Repeated 1 hour electrocardiographic monitoring of survivors of myocardial infarction at 6 month intervals: Arrhythmia detection and relation to prognosis

In a study of the relation between ventricular premature beats and sudden death among 1,739 male survivors of myocardial infarction enrolled in the Health Insurance Plan of Greater New York (HIP), patients underwent 1 hour of electrocardiographic monitoring at a baseline examination. During follow-up periods of up to 5 1/2 years, survivors underwent repeated monitoring at 6 month intervals for a maximum of four monitorings. At each monitoring a constant proportion of the men—25 percent—showed complex ventricular premature beats (runs of two or more, R on T phenomenon, bigeminal or multiform beats) during the hour. In comparison with men free of such arrhythmia, those demonstrating these complex forms in a given hour were three times as likely to show such beats in a subsequent monitoring hour. The mortality risk over 3 1/2 years after each of the four monitoring observations was in all cases elevated among men with complex ventricular premature beats. The risk of sudden death over this period was 6 percent for men without and 13 to 17 percent for men with such complexes. A study of the 1,445 men who underwent monitoring both at baseline examination and 6 months later identified the presence of runs of ventricular premature beats in either observation as a particularly important harbinger of sudden death.     

Identifying patients at risk of sudden death after myocardial infarction: Value of the response to programmed stimulation, degree of ventricular ectopic activity and severity of left ventricular dysfunction

The ability of programmed ventricular stimulation to identify risk of sudden death after acute myocardial infarction (MI) was compared with 24-hour electrocardiographic assessment of ventricular ectopic activity and determination of left ventricular (LV) dysfunction. Forty-six patients underwent programmed stimulation 8 to 60 days (mean 22) after documented MI. Programmed stimulation consisted of single and double extrastimuli from the right ventricular apex at 2 times diastolic threshold during ventricular pacing and normal sinus rhythm. Of the 46 patients, 44 underwent electrocardiographic monitoring at least 6 days after MI. In 43 of the 46 patients, LV ejection fraction (EF) and the presence of LV aneurysm were determined. In response to programmed ventricular stimulation, 5 patients had sustained ventricular tachycardia (VT), 5 had nonsustained VT (≥4 beats), 13 had intraventricular reentrant repetitive responses, and 23 had either bundle branch reentrant repetitive responses or no extra responses to programmed ventricular stimulation (negative study).

During a mean follow-up of 18 months, 10 patients died, 6 suddenly. One of the 10 patients with sustained or nonsustained VT died suddenly, compared with 3 of 13 patients with intraventricular reentrant responses and 2 of 23 patients with a negative study (difference not significant). Of 25 patients with Grade 0 to 2 ventricular ectopic activity, 3 died suddenly after MI, compared with 3 of 19 patients with Grade 3 or 4 activity (difference not significant). By comparison, the frequency of sudden death was greater in patients with an LVEF of <40% (5 of 16 versus 1 of 27 patients) or an LV aneurysm (5 of 13 versus 1 of 30 patients).

Thus, using the described protocol, the response to programmed ventricular stimulation is not helpful in identifying patients at risk for sudden death after MI. The presence of an LV aneurysm or EF of <40% appears to provide the greatest prognostic information with respect to risk for sudden cardiac death.     

Prognostic significance of repetitive ventricular response during programmed ventricular stimulation

To determine the incidence and prognostic significance of the repetitive ventricular response, a retrospective study was performed in 65 patients (49 male, 16 female, mean age ± standard deviation 55 ± 11 years) with coronary artery or myocardial disease and a variety of cardiac rhythm disorders. Programmed right ventricular stimulation was performed at a basic pacing rate of 120 beats/min using one (S₂) and two (S₂-S₃) premature stimuli. The data were analyzed as to the presence or absence of a repetitive ventricular response and the patients' outcome ([1] sudden death at 1 hour or less or documented ventricular fibrillation without myocardial infarction; [2] survival or death from noncardiac causes or nonsudden death).A repetitive ventricular response was observed in 23 (35.4 percent) of 65 patients after one and in 31 (48.4 percent) of 64 patients after two premature stimuli. It occurred in 9 of 9 patients with ventricular fibrillation and in 14 (82.4 percent) of 17 patients with ventricular tachycardia. The mean follow-up period was 76 ± 39 weeks. Sixteen patients were classified as dying suddenly; the remaining patients were considered surviving (or dying nonsuddenly). After one premature stimulus, a repetitive ventricular response was observed in 32.7 percent of patients surviving or with nonsudden death and in 43.8 percent of patients with sudden death or malignant ventricular arrhythmias. After two premature stimuli, the incidence of a repetitive ventricular response increased from 40.8 percent in patients surviving or with nonsudden death to 68.8 percent in patients with sudden death; 6 (12.2 percent) of 49 patients surviving or with non-sudden death and 9 (56.3 percent) of 16 patients with sudden death had more than three ventricular echo beats. All nonsurviving patients who demonstrated a repetitive ventricular response had intraventricular reentry. Depending on the rigidity of the criteria used (that is, the number of echo beats), the sensitivity of the test ranged between 37 and 88 percent and specificity ranged between 45 and 92 percent. The proportion of false positive results was high (33 to 66 percent); but the proportion of false negative results was low (8 to 18 percent).This retrospective study showed a correlation between sudden death and the incidence and number of repetitive ventricular responses (depending on the number of premature stimuli) and the type of reentrant beats (bundle branch reentry or intraventricular reentry).     

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.     

Ventricular arrhythmias after coronary artery bypass graft surgery: incidence, risk factors and long-term prognosis

The incidence, risk factors and long-term prognosis of complex ventricular arrhythmias after coronary artery bypass graft surgery are not known. Complex ventricular arrhythmias are defined as Lown grades 4a (couplets), 4b (ventricular tachycardia) and 5 (R on T phenomenon). Ninety-two patients with normal left ventricular function who underwent elective coronary artery bypass graft surgery were prospectively evaluated. Ventricular arrhythmias were documented by predischarge 24 hour ambulatory electrocardiographic monitoring; 43% of patients had no or simple ventricular arrhythmias (Lown grades 1 to 3) and 57% had complex ventricular arrhythmias. Risk factors analyzed included age, sex, diabetes, hypertension, smoking, preoperative digoxin or propranolol therapy, cardiopulmonary bypass time, aortic cross-clamp time, number of vessels bypassed, peak creatine kinase (CK) elevation and pericarditis. No risk factor identified patients at higher risk for complex ventricular arrhythmias. Patients were followed up for 6 to 24 months (mean 16). Patients with complex ventricular arrhythmias did not have a higher incidence of sudden death, cardiac death, syncope, angina, myocardial infarction or cerebrovascular accident. It was concluded that: Complex ventricular arrhythmias are common after coronary artery bypass graft surgery. None of the risk factors considered identify high risk patients. Complex ventricular arrhythmias after coronary artery bypass graft surgery do not indicate a poor prognosis in patients with normal left ventricular function.     

Lorcainide therapy for the high-risk patient post myocardial infarction

Nonsustained ventricular tachycardia (VT) in the late period (7 to 21 days) after myocardial infarction (MI) is reported to be a predictor of sudden death. Patients with 3-beat VT on Holter monitoring in the late infarction period would be suspected to demonstrate electrical instability on electrophysiologic studies. Forty-seven patients were identified as having at least 3-beat VT on Holter monitoring. Eighteen patients refused electrophysiologic studies or were not referred. Eight patients died; 3 were sudden deaths in 13 +/- 5 months, a 17% incidence. Twenty-nine patients underwent invasive electrophysiologic studies and 28 had inducible VT, 18 sustained and 10 nonsustained. Lorcainide prevented VT induction in 21 of the 28 patients, whereas 12 of the 22 patients studied on procainamide were protected. Lidocaine, tested in 21 patients, prevented VT induction in only 5. Lorcainide and procainamide prolonged refractoriness in those patients protected at programmed electrical stimulation (PES), whereas the QT interval was prolonged in patients in whom VT could still be induced. Twenty-seven of the 28 patients were placed on drugs predicted to be effective by PES studies, 19 on lorcainide. After a mean follow-up of 12.5 +/- 4 months the patient with noninducible arrhythmia is alive and 26 of the 28 patients with inducible arrhythmia are alive and well. Two patients died, 1 of stroke and 1 of pump failure after a second MI. No sudden deaths were observed in this group. Two patients had breakthrough arrhythmias and were treated by alternative antiarrhythmic therapy that was also effective on initial electrophysiologic studies.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term antiarrhythmic therapy with acetylprocainamide

Nineteen patients whose arrhythmias were initially suppressed with acetylprocainamide underwent long-term treatment with this drug. Eleven patients were still taking the drug at the end of 12 months. Drug withdrawal with substitution of a placebo caused an increase in ventricular premature beats. Thus, suppression of ventricular premature beats persisted for 1 year. The eight withdrawals from the study were due to death during the year (n = 6) or recurrence of arrhythmias. The deaths occurred in patients who were in New York Heart Association functional class II (one patient), III (three patients) and IV (two patients). Ventricular performance, assessed from systolic time intervals, improved with drug therapy and declined during drug withdrawal. Symptomatic effects were common, with seven patients requiring a reduction in dosage or discontinuation of therapy. Three patients treated for 3 years continued to show drug suppression of ventricular premature beats compared with the level during placebo substitution. Small amounts of procainamide were present in all patients because of in vivo deacetylation of acetylprocainamide. Many patients with good initial responses to this drug had recurrent arrhythmias during long-term therapy. For this reason, the usefulness of acetylprocainamide as an antiarrhythmic drug appears to be limited.     

Prognostic factors in nonsustained ventricular tachycardia

Electrophysiologic studies were performed in 83 consecutive patients with spontaneous nonsustained ventricular tachycardia (VT). VT was inducible in 52 patients (nonsustained VT only in 37 patients, nonsustained and sustained VT in 13 and sustained VT only in 2). During a follow-up of 3 to 111 months (mean 33), 10 patients died suddenly, 5 with coronary artery disease (CAD) and 5 with dilated cardiomyopathy. All patients with sudden death had an ejection fraction ≤0.40. Sudden death occurred in 4 of 15 patients with inducible sustained VT, 2 of 37 patients with only nonsustained VT and 4 of 31 patients without inducible VT. One patient with dilated cardiomyopathy and VT inducible only by isoproterenol died suddenly. Three of 5 patients with CAD who had sudden death had had inducible sustained VT, but 3 of 5 patients with cardiomyopathy who had sudden death had no inducible VT. Multivariate analysis revealed that patients with inducible sustained VT or an ejection fraction ≤0.40 had a 3-fold increased risk of sudden death, and patients with both factors had a 7-fold increased risk of sudden death. This study demonstrates that patients with nonsustained VT with an ejection fraction > 0.40 have an uncomplicated course; however, noninducibility does not predict such a course, particularly in patients with cardiomyopathy. The most powerful predictor of risk for sudden cardiac death is a left ventricular ejection fraction ?0.40, but the presence of inducible sustained VT is an independent risk factor for sudden death.     

Antiarrhythmic treatment: an overview

Atrial and ventricular arrhythmias cause significant morbidity and mortality. Abnormalities of impulse generation, e.g., abnormal automaticity or triggered activity, or abnormalities of impulse conduction, e.g., atrioventricular block or reentry, are the prime mechanisms of atrial or ventricular arrhythmias. The ventricular arrhythmias are of special interest because they are a key element in sudden cardiac death, the number 1 public health problem in the U.S. Electrocardiographic recording or provocative testing, e.g., exercise or programmed ventricular stimulation, are used to detect and classify ventricular arrhythmias. Drugs with different mechanisms of action are being rapidly developed to combat cardiac arrhythmias. Ventricular arrhythmias can be defined as benign, potentially malignant or malignant. Benign ventricular arrhythmias require no drug treatment; potentially malignant arrhythmias are subject to drug prophylaxis; and the malignant ventricular arrhythmias require aggressive therapy with drugs, surgery or electronic devices. The management of the malignant ventricular arrhythmias should be evaluated by 1 of 2 programmatic approaches: electrophysiologic or Holter/exercise. Both are complex, costly and inconvenient, but both are excellent for identifying effective treatment for malignant ventricular arrhythmias.     

QT及JT离散度对心性猝死预测价值的探讨

测定３２例心性猝死和３０例非猝死性心性死亡病人入院后的首次心电图ＱＴ离散度（ＱＴｄ）和ＪＴ离散度（ＪＴｄ），产以３０例存活病人作对照，结果显示：（１）心性猝死组ＱＴｄ，ＪＴｄ较存活组和非猝死性心性死亡组显著增大（前者Ｐ均〈０．０１，后者Ｐ均〈０．０５，而非猝死性心性死亡组与存活组ＱＴｄ，ＪＴｄ比较差异均无统计学意义。（２）在心性猝死病人中，死亡直接原因为快速室性心律失常组（２３例）的ＱＴｄ，ＪＴｄ     

Wavelet decomposition analysis of the signal averaged electrocardiogram used for risk stratification of patients with hypertrophic cardiomyopathy

Aims To study the predictive value of wavelet decomposition, as demonstratedby the signal-averaged ECG, in order to identify patients withhypertrophic cardiomyopathy at increased risk for malignantventricular arrhythmias or sudden death. Methods and Results Two hundred and forty-six patients with hypertrophic cardiomyopathywere studied. During a mean follow-up of 68±17 months32 patients died, of whom 17 died suddenly. Patients with suddendeath, together with eight patients with a history of ventricularfibrillation (sudden death/ventricular fibrillation group) wereanalysed and compared to the other 221 patients as well as toa subgroup of 82 patients without a history of syncope, ventriculararrhythmias on a long-term ECG recording or a family historyof sudden death. There were no differences in mean values ofthe four wavelet decomposition parameters among patients inthe sudden death/ventricular fibrillation group, those withoutsudden death/ventricular fibrillation or patients in the lowrisk group. There were, however, significant differences betweenpatients dying non-suddenly and patients being alive at theend of follow-up. Eighty-seven patients (35%) demonstrated evidenceof non-sustained ventricular tachycardia on a long-term ECG.Analysis of wavelet decomposition resulted in abnormal findingsin these patients more often than in those without ventriculararrhythmias. Conclusion The usefulness of wavelet decomposition analysis in predictingsudden death or ventricular fibrillation is limited in patientswith hypertrophic cardiomyop-athy. It may, however, play a rolein identifying patients at risk of dying non-suddenly and ofpatients with non-sustained ventricular tachycardia.     

Prognostic significance of 24 hour ambulatory electrocardiographic monitoring in patients with hypertrophic cardiomyopathy: A prospective study

The prevalence and prognostic significance of ventricular arrhythmias identified on 24 hour ambulatory electrocardiographic monitoring was prospectlvely assessed in 99 patients with hypertrophie cardiomyopathy. In the absence of antlarrhythmic therapy, high grade ventricular arrhythmias (grade 3 and above) were common; that is, they were identified in 66 percent of the patients, including 19 percent with episodes of asymptomatic ventricular tachycardia.Clinical outcome was assessed 3 years after the initial 24 hour ambulatory electrocardiogram. Of the 84 patients who did not undergo ventricular septal myotomy-myectomy, 6 died suddenly or experienced cardiac arrest, 1 died of progressive congestive heart failure and the other 77 have survived without a cardiac catastrophe. The prevalence rate of sudden death or cardiac arrest during the follow-up period was the same (3 percent) in patients with high grade arrhythmias other than ventricular tachycardia (1 of 37) as in those with no or low grade arrhythmias (1 of 29). However, the occurrence of a sudden cardiac catastrophe was significantly more common in patients with asymptomatic ventricular tachycardia of brief duration on 24 hour electrocardiography (4 [24 percent] of 17) than in patients without ventricular tachycardia (2 [3 percent] of 66) (p <0.02).In summary, (1) high grade ventricular arrhythmias are commonly found on continuous 24 hour electrocardiographic monitoring in patients with hypertrophic cardiomyopathy; and (2) although sudden death is relatively uncommon in patients with high grade ventricular arrhythmias other than ventricular tachycardia (annual mortality rate 1 percent), the finding of ventricular tachycardia on 24 hour electrocardlography identifies a subgroup of patients at high risk for sudden death (annual mortality rate 8.6 percent). Although no conclusions can be drawn regarding the impact of therapy, our findings suggest that 24 hour electrocardiographic monitoring should be performed in patients with hypertrophic cardiomyopathy and that it may be reasonable to initiate antlarrhythmic therapy if ventricular tachycardia is identified.     

Sudden death in patients with hypertrophic cardiomyopathy: Characterization of 26 patients without functional limitation

Sudden death is a recognized complication in symptomatic patients with hypertrophic cardiomyopathy. However, its occurrence in patients with no or transient previous cardiac symptoms presents a particularly challenging diagnostic and therapeutic dilemma. Therefore, 26 patients with hypertrophic cardiomyopathy whose death was the first definitive manifestation of cardiac disease were evaluated. Their ages ranged from 8 to 49 years (mean 18) and 23 were less than 25 years of age; 19 were male and 7 female. Of the 26 patients, 13 died during or immediately after moderate or severe physical exertion. Of 12 patients with previous cardiac catheterization, 6 had no or a small left ventricular outflow tract gradient under basal conditions and 6 had an outflow gradient of 50 mm Hg or greater. Left ventricular end-diastolic pressure was elevated in nine patients, and the ventricular septum was moderately to severely thickened (17 mm or more) in all patients. The electrocardiogram was abnormal in all 19 patients studied before death. Thus, sudden death may be the first definitive manifestation of cardiac disease in some patients with hypertrophic cardiomyopathy. Although the effects of patient selection in this study group cannot be excluded, sudden death was common in children and young adults and was often related to physical exertion; each patient showed a distinctly abnormal electrocardiogram and moderate to severe ventricular septal thickening.     

Predictors of sudden cardiac death in never previously treated patients with essential hypertension: long-term follow-up

Increased QT dispersion has been associated with ventricular arrhythmia and sudden death in a variety of cardiac disorders. Left ventricular hypertrophy (LVH) has also been associated with increased incidence of sudden cardiac death in patients with essential hypertension. Furthermore, patients with essential hypertension, particularly those with LVH, are more likely to develop ventricular arrhythmias than are the normal population. The relationship between LVH, QT dispersion, complex ventricular arrhythmia and sudden cardiac death in previously untreated patients over long-term follow-up in hypertension has not been reported before and is the purpose of this study. Fifty-nine adult subjects with essential hypertension, who had never been previously on antihypertensive treatment were followed up for a total of 119.2 +/- 26.2 months. QTc (corrected QT), blood pressure, electrocardiograms, and 24-h Holter ECG recordings were performed in all patients at the time of entry to the study. Ventricular arrhythmias were classified using a modified Lown's scoring system. During the follow-up period death occurred in 12 cases (20%) of which only six (10%) deaths were sudden. The findings of this study indicate that LVH and complex ventricular arrhythmias (Lown's score > or =3) are the only significant predictors of sudden death. Although patients who died suddenly had higher systolic and diastolic blood pressures and greater QTc dispersion compared to surviving patients, this difference was statistically not significant. Similarly, when those who died suddenly were compared to those non-cardiac deaths, LVH and complex ventricular arrhythmias were the only significant predictors of sudden death. In spite of increased QTc dispersion in hypertensive patients, this finding was not associated with increased risk of sudden death and only LVH and high grade ventricular arrhythmias identified hypertensive patients at risk of sudden cardiac death over a 10-year follow-up period.     

Mechanisms of Arrhythmia and Sudden Cardiac Death in Patients With HIV Infection

Long-term survival of HIV-infected patients has significantly improved with the use of antiretroviral therapy (ART). As a consequence, cardiovascular diseases are now emerging as an important clinical problem in this population. Sudden cardiac death is the third leading cause of mortality in HIV patients. Twenty percent of patients with HIV who died of sudden cardiac death had previous cardiac arrhythmias including ventricular tachycardia, atrial fibrillation, and other unspecified rhythm disorders. This review presents a summary of HIV-related arrhythmias, associated risk factors specific to the HIV population, and underlying mechanisms. Compared with the general population, patients with HIV have several cardiac conditions and electrophysiological abnormalities. As a result, they have an increased risk of developing severe arrhythmias, that can lead to sudden cardiac death. Possible explanations may be related to non-ART polypharmacy, electrolyte imbalances, and use of substances observed in HIV-infected patients; many of these conditions are associated with alterations in cardiac electrical activity, increasing the risk of arrhythmia and sudden cardiac death. However, clinical and experimental evidence has also revealed that cardiac arrhythmias occur in HIV-infected patients, even in the absence of drugs. This indicates that HIV itself can change the electrophysiological properties of the heart profoundly and cause cardiac arrhythmias and related sudden cardiac death. The current knowledge of the underlying mechanisms, as well as the emerging role of inflammation in these arrhythmias, are discussed here.     

Detailed analysis of 24 hour ambulatory electrocardiographic recordings during ventricular fibrillation or torsade de pointes

Although the terminal cardiac rhythm is often well documented in many cases of sudden cardiac death, the antecedent or premonitory arrhythmias are usually not retrievable. The ambulatory electrocardiographic recordings of 12 patients who sustained ventricular fibrillation or torsade de pointes while wearing a long-term electrocardiographic monitor were analyzed in detail. A printout of the entire electrocardiographic recording was made and hand counts of ventricular arrhythmias were correlated with heart rate, QTc interval, RR interval preceding ventricular fibrillation or torsade de pointes and (RR')/QT initiating ventricular fibrillation or torsade de pointes. Common ambulatory electrocardiographic features in these 12 patients experiencing ventricular fibrillation or torsade de pointes included: 1) a period of high density of increasingly frequent or complex ventricular arrhythmias, or both, preceding ventricular fibrillation or torsade de pointes (11 patients); 2) R on T beats frequently initiating ventricular fibrillation or torsade de pointes (9 patients); and 3) repolarization abnormalities present for several hours before ventricular fibrillation or torsade de pointes (7 patients). No consistent relation between the RR and RR' interval initiating ventricular fibrillation or torsade de pointes was found; no consistent alteration in heart rate occurred before ventricular fibrillation or torsade de pointes. Thus, ventricular arrhythmias leading to sudden death in an ambulatory population do not occur in isolation but are preceded by a period of increased ventricular ectopic activity. Future guidelines for assessment of antiarrhythmic drug efficacy should include an evaluation of a drug's impact not only on ectopic beat frequency but also on arrhythmia density.     

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.     

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.     

Idiopathic dilated cardiomyopathy. Role of programmed electrical stimulation and Holter monitoring in predicting those at risk of sudden death

The prognostic role of programmed electrical stimulation and Holter monitoring was evaluated in 21 patients with idiopathic dilated cardiomyopathy who had no prior history of ventricular tachyarrhythmias. During a mean follow-up period of 23 months, sudden death or ventricular fibrillation occurred in four (20 percent). One patient died of complications of sepsis, and one underwent cardiac transplantation. Programmed electrical stimulation (PES) resulted in five or more beats of induced ventricular tachycardia in seven patients (33 percent), but was a poor predictor of sudden death (sensitivity = 20 percent). Thirteen patients (62 percent) had complex ventricular ectopy (Lown class 4A or 4B) by ambulatory monitoring. This was a sensitive (80 percent) but not specific (31 percent) marker for sudden death. The predictive value of a negative Holter monitor study was high (80 percent) for identifying those at low risk of sudden death. The results of this prospective study suggest that programmed ventricular stimulation and routine ambulatory monitoring are poor predictors of sudden death in this population.