide and 1 propafenone. Five of the 28 patients treated with amiodarone were also given either procainamide or propafenone due to the early recurrence of ventricular tachycardia or fibrillation. One patient underwent early left ventricular aneurysmatic resection due to refractory ventricular fibrillation. Two groups of patients were distinguished on the basis of the electrophysiologic study results obtained during anti-arrhythmic treatment: group A consisted of 17 cases in which a sustained ventricular tachycardia was inducible (57%), group B consisted of 13 cases in which a sustained ventricular tachycardia was not inducible (43%). During a mean follow-up period of 31.6 +/- 26 months the total mortality rate was 23% in group A and 46% in group B (p = ns), the incidence of sudden death was 17% in group A and 23% in group B (p = ns), the incidence of non fatal ventricular tachycardia or ventricular fibrillation recurrences was 24% in group A and 0% in group B (0.05 less than p less than 0.1). One group A patient successfully underwent a heart transplant. The negative predictive value of ventricular stimulation in relation to sudden death and to non-fatal arrhythmic recurrences was 77% and 100%; the positive predictive value was 17 and 28%.(ABSTRACT TRUNCATED AT 400 WORDS)     

Risk stratification and prognosis of patients treated with amiodarone for malignant ventricular tachyarrhythmias after myocardial infarction

Summary Seventy-seven consecutive patients (mean age 62 years) with episodes of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) after acute myocardial infarction (AMI) were evaluated to assess the long-term efficacy of first-line amiodarone treatment and to identify clinical and laboratory factors associated with a high risk of death or arrhythmia recurrence. The presenting arrhythmia was VT in 41 cases (53%) and VF in 36 (47%). VT or VF occurred between the 4th and 90th day after AMI in 45 cases (58%) and later (more than 90 days) in the remaining 32 (42%). The mean number of arrhythmic episodes was 4.2. Forty patients (52%) were in New York Heart Association (NYHA) class I or II, and 37 (48%) were in class III or IV. Mean left ventricular ejection fraction was 32%; ventricular aneurysm was present in 41 subjects. Most patients had multivessel coronary artery disease. Amiodarone was administered as a first-choice drug in all patients, in combination with other antiarrhythmic drugs in 14. By ventricular stimulation after loading doses of amiodarone, sustained VT was inducible in 46 (62%) and noninducible in 28 (38%). During a mean follow-up of 28 months the incidence of cardiac mortality at 1, 3, and 5 years was 21%, 37%, and 47%; of sudden death was 7%, 19%, and 23%; of nonfatal VT recurrence was 13%, 13%, and 24%, respectively. The overall incidence of amiodarone side effects was 35%. Factors independently associated with mortality for all causes and cardiac mortality included NYHA class III or IV (p<0,01), ejection fraction -35% (p<0,01), and age -65 years (p=0,03). History of cardiac arrest was a weak predictor only by univariate analysis (p=0.05). No single variable was consistently related to an increased risk of sudden death and nonfatal VT recurrence, not even inducibility of sustained VT during electropharmacologic studies (18% of incidence in responders and 30% in nonresponders, p = ns). In this study, amiodarone treatment of patients with life-threatening ventricular tachyarrhythmias after myocardial infarction confirmed its beneficial, but not uniform, efficacy. Severe left ventricular dysfunction, age, and, less significantly, history of cardiac arrest, were independent predictors of death. Identification of patients at high risk of arrhythmia recurrence and sudden death remains undefined during amiodarone treatment.     

Current aspects of defibrillator therapy in congestive heart failure

The beneficial effects of implantable cardioverter defibrillator (ICD) therapy in patients (pts) with life-threatening ventricular tachyarrhythmias and impaired left ventricular (LV) function is still unclear. We studied the follow-up of 410 pts (368 males, 42 females, mean age 57 +/- 11 years) after ICD implant. The LV function was assessed by the New York Heart Association functional class of heart failure (NYHA). Fifty pts (12%) were in NYHA I-II, 151 pts (37%) in NYHA II, 117 pts (29%) in NYHA II-III and 92 pts (22%) in NYHA III. Epicardial ICD implantation was performed in 209 pts (51%) and 201 pts (49%) received nonthoracotomy ICDs. Perioperatively (within 30 days after implant), 12 pts (3%) died, significantly more frequent after epicardial (11 of 209 pts, 5%) than after transvenous ICD implant (1 of 201 pts, < 1%) (p < 0.05). During a mean follow-up of 28 +/- 24 months (range < 1 to 114 months), 90 pts (23%) died: 9 pts (2%) died from sudden arrhythmic death and 5 pts (1%) suddenly, but probably not from arrhythmic causes; 55 pts (14%) died from cardiac causes (congestive heart failure, myocardial reinfarction) and 21 pts (5%) from noncardiac causes. The 3-year, 5-year and 7-year survival was 92% to 96% for arrhythmic mortality in NYHA class I, II and III compared to the 3-year survival of 94%, and a 5-year and 7-year survival of 84% in patients with NYHA class II-III. 338 pts (82%) received ICD shocks (mean incidence 21 +/- 43 shocks per pt); pts in NYHA class II (83%), class II-III (84%), class III (90%) received ICD discharges significantly more frequently than in class I-II (64%) (p < 0.05). Our data show that pts with LV dysfunction benefit from ICD therapy and that these pts survive for a considerable time after the first shock. However, survival is clearly influenced by the degree of left ventricular dysfunction and, in addition to ICD therapy, aggressive treatment of heart failure is necessary.     

The value of the clinical history to assess prognosis of patients with ventricular tachycardia or ventricular fibrillation after myocardial infarction

Multivariate analysis using 70 variables in 200 patients who suffered from ventricular tachycardia or ventricular fibrillation after myocardial infarction detected eleven variables that were associated with an increased risk of sudden arrhythmic death and cardiac death during a mean follow-up period of 2 years. Four of the 11 variables came from the patient's clinical history: (1) cardiac arrest at the time of the first spontaneous episode of arrhythmia, (2) New York Heart Association functional class for dyspnoea = III, (3) ventricular tachycardia or ventricular fibrillation occurring early (after 3 days and within 2 months) after myocardial infarction, (4) multiple myocardial infarctions before the first episode of ventricular tachyarrhythmia. Total mortality, incidence of sudden arrhythmic death and of non-sudden cardiac death increased with an increasing number (zero, one, two, three, four) of variables seen in individual patients. Patients with zero or one variable had an incidence of sudden death of 2.8% and a 4.2% incidence of non-sudden cardiac death at 26 months, while patients with more than two variables had a 13.5% and a 20.3% incidence respectively of sudden and non-sudden cardiac death. The strongest predictor of sudden death was the occurrence of cardiac arrest during the first spontaneous episode of ventricular arrhythmia. The strongest predictor of non-sudden cardiac death was the New York Heart Association functional class. The use of the four variables to stratify risk revealed seven subgroups of patients with incidences of sudden death ranging from 0 to 28%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiac arrest and sudden death in patients treated with amiodarone for sustained ventricular tachycardia or ventricular fibrillation: risk stratification based on clinical variables

Multivariate analysis of 11 clinical variables was performed in 104 patients with sustained, symptomatic ventricular tachycardia (VT) or ventricular fibrillation treated with amiodarone to determine variables predictive of subsequent cardiac arrest or sudden death. Twenty-five patients (24%) had fatal or nonfatal cardiac arrest after 7.3 +/- 6.2 months (mean +/- standard deviation) of therapy. Multivariate analysis identified an ejection fraction of less than 0.40, syncope or cardiac arrest before amiodarone therapy, and VT (3 or more consecutive ventricular premature complexes) during predischarge ambulatory electrocardiographic monitoring as variables associated with a high risk of subsequent fatal or nonfatal cardiac arrest (p less than 0.03). Patients who had these 3 clinical variables had a much higher predicted incidence of cardiac arrest at 6 months (62%) and 12 months (76%) than did patients with an ejection fraction greater than 0.40, without syncope or cardiac arrest before amiodarone therapy, and without VT during predischarge ambulatory electrocardiographic monitoring (2% and 5%, respectively) (p less than 0.02). Risk stratification using clinical variables can predict which patients are at high risk of recurrent cardiac arrest or sudden death during amiodarone therapy.     

Prognosis of patients with sustained ventricular tachycardia and of survivors of cardiac arrest not inducible by programmed stimulation.

The aim of this study was to analyze the long-term clinical outcome of 60 prospectively studied patients with documented sustained ventricular tachyarrhythmia that was not inducible during baseline programmed ventricular stimulation: 39 with cardiac arrest due to noninfarction ventricular fibrillation (VF) and 21 with mild hemodynamically compromising sustained ventricular tachycardia (VT). Left ventricular ejection fraction was 55 +/- 14% in the VF group and 50 +/- 13% in the VT group (difference not significant). Patients were discharged without conventional antiarrhythmic drugs and received only empirical beta-blocker therapy. During a mean follow-up period of 21 +/- 16 months (mean +/- SD), 10 of 60 patients (17%) died suddenly. The actuarial incidence of sudden death at 1 and 4 years was similar in both groups (VF group, 10 and 20%; VT group, 16 and 16%) (p = 0.48). The actuarial incidence of sudden cardiac death was significantly higher in patients with left ventricular ejection fraction < or = 40% than in those with > 40% (1-year incidence in VF group, 40 vs 0%; VT group, 50 vs 0%) (p = 0.005 and p = 0.01, respectively). Multivariate regression analysis identified left ventricular ejection fraction < or = 40% and previous myocardial infarction as the only independent predictor of sudden cardiac death. The occurrence of frequent ventricular pairs during Holter monitoring was the only independent predictor of sustained VT recurrences. It is concluded that patients with sustained ventricular tachyarrhythmia in whom arrhythmia was non-inducible during baseline ventricular stimulation and not treated with antiarrhythmic therapy have a favorable outcome if left ventricular ejection fraction is high.(ABSTRACT TRUNCATED AT 250 WORDS)     

Value of serial electropharmacologic tests in the treatment of sustained ventricular arrhythmias

The value of electropharmacological testing in patients (pts) with sustained ventricular tachyarrhythmias was studied in 46 consecutive pts (24 with sustained ventricular tachycardia (SVT) and 22 with cardiac arrest due to a ventricular tachyarrhythmia. Forty-two pts underwent a baseline electrophysiological study. The ventricular stimulation protocol included up to 3 extrastimuli during spontaneous rhythm and during paced ventricular rhythm at 100/min, 130/min, 160/min and brief bursts pacing at 2 ventricular sites. Ventricular tachycardia was induced in 37/42 pts (88%) (sustained in 32 pts and non sustained in 5 pts). Twenty nine pts underwent 79 trials of different drug regimens (mean 2.72 per pt, range 1-8). A totally successful drug regimen was found in 15/29 pts (51.7%) and a partially successful drug regimen in 11/29 pts (37.9%). Twenty-three pts were discharged on a drug regimen successful during serial electropharmacological testing (Group I) and 23 pts were discharged on an empiric drug regimen (Group II). Each pt was followed-up for a mean period of 15 months (range 1-74). Group I pts had fewer arrhythmia recurrence (SVT and/or sudden death) than Group II pts (2/23 vs 13/23 p less than 0.01). In conclusion electropharmacological testing is an useful tool in the therapy of pts with sustained ventricular tachyarrhythmias.     

Arrhythmias in patients with Brugada-type electrocardiographic findings.

Brugada syndrome is characterized by marked ST-segment elevation in the right precordial leads (Bru-ECG) and is associated with a high risk for sudden death. However, it is unclear whether the arrhythmogenesis is caused by the mechanisms responsible for Bru-ECG. The present study investigated the risk of arrhythmias in patients with Bru-ECG by retrospectively analyzing 30 patients (28 men; mean age, 51+/-14 years) with Bru-ECG. Aborted sudden cardiac death (ventricular fibrillation or syncope) occurred in 9 patients (30%); paroxysmal atrial fibrillation was present in 9 (30%) patients in addition to malignant ventricular arrhythmias, and some type of arrhythmic event (aborted sudden cardiac death or paroxysmal atrial fibrillation) occurred in 15 patients (50%). Of all the arrhythmic events, 93% occurred at night or early in the morning, and 92% had pronounced ST-segment elevation. These results suggest that Bru-ECG may be associated not only with an increased risk of ventricular tachyarrhythmias but also with an increased risk of paroxysmal atrial fibrillation, and that the arrhythmogenesis may be related to the pronounced ST-segment elevation.     

Predictors of efficacy of amiodarone and characteristics of recurrence of arrhythmia in patients with sustained ventricular tachycardia and coronary artery disease

The value of serial electropharmacologic testing during long-term oral amiodarone therapy for prediction of long-term drug efficacy as well as characteristics of arrhythmia recurrence is controversial. One-hundred four consecutive patients with coronary artery disease and sustained ventricular tachyarrhythmias (VT) underwent initial electrophysiologic (EP) evaluation in the drug-free state and again after an amiodarone loading period of 25 +/- 14 days (mean +/- SD). Twenty-six patients (25%) had no inducible ventricular tachyarrhythmia during therapy with amiodarone (VT control group), whereas arrhythmia inducibility persisted in the remaining 78 patients (VT noncontrol group). During 17.4 +/- 13.7 months of follow-up, two patients in the VT control group either had VT recurrence or died suddenly compared with 21 VT recurrences and eight sudden cardiac deaths in the VT noncontrol group (actuarial event rates at 36 months of 0.11 and 0.56, respectively, p = .0065). The cycle lengths of recurrent VT in these 21 patients in the VT noncontrol group were compared with those observed at final EP testing. A significant linear correlation was demonstrated (r = .76, p = .0001). Subgroup analysis of patients in the VT noncontrol group showed no EP predictors of outcome, including cycle length of induced VT. However, patients dying suddenly during the follow-up period had a higher prevalence of new or worsening congestive heart failure (75%) compared with patients with VT recurrence (19%) or those with no arrhythmic event (29%) (p less than .02).2off     

Long-term low-dose amiodarone therapy in the management of ventricular and supraventricular tachyarrhythmias: Efficacy and safety

Background: Amiodarone hydrochloride has been in use for two decades for the control of ventricular and supraventricular arrhythmias. Established and emerging evidence indicates that amiodarone has an antiarrhythmic efficacy superior to that of most other drugs. Hypothesis: The study was undertaken to evaluate the efficacy and acceptability of low-dose amiodarone therapy in the long-term management of supraventricular and ventricular tachyarrhythmias. Methods: A total of 124 patients with symptomatic drug-refractory or life-threatening arrhythmias managed with low-dose oral amiodarone therapy over a 10-year period was analyzed retrospectively. Of these, 45 patients (36%) had ventricular arrhythmias, 52 (42%) had atrial arrhythmias, and 27 (22%) had atrioventricular reentry tachycardia. Loading doses of amiodarone 600 mg daily for 1 week were administered for supraventricular arrhythmias and 600–1200 mg daily for 2 weeks for ventricular arrhythmias. Maintenance daily doses were 194 ± 48 and 206 ± 55 mg, respectively. Mean treatment duration was 32 ± 28 months, with 326.3 patient years of therapy. Results: Of 39 patients with sustained ventricular tachyarrhythmias, the actuarial incidence of satisfactory arrhythmia control (absence of sudden cardiac death or nonfatal arrhythmia recurrence) was 78% at 1 year and 71 % at 2 years. Satisfactory control of supraventricular arrhythmias (mean ventricular rate < 100/min with significant symptomatic improvement for sustained atrial arrhythmias and < 1 attack per year for paroxysmal atrial or atrioventricular arrhythmias) was achieved in 73, 65, and 62% of patients at 1, 2, and 3 years, respectively. The cumulative incidence of amiodarone-related adverse effects was 5.8 per 100 patient years, with drug withdrawal required in 12 patients (9.7%). Fifteen patients had thyroid dysfunction, 2 had hepatic toxicity, and 1 developed nonfatal pulmonary fibrosis. Overall, the incidence of successful use of amiodarone (satisfactory arrhythmia control and freedom from side effects) was 67, 59, and 53% at 1, 2, and 3 years, respectively. Conclusions: The results of this study suggest that the efficacy of low-dose amiodarone therapy in the management of serious ventricular and supraventricular arrhythmias would be similar to those achieved with higher doses, but with a much more acceptable side effect profile.     

Amiodarone in patients with recurrent sustained ventricular tachyarrhythmias: results of programmed electrical stimulation and long-term clinical outcome in chronic treatment

Thirty-three patients with clinically recurrent ventricular tachyarrhythmias were treated with amiodarone (200 to 600 mg/day) during a mean follow-up period of 23.7 months. Prior to amiodarone therapy, sustained ventricular tachycardia or ventricular fibrillation was initiated in all patients at control electrophysiologic study; patients failed a mean of 5.7 drugs, as assessed by programmed electrical stimulation. At electrophysiologic study after a loading phase (1000 mg/day for 10 days), 10 patients had no inducible ventricular tachycardia, nine patients had nonsustained ventricular tachycardia, 13 patients had persistent sustained ventricular tachycardia, and one patient had ventricular fibrillation. Patients were continued on amiodarone alone regardless of the findings at the electrophysiologic study, and during follow-up patients with no inducible sustained ventricular tachycardia or fibrillation on amiodarone had no recurrent arrhythmias or sudden death. Six of 14 patients (43%) with sustained ventricular tachyarrhythmias still inducible had recurrent ventricular tachycardia/fibrillation, and four of them died suddenly (29%). Programmed electrical stimulation predicts a good clinical long-term outcome during amiodarone therapy. Patients with persisting fast tachyarrhythmias (cycle length less than or equal to 300 msec) on amiodarone and a low ejection fraction (less than 35%) seem to have a higher incidence of sudden death. In these patients, therapeutic approaches such as antiarrhythmic surgery or implantation of antitachycardia devices should be considered.     

Does the appearance of pro-arrhythmic response to anti-arrhythmic drugs have prognostic significance?]

Study was undertaken to assess whether proarrhythmic response to antiarrhythmic drug is a risk factor for cardiac death in patients (pts) with ischaemic heart disease (IHD). In 782 pts with IHD and frequent and/or complex ventricular ectopic beats (VEB) 1041 drug tests guided by 24 hour Holter monitoring were conducted. The following drugs were assessed: propranolol, disopyramide, mexiletine, amiodarone. Pro-arrhythmia was defined according to Velebit: 1/greater than or equal to 4-fold increase in VEBs, 2/greater than or equal to 10-fold increase in repetitive forms of 3/new occurrence of ventricular tachycardia or ventricular fibrillation (VT/VF). Proarrhythmic effect was observed in 8.4% of pts and in 7.9% of drug tests. The frequency with individual drugs ranged from 5.7% to 9%. No drug was completely free of this type of reaction. Antiarrhythmic drugs inducing arrhythmogenic response were eliminated. Pts were followed-up for a mean of 22 months (range 1-49). Chronic antiarrhythmic treatment was conducted. Pts were discharged taking the agent deemed most effective for suppression of arrhythmia. Follow-up visits were made every 6-12 months. All cases of death were verified. In long-term observation cardiac death and sudden death occurred in 53 and 32 pts. With actuarial analysis (Kaplan-Meler method, log rank test) there was significant difference in cardiac death (p less than 0.05) of pro-arrhythmia (+) compared with ++pro-arrhythmia (-) pts at yr (11% v 4%, 7% v 3%) and 3 yr (24% x 11%, 16% v 7%). The relative importance of baseline clinical variables in predicting survival was assessed with a stepwise Cox regression.(ABSTRACT TRUNCATED AT 250 WORDS)     

Treatment of malignant ventricular tachyarrhythmia with amiodarone: comparison of empirical administration and administration guided by Holter or ventricular stimulation. Results of the parallel test

To assess the most appropriate method of administering amiodarone and predicting its efficacy (empiric vs guided by Holter or by ventricular stimulation), 19 patients with sustained ventricular tachycardia or ventricular fibrillation underwent a "parallel study". Fifteen patients were men and 4 women, with a mean age of 65 years. A coronary artery disease with previous myocardial infarction was present in 15 patients, dilated cardiomyopathy in 3 and arrhythmogenic right ventricular dysplasia in 1 (mean left ventricular ejection fraction = 35%). All 19 patients had, as inclusion criteria, 1) frequent (greater than or equal to 30/hour) and/or repetitive (greater than or equal to 10/24 hours) ventricular premature beats during 24-hour Holter monitoring and 2) inducible sustained (greater than 30/sec) ventricular arrhythmias during programmed ventricular stimulation (1-3 extrastimuli from 2 right ventricular sites). Amiodarone was given at an initial dosage of 15 mg/kg/day for 2 weeks and then at a dosage of 5 mg/kg/day. After 15 days 24-hour Holter monitoring and programmed ventricular stimulation were repeated. The data of these tests, however, were not used to guide the therapy that remained empiric, but served only to assess retrospectively the predictive value of Holter monitoring and ventricular stimulation. The following main results were obtained: The mean duration of follow-up was 25 +/- 13 months. During this period 6 patients (32%) died, 3 from sudden and 3 from non-sudden cardiac death. Two other patients had recurrence of sustained ventricular arrhythmias. After 15 days of therapy amiodarone was effective at Holter monitoring in 15 patients (79%) and not effective in 4 (21%). Two of the 15 patients considered responders died suddenly during the follow-up and 2 had arrhythmic recurrence, vs 1 of the 4 non-responder patients who died suddenly (negative predictive value of Holter monitoring: 73%; positive predictive value: 25%; predictive accuracy: 63%). After 15 days of therapy amiodarone was effective at ventricular stimulation in 10 patients (53%) and not effective in 9 (47%). None of the 10 patients considered responders had arrhythmic events during the follow-up, vs 5 of the 9 non-responders, 3 of whom died suddenly and 2 of whom had arrhythmic recurrences (negative predictive value of ventricular stimulation: 100%; positive predictive value: 56%; predictive accuracy: 79%). Only 1 patient discontinued amiodarone after 25 months of follow-up because of development of an important blue-grey skin discoloration.(ABSTRACT TRUNCATED AT 400 WORDS)     

Value of Holter monitoring in identifying risk for sustained ventricular arrhythmia recurrence on amiodarone

Seventy-four patients with sustained ventricular tachyarrhythmias had 22 +/- 3 hours of Holter monitoring before and after 11 +/- 6 days of amiodarone treatment. On control Holter recordings, 55 patients (group I) had frequent (more than 10 extrasystoles per hour) and/or complex (at least couplets) ventricular ectopic activity (VEA), and 19 patients (group II) had infrequent and simple VEA. A positive Holter monitor response to amiodarone was defined as a decrease in VEA by more than 85% and abolition of all complex VEA. In group I, 34 patients (62%) had a positive Holter monitor response. In group II, 16 patients (84%) had persistent, infrequent and simple VEA and 3 had frequent and/or complex VEA. During a mean follow-up of 13 +/- 12 months, 22 patients (30%) had ventricular tachycardia (VT) or sudden death. In group I, VT or sudden death occurred in 6 of 34 (18%) patients with a positive Holter monitor response and 11 of 21 (52%) with a negative Holter monitor response (p less than 0.01), and in group II, VT or sudden death occurred in 5 of 16 patients (31%) with persistent, infrequent and simple VEA. All episodes of VT or sudden death occurred after at least 2 weeks of amiodarone therapy (mean 5 +/- 6 months). The predictive accuracy of a positive Holter monitor response as an indicator for subsequent prevention of sustained ventricular tachyarrhythmias and sudden cardiac death was 82% and for a negative Holter monitor response as an indicator of tachyarrhythmia or sudden death recurrence on therapy it was 52%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sudden cardiac death in Chagas' heart disease in the contemporary era

This article reviews epidemiology, clinical-morphological aspects, and primary and secondary prevention of sudden cardiac death in patients with chronic Chagas' heart disease in the current era. Chagas' disease patients with life-threatening ventricular tachyarrhythmias are at risk of sudden cardiac death. No evidence-based support is available for guiding prophylaxis of sudden cardiac death in patients with this condition. Therefore, measurements for sudden cardiac death prevention in Chagas' disease patients have been derived from data obtained in non-Chagas' disease patients as well as on expertise of physicians dealing with this disorder in areas where Chagas' disease is endemic. For primary prevention, therefore, we suggest that patients with non-sustained VT be referred to programmed ventricular stimulation. Patients with inducible VT will be better treated with Implantable Cardioverter-Defibrillator (ICD) than with amiodarone therapy. For secondary prevention, we suggest that patients with malignant ventricular tachyarrhythmias with hemodynamic instability receive ICD therapy. For patients with life-threatening ventricular arrhythmias and no hemodynamic instability, however, secondary prevention can be accomplished with ICD therapy or catheter ablation in those with a left ventricular ejection fraction (LVEF) of 30% or less, and with electrophysiologic testing-guided drug therapy or empiric treatment with amiodarone in those with a LVEF of 30% or high.     

Electrophysiologically guided amiodarone therapy versus the implantable cardioverter-defibrillator for sustained ventricular tachyarrhythmias after myocardial infarction: results of long-term follow-up

OBJECTIVES: We sought to compare the long-term survival rates of patients with sustained ventricular tachyarrhythmia after myocardial infarction (MI) who were treated according to the results of electrophysiological (EP) study either with amiodarone or an implantable cardioverter-defibrillator (ICD). BACKGROUND: Patients with sustained ventricular tachyarrhythmias after MI are at high risk of sudden cardiac death (SCD). However, data comparing the long-term survival rates of patients treated with amiodarone or ICD, according to the results of EP testing, are lacking. METHODS: Patients underwent a first EP study at baseline and a second one after a loading dose of amiodarone of 14 +/- 2.9 g. According to the results of the second EP study, patients were classified either as responders or non-responders to amiodarone; non-responders were eventually treated with an ICD. RESULTS: Eighty-four consecutive patients with MI (78 men; 21-77 years old; mean left ventricular (LV) ejection fraction 36 +/- 11%) were consecutively included. Forty-three patients (51%) were responders, and 41 patients (49%) were non-responders to amiodarone therapy. During a mean follow-up period of 63 +/- 30 months, SCD and total mortality rates were significantly higher in the amiodarone-treated patients (p = 0.03 and 0.02, respectively). CONCLUSIONS: The long-term survival of patients with sustained ventricular tachyarrhythmias after MI, with depressed LV function, is significantly better with an ICD than with amiodarone therapy, even when stratified according to the results of the EP study. These patients should benefit from early ICD placement, and any previous amiodarone treatment seems to have no additional value.     

Long-term follow-up of arrhythmias in patients with myotonic dystrophy treated by pacing: a multicenter diagnostic pacemaker study

OBJECTIVES: We hypothesized that pacemaker (PM) implantation in patients with myotonic dystrophy (MD) with a prolonged HV interval, even asymptomatic, may protect them against sudden death related to atrioventricular (AV) block. We sought to prospectively document the true incidence of AV block episodes in this high-risk population and accurately trace, in the long term, by the PM, the occurrence of arrhythmias that may remain undetected during conventional follow-up. BACKGROUND: Myotonic dystrophy is associated with a high risk of sudden death, commonly attributed to AV block or ventricular arrhythmias, but cardiac pacing is only recommended as a secondary prevention. METHODS: Patients with MD with an HV interval > or =70 ms, even in the absence of related symptoms, prospectively received a cardiac PM, including an algorithm capable of diagnosing episodes of bradycardia and tachyarrhythmias. RESULTS: The population consisted of 49 patients (45.5 +/- 8.9 years old) followed for 53.5 +/- 27.2 months. Paroxysmal arrhythmias were recorded in 41 patients (83.7%), consisting of complete AV block (n = 21), sino-atrial block (n = 4), or atrial (n = 25) or ventricular (n = 13) tachyarrhythmias. No patient died of AV block during follow-up, but 10 deaths occurred, 4 of them sudden. An arrhythmic cause could be excluded by postmortem PM interrogation in two cases of typical sudden death. CONCLUSIONS: Arrhythmias are common in patients with MD with infrahisian conduction abnormalities. The prophylactic implantation of a pacing system when the HV interval is > or =70 ms seems appropriate. The PM protects the patient against the clinical consequences of paroxysmal profound bradycardia and facilitates the diagnosis and management of frequent paroxysmal tachyarrhythmias.     

Ventricular fibrillation in chronic heart disease

The objective of the work was to describe in subjects with spontaneous ventricular fibrillation, after elimination of acute cardiac disease, the strategy of antiarrhythmic treatment and to evaluate, based on prospective follow-up, the effectiveness of this treatment. The authors included in the group 36 patients (30 men and 6 women) within the range from 34 to 78 years (mean age 58 +/- 11 years) with spontaneous ventricular fibrillation. They divided the group into a subgroup (15 subjects) without revascularization of the heart muscle, into a subgroup (17 subjects) with revascularization of the myocardium (coronary angioplasty and bypasses) and a subgroup (4 subjects) where ischaemic heart disease was ruled out (mostly cardiomyopathies). In all subgroups they used programmed ventricular stimulation (apparatuses of Quinton Co. USA, Biotronik Co. GFR), in the subgroup with revascularization within 3 months. During the diagnostic procedure of ventricular stimulation they tested antiarrhythmic drugs most frequently amiodarone per os (for 4 weeks). An implantable cardioverter--defibrillator was implanted in 17 patients (8 subjects without revascularization, 6 subjects with revascularization, 3 subjects without ischaemic heart disease). All patients were followed up till death, maximum 24 months. The authors evaluated the rate of cardiac deaths (death on cardiac grounds, incl. sudden arrhythmic death) and sudden arrhythmic deaths (within one hour after the onset of symptoms or the first malignant ventricular tachyarrhythmia recorded after implantation of the defibrillator). In the subgroup without revascularization with electric instability of the ventricles according to programmed stimulation 66.7% they described seven cardiac deaths (46.7%) and 6 sudden "arrhythmic" deaths (40%) incl. 5 subjects with ineffective testing of antiarrhythmic drugs. Conversely in the subgroup with revascularization and with diagnostic programmed stimulation in 47.1% they found 3 cardiac deaths (17.7%), one sudden "arrhythmic" death (5.9%)--a subject with ineffective testing. In the subgroup without ischaemic heart disease they recorded cardiac and sudden "arrhythmic" deaths in half the subjects, in all instances in subjects without inducible ventricular tachyarrhythmia. The authors found in the course of a two-year investigation a relapse of cardiac arrest in 25% of subjects after spontaneous ventricular fibrillation. A third of these subjects (all without a cardioverter-defibrillator) died. They confirm the benefit of implantation of a defibrillator for all subjects regardless of the basic diagnosis and revascularization of the heart muscle.     

Significance and control of cardiac arrhythmias in patients with congestive cardiac failure

A wide spectrum of ventricular and supraventricular tachyarrhythmias occurs in the setting of congestive cardiac failure. However, the two most clinically significant are atrial fibrillation and ventricular tachycardia and fibrillation.In the past there has been much emphasis on premature ventricular contractions and more recently, on nonsustained ventricular tachycardia. For the most part, these arrhythmias are asymptomatic in heart failure. They are markers of sudden arrhythmic death but their suppression by antiarrhythmic drugs have not resulted in a reduction of total mortality. Two approaches have been used to this end. The first is the use of beta-adrenergic blocking drugs and antiarrhythmic agents such as amiodarone. Beta-blockers have been shown to significantly reduce sudden death as well as total mortality, while the effects of amiodarone have been less decisive. The prospective role of the implantable cardioverter defibrillator (ICD) is undergoing critical evaluation in patients with cardiac failure at high risk for sudden death. The elective role of the ICD is well established as first-line therapy in patients with heart failure resuscitated from sudden death and in those with sustained ventricular tachycardia in conjunction with conventional therapies for cardiac decompensation.The prevalence of atrial fibrillation rises as a function of severity of cardiac failure, but it is also in known that persistent atrial fibrillation with an uncontrolled ventricular response may induce heart failure. Controlled ventricular response may prevent congestive heart failure and improve left ventricular function. The two most common causes of atrial fibrillation in cardiac failure in Europe and America are ischemic heart disease and hypertension, while mitral valve disease remains the prevalent cause elsewhere. The choice of antiarrhythmic drugs for maintaining sinus rhythm is critical in the prevention of heart failure aggravation and proarrhythmic reactions of antiarrhythmic drugs. Amiodarone and dofetilide are most widely used in this context.