Significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy

The incidence and prognostic significance of ventricular arrhythmias identified by 24-hour ambulatory electrocardiography (Holter) was prospectively assessed in 74 patients with idiopathic dilated cardiomyopathy (IDC). The criteria for diagnosis of IDC were based on clinical and cardiac catheterization findings. Holter monitoring was performed at the time of entry into the study. Patients were followed for 2 to 21 months (mean 11 +/- 3). Frequent ventricular premature complexes (VPCs) (greater than 1,000/24 hours) were seen in 35%, and complex VPCs (Lown grade III and IV) in 87% of the patients. Forty-nine percent of the patients had nonsustained ventricular tachycardia (VT) consisting of 3 to 32 beats with rates from 110 to 230 beats/min, and 20% had ventricular pairs. No correlation was found between clinical symptoms or the degree of left ventricular (LV) impairment and the number of ventricular pairs or episodes of VT. During follow-up, 19 patients died, 7 from congestive heart failure (CHF) and 12 suddenly. Patients who died suddenly had significantly more episodes of VT, ventricular pairs or total VPCs (p less than 0.01 each) compared with survivors and those who died from CHF. No significant differences were found between patients who died from CHF or suddenly with respect to LV end-diastolic pressure, LV end-diastolic volume index, LV ejection fraction (EF) and cardiac index. A linear stepwise discriminant function analysis using hemodynamic (LVEF and cardiac index) and arrhythmic (number of VT episodes and ventricular pairs) variables resulted in a meaningful separation between survivors and patients who died from CHF or suddenly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arrhythmia profile and sudden cardiac death in early and late resuscitated patients following myocardial infarct

The arrhythmia profile has been studied in 40 patients (pts) with acute myocardial infarction (MI) resuscitated early (less than 24 hours post MI, group I) and late (4-12 weeks post MI, group II) using 24 h Holter monitoring (HM) at the time of LV- and coronary angiography (HM A) with an average follow-up of 27 months (7-61) (HM B). Forty pts with an acute MI without resuscitation served as controls (group III). Mortality for sudden cardiac death (scd) (death within 24 hours after beginning of symptoms) was significantly higher in group II (6/14 or 42.9%; 13% per year) than in group I (4/26 or 15.4%; 5.9% per year) (p less than 0.05) or in group III (3/40 or 7.5%; 1.8% per year) (p less than 0.001). In HM A there were no significant differences with regard to PVCs and complex arrhythmias using qualitative and quantitative analysis in groups I-III as well as between survivors and scd-pts. In HM B survivors in group II had significantly more PVCs (mean = 1347), couplets (mean = 29) and salvos (mean = 11) than in group I (PVC, mean = 355; couplets, mean = 3; salvos, mean = 0.1; p less than 0.05) or in group III (PVC, mean = 455; couplets, mean = 4; salvos, mean = 0.8; p less than 0.05). They also showed significantly more PVCs (mean = 1480), couplets (mean = 35) and salvos (mean = 15) than in HM A (PVC, mean = 1347; couplets, mean = 3; salvos, mean = 0; p less than 0.05). There were no significant differences between HM A and HM B in groups I and III. It can be concluded that the risk of sudden cardiac death was increased in pts resuscitated 4-12 weeks post MI in comparison to pts with early resuscitation or without resuscitation post MI. In these high risk pts repeated studies using Holter monitoring were helpful in estimating the further risk of sudden cardiac death.     

室性心律失常对老年心力衰竭患者预后的影响

目的　探讨室性心律失常对心力衰竭老年患者预后的影响。方法　 180例心力衰竭老年患者行 2 4h动态心电图检查 ,随访 3个月。观察猝死与各种室性心律失常的关系。结果　 16 9例(93 9% )患者有室性心律失常。 2 4h >10 0 0个室性早搏 (PVCs)者 6 9例 (38 3% ) ,多形PVCs 34例(18 9% ) ,成对PVCs 6 6例 (36 7% )。非持续性室性心动过速 81例 (45 0 % ) ,随访 3个月 7例发生猝死 ,无心动过速的患者猝死 1例。结论　非持续性室性心动过速是心力衰竭老年患者猝死的危险因素     

Arrhythmia Profile and Sudden Death After Myocardial Infarction and Cardiac Arrest

Incidence of sudden death and arrhythmia pattern were studied using ambulatory monitoring in 40 patients resuscitated < 24 hours (n = 26, Group I) or 4–12 weeks (n = 14, Group II) after myocardial infarction. Forty patients with myocardial infarction and no resuscitation served as controls (Group III). Ambulatory ECGs were recorded with an average of 2 months (Recording 1) and 28 months (Recording 2) after myocardial infarction. Incidence of sudden death was significantly higher in Group II (43%) than in Group I (15%) or Group III (8%) (p < 0.01). In Recording 1, there were no significant differences in the incidence of premature ventricular beats and complex arrhythmias (couplets or salvos) between survivors and sudden death patients in Groups I, II and III, whereas in Recording 2 the mean incidence of premature ventricular beats and complex arrhythmias was significantly higher in survivors in Group II than in Group I or Group III (p < 0.05). In addition, in survivors in Group II, incidence of premature ventricular beats and complex arrhythmias was significantly higher in Recording 2 than in Recording 1 (p < 0.05). Our data show that the risk of sudden death is high in patients with cardiac arrest 4–12 weeks after myocardial infarction. Repeated studies using ambulatory monitoring are helpful in estimating the risk of sudden death in patients with myocardial infarction and cardiac arrest.     

Heart rate variability and sudden death secondary to coronary artery disease during ambulatory electrocardiographic monitoring

Data are analyzed from 5 patients who died suddenly during ambulatory electrocardiographic monitoring. Three of the patients were also assessed in terms of 2 recently developed indexes of heart rate (HR) variability. One of these, the standard deviation of RR intervals during successive 5-minute segments averaged over 24 hours, has been reported to be a putative index of vagal tone. Comparisons were made with HR variability findings in 20 normal volunteers. Sudden death was due to ventricular tachycardia degenerating into ventricular fibrillation in all cases. Both early (3 patients) and late cycle (2 patients) ventricular premature complexes initiated the terminal dysrhythmia. An increased density of ventricular ectopic activity was noted in the hour before onset of ventricular fibrillation. HR variability as measured by the standard deviation was significantly (p less than 0.01) lower in the patients who died suddenly (30 +/- 10 ms) than in the normal subjects (76 +/- 14 ms). These findings support suggestions that HR variability analysis may be useful in identifying patients at a higher risk of sudden death.     

Comparison of programmed stimulation and Holter monitoring for predicting long-term efficacy and inefficacy of amiodarone used alone or in combination with a class 1A antiarrhythmic agent in patients with ventricular tachyarrhythmia

The values of two Holter ambulatory electrocardiographic monitoring criteria and one programmed stimulation efficacy criterion reported to be predictive of the efficacy of amiodarone were compared in 70 patients taking amiodarone for sustained ventricular tachyarrhythmias. At baseline, all patients had ventricular tachycardia inducible by programmed stimulation. After amiodarone loading (935 +/- 271 mg for 16 +/- 7 days), efficacy was determined by a programmed stimulation criterion (ventricular tachycardia no longer inducible or less than or equal to 15 beats) and two Holter monitoring criteria (Holter I = greater than or equal to 85% reduction of ventricular premature complexes and abolition of couplets and triplets in 64 patients who had greater than or equal to 10 ventricular premature complexes/h or couplets or triplets or both before therapy; Holter II = abolition of triplets in 41 patients who had triplets before therapy). Amiodarone was effective in 12 of 70 patients by the programmed stimulation criterion, in 49 of 64 patients by Holter criterion I and in 37 of 41 patients by Holter criterion II. In assessing efficacy of amiodarone, programmed stimulation and Holter criteria were discordant in 69% of patients or more (p less than 0.001). There were 16 recurrences or sudden deaths during the entire follow-up period (19 +/- 19 months). Arrhythmia-free survival rates at 24 months of patients with efficacy and inefficacy by each criterion, respectively, were 90 and 78% by programmed stimulation, 84 and 62% by Holter criterion I (p less than 0.05) and 73 and 50% by Holter criterion II (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Sudden cardiac death after aortic valve surgery: incidence and concomitant factors

A retrospective analysis of 599 consecutive patients after aortic valve surgery aged 7-82 years (mean 56) was performed. During a follow-up of 1-14 years (mean 4.7 years) a 4-week perioperative mortality of 6.9% and a late annual mortality of 3.6% were observed. Sudden cardiac death was the most frequent single cause of death, accounting for 24% of all deaths. Patients dying suddenly were younger than patients dying from other causes (51 +/- 17 vs. 59 +/- 14 years, p less than 0.05) and showed more left ventricular hypertrophy by electrocardiographic criteria when compared with matched survivors (mean Estes score 5.2 +/- 2.4 vs. 2.8 +/- 1.9; p less than 0.01) and with patients dying nonsuddenly (mean Estes score 5.2 +/- 2.4 vs. 1.8 +/- 1.8; p less than 0.01). Ventricular premature beats in the resting electrocardiogram were more prevalent in patients dying suddenly than in matched survivors (55 vs. 20%; p less than 0.025) as well as in patients dying from other causes (55 vs. 25%; p less than 0.05). In addition, there were more intracardiac conduction disturbances and more ungrafted coronary vessels with insignificant stenoses at the time of surgery in sudden death patients. Our findings suggest that after aortic valve replacement patients with left ventricular hypertrophy, bundle-branch block, and ventricular premature beats in the resting electrocardiogram are at increased risk for sudden cardiac death. A possible etiological role of concomitant coronary artery disease must be considered.     

Sudden cardiac death while wearing a Holter monitor

The Holter tapes of 61 patients (46 men, mean age +/- standard deviation 65 +/- 11 years) with sudden cardiac death while being monitored were analyzed. Thirty-eight patients were known to have coronary artery disease, 5 had cardiomyopathy, and 7 had aortic valve disease. Etiology remained unknown in 11 patients. Mean New York Heart Association functional class was 2.5 +/- 0.7. Thirty patients had received antiarrhythmic drugs and 32 had received digitalis. Sudden death occurred at rest in 73%. In the hours before death, repetitive ventricular arrhythmias were found in 50 patients (82%), with atrial fibrillation in 34%. Patients with bradyarrhythmic death (18%) had less complex ventricular activity compared to patients with tachyarrhythmic death (p less than 0.01). Lethal arrhythmias--monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, torsades de pointes, primary ventricular fibrillation, and 1:1 conducting atrial tachycardia--were found in 26 (43%), 15 (25%), 5 (8%), 3 (5%), and 1 patient, respectively. The coupling interval of the final ventricular tachycardia correlated inversely with the initial frequency of ventricular tachycardia (p less than 0.05). For patients with tachyarrhythmic death, an increase of heart rate within the last 3 hours was noted (83 vs 89 beats/min, p less than 0.05). Ventricular premature complexes and the proportion of patients with greater than 2 couplets and greater than 2 triplets increased significantly only within the last hour before death.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arrhythmia control and other factors related to sudden death in coronary disease patients at intermediate risk

Thirty-three patients with coronary artery disease and frequent, complex ventricular arrhythmias (VA) were followed long-term to evaluate factors related to sudden death (SD). Patients with malignant VA (sustained ventricular tachycardia (VT), resuscitated SD, or acute myocardial infarction) were excluded. Baseline data included angiographic ejection fraction (EF), segmental wall motion, and Holter evidence of frequent (greater than 30/hr) and complex (repetitive) ventricular premature beats (VPBs). Control of VA was attempted with conventional or experimental agents and was defined as greater than or equal to 70% reduction in VPBs, greater than or equal to 90% reduction in couplets, and abolition of nonsustained VT on two consecutive Holter tapes. After 24 +/- 15 months of follow-up on the single most effective agent, 18 patients survived while 15 patients died suddenly. There was no difference between these groups with respect to age, sex, or baseline VA. Survivors had a higher EF (51% vs 34%, p less than 0.001), fewer dyskinetic segments (0.05 vs 1.0, p less than 0.01), and better VA control (83% vs 40%, p less than 0.01) than nonsurvivors. By analysis of variance, VA control was not independent of EF (F = 6.98, p less than 0.01). The 1-, 2-, and 3-year survival rates were 90%, 90%, and 82% for patients with EF greater than or equal to 40% and 22%, 11%, and 11%, for those with EF less than 40% and uncontrolled VA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Analysis of ambulatory electrocardiograms in 14 patients who experienced sudden cardiac death during monitoring

The Holter monitors of 14 patients (out of 58,000 Holter recordings performed between 1978 and 1984) who experienced cardiac arrest and expired during the recording period were analyzed. Tachyarrhythmic arrest patients frequently had coronary heart disease, congestive heart failure, and prolonged QTc intervals. The highest incidence of intermediately frequent premature ventricular complexes (PVCs) occurred between 15 and 6 hours prior to death. The frequency of ventricular couplets increased toward the time of arrest. The hours with greatest frequency of ventricular tachycardia (VT) were found to be the last 5 hours of life. An increasing incidence of ST-segment changes greater than 2 mm was noted throughout all of the risk periods until the third hour prior to arrest when the incidence diminished. Conversely, the incidence of lower amplitude ST-segment changes (usually elevation) increased over the final 6 hours. The mean time of death was 0228 hours +/- 5:20. In conclusion, we observed two patterns of Holter-monitored changes which usually occurred prior to death and may represent predictors of sudden death: (1) an increasing incidence of intermediately frequent isolated PVCs followed by increased ventricular couplets and runs of VT; (2) return of high amplitude ST-segment changes toward baseline. To our knowledge, the temporal relationship of the degree of ST-segment deviation to sudden death and the time of sudden death have not been reported in large studies of Holter-monitored sudden death patients.     

Relation of ventricular arrhythmias in the late hospital phase of acute myocardial infarction to sudden death after hospital discharge.

To determine the prognostic significance of ventricular arrhythmias persisting during the hospital ambulatory phase of acute myocardial infarction, 64 patients with acute myocardial infarction underwent continuous 10-hour Holter monitoring an average of 11 days after discharge from the coronary care unit (CCU). Patients were categorized according to the results of ambulatory monitoring: 27 patients had ventricular extrasystoles, which were complicated (multifocal, R on T, paired, more than 5/min), or ventricular tachycardia; 22 had uncomplicated premature ventricular contractions; and 15 exhibited no ventricular arrhythmias. The 64 patients were followed prospectively for an average course of 25.8 months; 12 died suddenly; 8 died of other causes, and 44 survived. In all patients who died suddenly, ventricular ectopy was recorded on Holter monitoring before their discharge from the hospital (complicated premature ventricular contractions, eight patients; uncomplicated premature ventricular contractions, four patients); there were no sudden deaths in the patients without ventricular arrhythmias. Patients who died suddenly and those survived were similar in respect to age (60, 62 years), sex, location of infarction, presence of coronary risk factors, severity of acute myocardial infarction (Q waves, cardiac enzymes), serum cholesterol levels, evidence of cardiomegaly on roentgenograms, presence of ventricular gallop and drug therapy received. The occurrence of acute arrhythmias in the CCU did not separate patients who died suddenly from those who survived; there were no differences in ventricular tachycardia or ventricular fibrillation (3 or 12 patients who died suddenly, 6 of 44 patients who survived) or complicated premature ventricular contractions (4 or 12 patients who died suddenly, 18 of 44 patients who survived). Electrocardiograms obtained late in the hospital course revealed no differences in the extent of Q or T wave changes between these two groups. However, the extent of S-T segment abnormality was greater in patients who died suddenly than in patients who survived (5.6 compared to 1.8 leads/standard tracing, p smaller than 0.02) suggesting that the arrhythmias in the former were related to persistent ischemia or segmental ventricular dyssynergy. Thus, in this relatively small number of patients, ventricular arrhythmias persisting late in the hospital course of patients admitted for acute myocardial infarction are shown to predispose to subsequent sudden death.     

Long-term prognostic significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy

The prognostic significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy is controversial. Thus, 73 patients with idiopathic dilated cardiomyopathy who had both 24-hour Holter monitoring and angiography were followed for greater than or equal to 3 years. Twenty-eight patients (38%) died, 14 patients (19%) due to pump failure and 14 patients (19%) due to sudden death. Univariate analysis revealed ventricular tachycardias as a major risk indicator, among others. However, multivariate analysis determined the major independent risk factors in the following order: patients who died from pump failure, left ventricular filling pressure, left bundle branch block, the number of beats in the longest episode of ventricular tachycardia and left ventricular ejection fraction; patients who died from sudden death, left bundle branch block and left ventricular ejection fraction, but not any form of ventricular arrhythmias. Reclassification by means of the risk factors resulted in a meaningful identification of patients who died from pump failure; however, patients who died from sudden death could not be separated from survivors. Thus, in the present study Holter monitoring was unable to distinguish between patients who died from subsequent pump failure and patients who died from subsequent sudden death.     

Evaluation of antiarrhythmic drug effects with simultaneous analysis of single ventricular premature contractions, couplets and salvos.

To improve the clinical value of ambulatory Holter electrocardiographic (ECG) monitoring as a tool of antiarrhythmic therapy control, a new statistical model was developed. In a patient group at increased risk of sudden cardiac death, the spontaneous variability of ventricular arrhythmias was assessed, with simultaneous consideration of single ventricular premature complexes, couplets and salvos. The study included 100 patients who suffered from coronary heart disease or idiopathic dilated cardiomyopathy and for whom greater than 30 ventricular premature complexes/h and couplets had been demonstrated on the last Holter ECG before the study. Between 3 and 12 Holter recordings were made for each patient in a drug-free state; the mean follow-up period was 260 days (maximum 1,403). The mean hourly values of the ectopic events (EE) were assessed separately for ventricular premature complexes, couplets and salvos. The spontaneous variability (SV) was calculated for single ventricular premature complexes, couplets and salvos as SV = log (EEday 2 + 0.01/EEday 1 + 0.01) and linked in one, two and three dimensions. Compared with the consideration of only one type of arrhythmia (one-dimensional model), the simultaneous use of two or three types of arrhythmia (two- or three-dimensional model) resulted in considerably lower reduction and aggravation rates as sufficient proof of drug effects. With control intervals up to 1 week, the one-dimensional model yielded reduction rates for ventricular premature complexes, couplets and salvos of -63%, -90% and -95%, respectively. In contrast, with the three-dimensional model, the rates were -28%, -72% and -88%. The corresponding aggravation values were +370, +1,114% and +2,189% versus +38%, +256% and +747%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Value of Holter monitoring in predicting long-term efficacy and inefficacy of amiodarone used alone and in combination with class 1A antiarrhythmic agents in patients with ventricular tachycardia

The value of two reported and two new ambulatory electrocardiographic (Holter) criteria was studied in 80 patients taking amiodarone for refractory recurrent sustained ventricular tachycardia. In the 80 patients, the four Holter criteria were as follows: I-85% or greater reduction of ventricular premature complexes and abolition of couplets and nonsustained ventricular tachycardia in 74 patients who had 10 or more ventricular premature complexes/h, or any couplets or nonsustained ventricular tachycardia/24 hours at baseline; II-abolition of nonsustained ventricular tachycardia in 51 patients who had nonsustained ventricular tachycardia at baseline; III-85% or greater reduction of ventricular premature complexes and abolition of nonsustained ventricular tachycardia in 64 patients who had 30 or more ventricular premature complexes/h at baseline; and IV-85% or greater reduction of ventricular premature complexes and abolition of nonsustained ventricular tachycardia in 73 patients who had 10 or more ventricular premature complexes/h at baseline. Amiodarone was judged effective in, respectively, 51 of 74, 44 of 51, 51 of 64 and 61 of 73 patients by criterion I, II, III or IV. During the follow-up period (19 +/- 20 months), there were 19 instances of recurrence of ventricular arrhythmia or sudden death. Actuarial arrhythmia-free survival rate at 24 months was 84, 74, 86 and 85%, respectively, in patients with efficacy by criterion I, II, III or IV and 61, 43, 48 and 39%, respectively, in patients with inefficacy (p less than 0.015 for all). Many patients with efficacy by Holter criteria, however, had a recurrence of arrhythmia, suggesting insensitivity of these Holter criteria.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy of amiodarone during long-term treatment of malignant ventricular arrhythmias in patients with chronic chagasic myocarditis

Oral amiodarone was administered to 24 patients with chronic chagasic myocarditis (CCM) and malignant ventricular arrhythmias. Control 24-hour Holter recordings revealed frequent ventricular premature beats (VPBs) (157 to 2572/hr; mean 714 ± 125), multiform VPBs, and countless numbers of ventricular couplets in all patients, R-on-T phenomenon in 17 patients, and ventricular tachycardia in 21 patients. Amiodarone caused total and persistent suppression of ventricular couplets and tachycardia and greater than 93% reduction of VPB number in 22 patients, during a follow-up of 26.6 months (range 2 to 55 months). In 1 patient, ventricular couplets and tachycardia persisted despite the fact that a 98.2% reduction of VPB number was achieved. This latter patient was the only one in the whole group who experienced sudden death. The maximal antiarrhythmic effect was attained gradually after 3 to 26 weeks (mean 7.4). In four patients in whom treatment was discontinued after 3 to 12 months, the antiarrhythmic protection lasted 4 to 9 weeks. In nine patients the dose of amiodarone was 600 to 800 mg/day. In 15 patients the dose had to be increased to 800 to 1000 mg/day. Despite the presence of congestive heart failure in seven patients and intraventricular block in 17 patients, no limiting side effects were observed. Amiodarone proved to be extremely effective and safe against the most malignant ventricular arrhythmias of CCM.     

Spectrum and prognostic significance of arrhythmias on ambulatory Holter electrocardiogram in hypertrophic cardiomyopathy

OBJECTIVES: The goal of this study was to assemble a profile and assess the significance of arrhythmias in a nontertiary-based hypertrophic cardiomyopathy (HCM) cohort. BACKGROUND: Hypertrophic cardiomyopathy is associated with arrhythmia-related consequences, particularly sudden death. Ventricular tachyarrhythmias on Holter electrocardiograms (ECG) have been reported as markers for sudden death in highly selected HCM populations. METHODS: We assessed the profile of ventricular and supraventricular ectopy and bradyarrhythmia on ambulatory 24-h Holter ECG and also related these findings to clinical outcome in 178 HCM patients. RESULTS: Of the 178 study patients, 157 (88%) had premature ventricular complexes (PVCs), including 21 (12%) with >/=500 PVCs, 74 (42%) had couplets, 67 (37%) had supraventricular tachycardia (SVT), and 56 (31%) had nonsustained ventricular tachycardia (NSVT). Mean number of PVCs was 330 +/- 763 (range 1 to 5,435) and increased with age (p < 0.01); NSVT was associated with greater left ventricular hypertrophy (p = 0.01) and severe symptoms (New York Heart Association functional classes III and IV) (p = 0.04); SVT occurred more commonly in patients with outflow obstruction (p = 0.02). Over a follow-up of 5.5 +/- 3.4 years, 11 (6%) patients died suddenly (annual mortality rate, 1.1%) including 5 patients with NSVT. For sudden death, NSVT on Holter ECG had negative and positive predictive values of 95% and 9%, and sensitivity and specificity of 45% and 69%, respectively. CONCLUSIONS: In this nontertiary-based HCM cohort, ventricular and supraventricular tachyarrhythmias were particularly frequent and demonstrated a broad spectrum on ambulatory (Holter) ECG. Paradoxically, despite such a highly arrhythmogenic substrate, sudden death events proved to be relatively uncommon. Ventricular tachyarrhythmias had a low positive and relatively high negative predictive value for sudden death in this HCM population.     

Empiric treatment with amiodarone in patients with sustained ventricular tachyarrhythmia. Results of a long-term follow-up

The long-term follow-up of 52 pts (36 M, 16 F, mean age: 62 years) with sustained ventricular tachyarrhythmias (SVT) was analyzed to assess the efficacy and feasibility of empiric amiodarone treatment. Forty-five pts had organic heart disease (mean EF: 38.3%) and 7 pts no overt heart disease. Twenty pts suffered from syncope or cardiac arrest secondary to sustained ventricular tachyarrhythmias (mean: 2.35 episodes) and 32 did not. All pts were given amiodarone empirically (mean dose: 390 mg) and followed-up for a mean period of 29.5 months (range 1-137). Two pts (3.8%) died of non cardiac causes, 5 (9.6%) of non sudden cardiac death and 7 (13.4%) of sudden death. Fifteen pts (28.8%) experienced non fatal arrhythmic recurrences. Four out of 7 pts who died suddenly experienced non fatal arrhythmic recurrence before death. The actuarial incidence of cardiac death was 10.8, 22.7, 31.5, 31.5% at 1, 2, 3 and 5 years; the actuarial incidence of sudden death was 8.9, 12, 22.1, 22.1% at 1, 2, 3 and 5 years; the actuarial incidence of non fatal arrhythmic recurrences was 17.4, 26.3, 26.3, 26.3, 44.7% at 1, 2, 3, 4 and 5 years. Univariate analysis identified recent myocardial infarction, NYHA functional class, detection of frequent and/or repetitive premature ventricular contractions on Holter monitoring and non fatal arrhythmic recurrences as predictors of cardiac death (p less than 0.05), while only non fatal arrhythmic recurrences were associated with sudden death (p less than 0.05). Twenty-two pts (42.3%) developed side effects. Nine (17.3%) discontinued amiodarone: 6 pts (11.5%) because of side effects and 3 inadvertently.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relation between myocyte disarray and outcome in hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HC) is associated with an increased risk of sudden cardiac death or death from heart failure. Little is known of the pathologic substrate for risk of premature death in this disease. We therefore set out to correlate the pathologic findings with the mode of death and risk profile in 75 patients with HC. Hearts with HC were obtained after death or transplantation. The clinical details were correlated with the macroscopic findings and the percent fibrosis, disarray, and small-vessel disease across 19 sections of each heart. Thirty-nine patients died suddenly, 28 had end-stage heart failure, and 8 died of other causes. Myocyte disarray correlated positively with evidence of ischemia (r = 0.5, p <0.0001), and was greater in patients who died before age 21 years (mean disarray 33% vs 18%, p <0.0001) and in those with an abnormal vascular response to exercise (mean disarray and 30% vs 19%, p = 0.04). Myocardial fibrosis was greater in patients who died in heart failure (mean percent fibrosis was 2.8% versus 0.9%, p = 0.003), and in patients with nonsustained ventricular tachycardia or a high risk fractionation study (4.9% vs 2.7%, p = 0.04, and 6.84% vs 2.8%, p = 0.03, respectively). In conclusion, young patients who die with HC have greater disarray than their older counterparts. In contrast, myocardial fibrosis is the substrate for premature deaths from heart failure and is associated with an increased risk of a primary ventricular arrhythmia.     

Relation of dispersion of QRS and QT in patients with advanced congestive heart failure to cardiac and sudden death mortality

This study examined the usefulness of 01 and QRS dispersion in the prognosis of patients with advanced congestive heart failure (CHF). One hundred four patients in New York Heart Association functional classes II to IV, with a left ventricular ejection fraction of <35%, and untreated with antiarrhythmic drugs, were followed prospectively. QRS and QT dispersion were defined as the maximum difference in QRS and QT interval duration, respectively, measured on all leads of standard 12-lead electrocardiograms. The end points of the study were non-sudden and sudden cardiac mortality. During an average follow-up of 20 months, there were 13 non-sudden and 10 sudden deaths. The average QRS duration was significantly longer in nonsurvivors than in survivors (125 ? 34 vs 113 ? 34 ms, respectively, p <0.04). Similar results were obtained with 01 dispersion (95 ? 48 ms vs 78 ? 31 ms, respectively, p <0.03) and QRS dispersion (54 ? 17 ms vs 46 16 ms, respectively, p <0.02). Furthermore, patients who died suddenly had significantly greater QRS dispersion than patients who survived (56 ? 13 vs 46 ? 16 ms, respectively, p <0.02). In a multivariate analysis, QT and QRS dispersion were both independent predictors of non-sudden cardiac death (p = 0.01 and p = 0.001, respectively), and QRS dispersion was also an independent predictor of sudden cardiac death (p = 0.04). Death rate in patients with 01 dispersion >90 ms was 2.8-fold higher than those with 01 dispersion 90 ms (95% confidence intervals [CI] 1.2 to 6.4). Similarly, the death rate in patients with QRS dispersion >46 ms was 3.9-fold higher than in those with QRS dispersion 46 ms (95% Cl 1.6 to 9.5). These findings suggest that QT and QRS dispersion are useful predictors of mortality in patients with advanced CHF. ?2000 by Excerpta Medica, Inc.     

Clinical,electrocardiographic and follow-up observations in patients having ventricular fibrillation during holter monitoring: Role of quinidine therapy

Ventricular fibrillation occurred during Holter electrocardiographic monitoring in 5 of 3,307 consecutive patients. All five patients had Holter studies for evaluation of antiarrhythmic drug therapy; their ages ranged from 51 to 65 years. No patient had acute myocardlal infarction; all had congestive heart failure and severe left ventricular dysfunction. One patient had ischemic and four had nonischemic cardiomyopathy. All patients had recently begun treatment with oral quinidine and had plasma quinidine levels of 1.24 to 5.18 μg/ml. The Holter monitoring revealed that all had a long Q-T interval and that ventricular fibrillation began during frequent ventricular premature beats and was immediately preceded by ventricular tachycardia of the torsade de pointes type. The coupling interval of the ventricular premature beats initiating torsade de pointes was late (440 to 720 ms) and followed long preceding cycles (840 to 1920 ms). Ventricular fibrillation resolved spontaneously in two patients, but two of the remaining three patients died despite attempted cardiopulmonary resuscitation.It is concluded that (1) left ventricular dysfunction, chronic ventricular arrhythmias and initiation of quinidine therapy were the common findings in these patients; (2) a long Q-T interval, late coupled ventricular premature beats and long preceding cycles facilitate initiation of ventricular fibrillation in quinidine-treated patients; and (3) direct on-line monitoring should be utilized in the management of these patients.