Clinical and electrophysiologic determinants, treatment and survival of patients with sustained malignant ventricular tachyarrhythmias occurring late after myocardial infarction

To assess the clinical and electrophysiologic determinants, treatment and survival of patients with sustained malignant ventricular tachyarrhythmias late after myocardial infarction, a total of 108 patients (mean age 61 +/- 10 years) were studied. Thirty-two patients (Group I) had sustained ventricular tachyarrhythmias 8 to 60 days (mean 13 +/- 9) after acute myocardial infarction. The remaining 76 patients (Group II), who served as a control group, had no sustained ventricular tachyarrhythmias less than or equal to 60 days after infarction. The most significant independent determinants of sustained ventricular tachyarrhythmias late after infarction were the presence of late potentials (chi square = 16.07, p = 0.0001), defined as an abnormal signal-averaged QRS complex in association with an abnormal root-mean-square voltage in the terminal 40 ms of the QRS complex, and an abnormal ejection fraction of less than 40% (chi square = 10.09, p = 0.001). Sustained ventricular tachycardia was induced in 27 (96%) of 28 Group I patients. Among the 32 patients in Group I, antitachycardia therapy included antiarrhythmic drug therapy as the sole preventive measure in 14 (44%); map-guided surgery or coronary artery bypass surgery, or both, in 14 (44%) and the automatic cardioverter-defibrillator in 4 (12%). The arrhythmias were rendered noninducible in 83% of patients after map-guided surgery and in 41% after drug therapy. During a follow-up period of 20 +/- 14 months, five Group I patients (15%) had an arrhythmic event and four (9.3%) had a cardiac-related death. All five patients who had an arrhythmic event were receiving antiarrhythmic drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognosis following sustained ventricular tachycardia occurring early after myocardial infarction

Eighty-seven patients with sustained ventricular tachycardia (VT) between 3 and 90 days after acute myocardial infarction (AMI) were evaluated to define factors associated with a high risk of arrhythmia recurrence or death. Most patients had poor left ventricular function (mean ejection fraction 29 +/- 12%), multivessel coronary artery disease (71%) and inducible sustained VT with programmed stimulation (87%). During a mean follow-up of 26 months, 36 patients (41%) died and 21 patients had arrhythmia recurrence (with 19 sudden deaths). Factors independently associated with mortality included: (1) treatment before 1981 (p less than 0.01); (2) anterior AMI (p less than 0.05); (3) short time from AMI to first episode of VT (p less than 0.06); and (4) multivessel coronary artery disease (p less than 0.07). Factors independently associated with arrhythmia recurrence were: (1) medical treatment (as opposed to surgical) (p less than 0.01); (2) greater than or equal to 3 episodes of spontaneous VT (p = 0.01); (3) multivessel coronary disease (p less than 0.05); and (4) anterior AMI (p less than 0.07). Medically and surgically treated patients did not differ significantly in overall survival (49 vs 61%, respectively), although short-term (6 month) surgical survival improved from 31% during the first half of the study to 96% in the latter half (p less than 0.01). For patients with sustained VT early after AMI the risk of death and arrhythmia recurrence can be assessed based on clinical and angiographic characteristics; in addition, surgical treatment is associated with a lower incidence of arrhythmia recurrence than medical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inducible sustained ventricular tachycardia 4 years after experimental canine myocardial infarction: electrophysiologic and anatomic comparisons with early healed infarcts

We studied a group of 17 dogs 4 to 6 years after infarction produced by 2 hr occlusion of the anterior descending coronary artery followed by reperfusion. Dogs in this "late" infarct group were compared with a group of 24 dogs with "early" healed infarcts (2 to 24 weeks old). With signal-averaging techniques body surface potentials were recorded during sinus rhythm. After thoracotomy epicardial electrograms were recorded from 45 standardized sites within the infarcted region and characteristics of selected electrograms were compared with anatomic features of underlying myocardium. Epicardial recordings from the late infarct group demonstrated earlier local activation (p less than .001) and shorter electrogram duration (p less than .001) when compared with recordings from the early infarct group. There was less temporal dispersion of activation and electrogram duration among the 45 sites in dogs with late infarcts as measured by respective coefficients of variance (p = .007 and less than .001). With programmed stimulation six dogs in the late and eight in the early infarct group exhibited inducible sustained ventricular tachycardia. Mean cycle length of the tachycardia in dogs with late infarcts was significantly shorter (p = .035). Late potentials were notably less prominent in dogs in the late infarct group with ventricular tachycardia than in dogs in the early infarct group. Fewer abnormal electrophysiologic characteristics of late infarcts coincided with relatively less scar in the underlying myocardium. Moreover, the strength of electrophysiologic-anatomic correlations differed in late as opposed to early infarcts. The latter findings suggest long-term evolution of infarct anatomy. We conclude that a substrate for reentrant tachycardia is present in dogs 4 to 6 years after reperfused infarction. Conduction characteristics are less abnormal in these late healed infarcts and are associated with a shorter ventricular tachycardia cycle length and less pronounced late potentials on the body surface.     

Myocardial infarction and sudden death after sport: acute coronary angiographic findings

Thirteen patients, seven with acute myocardial infarction and six survivors of sudden death after sport, underwent coronary angiography within a mean of 104 min after the onset of symptoms. The admission electrocardiogram showed transmural myocardial ischemia in all patients. The ischemia-related vessel was occluded in all cases of sudden death and in three cases of acute myocardial infarction. Reperfusion was achieved in eight vessels: after intracoronary streptokinase in three, after intracoronary nitroglycerin in three, and mechanically in two. Coronary spasm was demonstrated in three vessels, and coronary thrombi, in four. The coronary lesion was described as either concentric in two or eccentric with irregular borders in eight. There was a high incidence of eccentric lesions consistent with ruptured plaques. The acute coronary angiographic findings of acute myocardial infarction and sudden death after sport are similar. Physical exercise can provoke myocardial infarction and sudden death probably by inducing plaque rupture that can evoke coronary spasm, thrombosis, or both.     

What is the best predictor of spontaneous ventricular tachycardia and sudden death after myocardial infarction?

BACKGROUND. Death during the first year after myocardial infarction is most commonly due to spontaneous ventricular tachycardia (VT) or fibrillation (VF). The purpose of this study was to compare, in a single cohort of patients, the values of inducible VT, delayed ventricular activation, low left ventricular ejection fraction, high-grade ventricular ectopy, and ST segment displacement on exercise in predicting electrical events (witnessed instantaneous death and spontaneous VT or VF) during the first year after myocardial infarction. METHODS AND RESULTS. Three hundred sixty one patients aged less than 71 years underwent electrophysiological study, signal-averaged electrocardiogram, gated blood-pool scan, 24 hour ambulatory electrocardiographic monitoring, and exercise testing 1-2 weeks after myocardial infarction and were then followed up for at least 1 year. There were 34 deaths (eight witnessed instantaneous, 26 other), and nine patients survived one or more episodes of spontaneous VF or VT. Patients with inducible VT were 15.2 times more likely to suffer electrical events than patients without inducible VT. No proportional-hazards model excluding inducible VT was as good a predictor of electrical events as was inducible VT alone. CONCLUSIONS. Inducible VT at electrophysiological study was the single best predictor of spontaneous VT and sudden death after myocardial infarction.     

Results of signal-averaged electrocardiography and electrophysiologic study in patients with nonsustained ventricular tachycardia after healing of acute myocardial infarction

Programmed stimulation and signal-averaged electrocardiography were performed in 43 consecutive patients with nonsustained ventricular tachycardia (VT) after healing of inferior (29 patients) or anterior wall (14 patients) acute myocardial infarction. Twenty-two patients had inducible sustained VT. Patients with inferior infarction and inducible sustained VT had significantly longer filtered QRS durations (125 +/- 19 vs 112 +/- 15 ms, p less than 0.01) and significantly lower voltage in the last 40 ms of the filtered QRS complex (19 +/- 5 vs 30 +/- 14 microV, p less than 0.05) than those without inducible sustained VT. In contrast, the signal-averaged electrocardiographic measurements in patients with anterior infarction and inducible sustained VT did not differ significantly from those without inducible sustained VT. The results of these studies were compared with those of 2 control groups: 45 patients without ventricular arrhythmias after myocardial infarction and 95 patients with spontaneous and inducible sustained VT after myocardial infarction. The signal-averaged electrocardiographic measurements in patients with spontaneous nonsustained VT after inferior infarction were intermediate between the control group without arrhythmias and the control group with sustained VT. The signal-averaged electrocardiograms in patients with nonsustained VT after anterior infarction were not significantly different from those in patients without ventricular arrhythmias. The study shows that the site of infarction influences the signal-averaged electrocardiogram in patients with VT after myocardial infarction. The signal-averaged electrocardiogram may be useful in identifying patients with nonsustained VT after a remote inferior myocardial infarction who have inducible sustained VT.     

Clinical and electrophysiologic findings in patients with repetitive monomorphic ventricular tachycardia and otherwise normal electrocardiogram

Natural history, structural substrate, electrocardiographic and electrophysiologic characteristics and therapy were evaluated in 18 patients who demonstrated repetitive ventricular tachycardia, defined as repeated episodes of ventricular tachycardia that had a uniform QRS configuration and normal sinus-conducted QRS complexes between the episodes of tachycardia. The patients were young (mean age 37 years) and frequently had a long history of arrhythmia before this evaluation; only two patients had a history of syncope and six were completely asymptomatic. Fourteen patients had no evidence of underlying structural heart disease, three had mitral valve prolapse and one had congestive cardiomyopathy. Episodes of ventricular tachycardia tended to occur in clusters over a 24 hour electrocardiographic recording period.Repetitive ventricular tachycardia was induced in two of nine patients by programmed electrical stimulation, and in seven patients incremental atrial and ventricular pacing suppressed spontaneous arrhythmia. In the one patient whose tachycardia was induced by incremental ventricular pacing there was an inverse relation between pacing cycle length and the interval from the last paced complex to the first complex of ventricular tachycardia, indicating there was overdrive suppression.At a follow-up time of 0.5 to 8 years no patient had died or had worsening of symptoms. Encainide completely eliminated episodes of ventricular tachycardia during acute treatment in five of six patients tested. Seven patients received no antiarrhythmic therapy and the arrhythmia appeared to have spontaneously resolved in four of these patients. Repetitive ventricular tachycardia appears to have distinct clinical and electrophysiologic characteristics. In this series the arrhythmia had a good prognosis and often required no treatment. The electrophysiologic features are consistent with a mechanism of automaticity.     

Amiloride. Antiarrhythmic and electrophysiologic actions in patients with inducible sustained ventricular tachycardia

This study assessed the antiarrhythmic activity of amiloride in 35 patients with inducible sustained ventricular tachycardia. Patients had failed to respond to 3.6 +/- 1.0 antiarrhythmic drugs. Ventricular tachycardia was reproducibly induced by programmed electrical stimulation in all patients at the baseline study. Amiloride was given at 10 and 20 mg/day p.o. on a twice-daily schedule that achieved serum concentrations of 21 +/- 17 and 36 +/- 18 ng/ml, respectively. The mean left ventricular ejection fraction was unchanged from 36 +/- 14% at baseline to 37 +/- 17% during amiloride treatment. Amiloride significantly increased serum potassium from 4.6 +/- 0.4 to 5.1 +/- 0.4 mM. Four patients failed amiloride therapy with spontaneous nonsustained ventricular tachycardia. The remaining 31 patients were assessed by repeat programmed stimulation. Six patients had complete antiarrhythmic response, and an additional six patients had less than 15 beats of ventricular tachycardia induced. Therefore, amiloride was an efficacious antiarrhythmic treatment in 12 of 35 (34%) patients. Amiloride concentrations were significantly higher (52 +/- 20 ng/ml) in patients that responded than in patients that did not respond (30 +/- 15 ng/ml). The only electrophysiologic measurement that changed significantly was the ventricular functional refractory period (from 269 +/- 24 to 283 +/- 25 msec, p less than 0.05). Amiloride also suppressed frequent, spontaneous ventricular premature beats in eight of 15 patients (53%). No somatic side effects occurred. Two of the five patients discharged on amiloride therapy developed asymptomatic nonsustained ventricular tachycardia, and this prompted a change in antiarrhythmic therapy. Both died suddenly of arrhythmia during substitute empiric antiarrhythmic drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Correlation between the signal-averaged electrocardiogram and electrophysiologic study findings in patients with coronary artery disease and sustained ventricular tachycardia

Ventricular late potentials at the end of the surface QRS, detected on the signal-averaged electrocardiogram (SAECG) have been shown to be markers for spontaneous and/or inducible ventricular tachycardia (VT) in patients with coronary artery disease (CAD). We examined the correlations between electrophysiologic study (EPS) findings and SAECG indexes in 50 patients with chronic CAD with documented spontaneous VT/ventricular fibrillation (VF), who had either syncope (24 patients) or aborted sudden cardiac death (SCD). The prevalence of late potentials was significantly higher in the syncope patients (75%) compared with the SCD group (46%) (p less than 0.05). No correlation was found between the ventricular refractoriness and the SAECG indexes. There was a significant difference in quantitative SAECG indexes comparing the induction mode of the sustained VT/VF by single and double versus triple extrastimuli; the types of the induced VT (sustained monomorphic, sustained pleomorphic or VF, noninducible); and the cycle length of the induced sustained monomorphic VT with the high frequency QRS duration (QRSD). In conclusion, differences in prevalence and characteristics of ventricular late potentials were found between patients with syncope and with SCD. The degree of abnormality of SAECG indexes correlated with the type and the mode of induction of sustained VT. The magnitude of QRSD of the SAECG correlated with the cycle length of monomorphic VT. The above findings suggest that in patients with CAD and sustained VT/VF the SAECG variables are related to the area of reentry.     

Noise in the signal-averaged electrocardiogram and accuracy for identification of patients with sustained monomorphic ventricular tachycardia after myocardial infarction

Late potentials are detected at various noise levels in clinicalstudies. The aim of this study was, in a case-control design,to assess the effect of residual noise level on the identificationof patients with sustained monomorphic ventncular tachycardiaafter myocardial infarction. Electrocardiograms from 16 patientswith prior myocardial infarction and documented sustained monomorphicventricular tachycardia and 41 patients with prior myocardialinfarction and without ventncular tachycardia, were analysedby two signal averaging procedures to noise level 0·2and 0·4 µV Standard time domain parameters weremeasured. Two definitions of late potential were analysed: (1)if any two of the following criteria were present (signal-averagedQRS duration >120 ms, late potential duration >40 ms,and root-mean-square voltage of the terminal 40 ms of the filteredQRS <25µV); or (2) if the signal-averaged QRS duration120 ms. Overall the signal-averaged electrocardiogram performedbetter at noise level 0·4µV compared to noise level0·2µV with respect to identification of patientswith or without ventricular tachycardia after myocordial infarction.Reducing noise level from 0·4 to 0·2 µVincreased the sensitivity, but the consequence was a substantialdecrease in specificity. Our data indicate that when a highsensitivity is the goal, the definition based only on signal-averagedQRS duration 120 ms should be applied; sensitivity was 88% andspecificity 59% at noise level 0·4 µV. If a highspecificity is the goal, the definition should be based on thedefinition with two abnormal parameters; sensitivity was 69%and specificity 68% at noise level 0·4µV.     

Incidence and timing of recurrences of sudden death and ventricular tachycardia during antiarrhythmic drug treatment after myocardial infarction.

Incidence and timing of recurrences of sustained ventricular tachycardia (VT) or sudden death were studied in 206 patients who survived their first episode of ventricular fibrillation (VF; n = 52) or sustained VT (n = 154) after myocardial infarction. All patients were treated with (empirically selected) antiarrhythmic drugs; 49% received amiodarone. After a mean follow-up of 36 months, 64 patients (41%) in the VT group and 10 (19%) in the VF group had nonfatal VT recurrences. Sudden death occurred in 22 (14%) and 9 (17%) patients in the VT and VF groups, respectively. Incidence of sudden death had 2 peaks at approximately 3 and 12 months. Nonfatal VT recurrences were more frequent (most often occurring in first 6 months) in the VT than in the VF group. Sudden death occurred during the following 3 years in only 10% of patients who survived 1 year. There was a much higher incidence of sudden death in patients with left ventricular ejection fraction (LVEF) less than or equal to 40% than in those with LVEF greater than 40% (28 of 65 vs 3 of 141; p less than 0.0001), but no relation between LVEF and nonfatal VT recurrences.     

Early ventricular fibrillation in patients with acute myocardial infarction: correlation with coronary angiographic findings

To define coronary angiographic characteristics of patientsexperiencing early primary ventricular fibrillation (VF) inthe acute phase of myocardial infarction we studied 266 consecutivepatients without clinical evidence of heart failure. Twenty-sixpatients (group 1) experienced early (< 12 h from the onsetof symptoms of myocardial infarction) primary VF whereas 240patients (group 2) with the same clinical characteristics servedas an appropriately matched cohort. All patients were catheterizedbefore or soon after hospital discharge (1 to 8 weeks afterthe acute event). There was no significant difference in left ventricular ejectionfraction between the two groups of patients (39.6±6%vs 36.9±8%, P = ns). Patients with early VF had a significantlygreater number of diseased vessels than those without VF (3.38±1.05vs 2.03±1.25. P <0.001) and a higher coronary arteriographicGensini score (29.31±4.80 vs 20.16±4.14, P <0.001).The left anterior descending coronary artery was identifiedas the infarct-related vessel in 53.6% of group 1 vs 44.5% ofgroup 2 patients (P <0.05). The mean maximal serum creatinekinase values were not significantly different (1897±1062vs 1426 ±839 IU.l–1, P=ns) between the two groups. These data indicate that patients with early primary VF in thesetting of acute myocardial infarction may have more extensivecoronary artery disease than similar patients without VF. Aworse prognosis could be anticipated for these patients on thebasis of worse coronary anatomy. A more aggressive therapeuticapproach with routine coronary angiography before hospital dischargecould reasonably be justified for patients with early primaryVF complicating acute myocardial infarction.     

Flecainide: steady state electrophysiologic effects in patients with remote myocardial infarction and inducible sustained ventricular arrhythmia

The effect of flecainide in 24 patients with inducible sustained ventricular arrhythmia and a history of remote myocardial infarction was determined. Flecainide was administered in oral doses individually adjusted to suppress all spontaneous ventricular tachycardia and 80% of ventricular premature complexes on 24 hour ambulatory (Holter) electrocardiography. Antiarrhythmic therapy, as assessed by Holter monitoring, was adequate in 20 (83%) of the study patients at a mean dose of 144 +/- 28 mg every 12 hours; the mean plasma flecainide level was 583 +/- 329 ng/ml. In 18 patients, the mean sinus cycle length, sinus node recovery time and atrial, atrioventricular nodal and ventricular refractory periods were unchanged. The AH interval increased by 15 +/- 15%, the HV interval by 35 +/- 32% and the QRS duration by 24 +/- 21%. Toxicity or failure to suppress ventricular premature complexes and ventricular tachycardia by Holter monitoring precluded electrophysiologic study with flecainide in four patients; two patients refused electrophysiologic study with flecainide for nonmedical reasons. Ventricular tachycardia was not inducible in 4 (22%) of 18 patients receiving flecainide. Sustained arrhythmia remained inducible in 14 patients (78%) despite evidence of antiarrhythmic efficacy on Holter monitoring, but the rate of the induced ventricular tachycardia was slower and symptoms were alleviated during ventricular tachycardia in 10 (56%) of 18 patients. The 4 patients who had no inducible ventricular tachycardia with flecainide, and the 10 patients who had inducible ventricular tachycardia with a longer cycle length and alleviation of their symptoms, have been followed up as outpatients for 16 +/- 7 months.(ABSTRACT TRUNCATED AT 250 WORDS)     

急性心肌梗死非持续和持续室性心动过速的Q—T离散度

为研究急眭心肌梗死伴持续和非持续室性心动过速患者间Q-T离散度和其它心电图参数之间的关系。比较14例急性心肌梗死伴持续室性心动过速和26例伴非持续室性心动过速患者的心室Q-T离散度、Q-T和Q-T_c间期。结果显示持续和非持续室性心动过速患者之间的Q-T离散度以及相邻胸导联Q-T离散度差异有显著意义(110.1±7.80对80.8±4.4,105.9±6.9对67.6±4.0,P<0.01)。我们认为相邻导联Q-T离散度增大极易出现室性心动过速,Q-T离散度大于110ms有发生持续室性心动过速的危险。而Q-T离散度在80—110ms之间有非持续室性心动过速的可能性。     

Prediction of sudden death by electrophysiologic studies in high risk patients surviving acute myocardial infarction

Seventy patients surviving a myocardial infarction complicated by heart failure or arrhythmias, or both, were studied 7 to 20 days after the infarction. Twenty-four hour electrocardiographic ambulatory monitoring and intracardiac electrophysiologic studies were performed in each patient. Electrophysiologic studies included introduction of single right ventricular premature stimuli during sinus rhythm (70 patients), atrial pacing (35 patients) and ventricular pacing (70 patients) at a stimulating voltage of 2 V, with the use of higher stimulating voltages (up to 10 V), and double right ventricular premature stimuli in 33 patients and pacing at a second right ventricular site in 50 patients. A repetitive response was defined as two or more spontaneous ventricular depolarizations in response to the premature stimuli, with His bundle reentry and aberrant conduction of supraventricular impulses excluded by a His bundle recording. Repetitive responses were initiated in 20 patients, and 12 patients had responses that were either sustained ventricular tachycardia or self-terminating ventricular tachycardia of more than five complexes in duration. The finding of a repetitive response was not related to the occurrence of complex ventricular arrhythmias during ambulatory monitoring or in the coronary care unit.Five of the 12 patients with sustained or self-terminating responses of more than five complexes died during the 12 month follow-up period, 4 suddenly, and these responses were significantly associated with late sudden death (p < 0.05), because only 1 of 25 patients with responses of fewer than five complexes or no response to maximal provocation died suddenly. It is concluded that induced responses of more than five complexes in duration may be an important indicator of a potentially reversible risk of sudden death after myocardial infarction.     

Subendocardial resection for sustained ventricular tachycardia in the early period after acute myocardial infarction

One hundred nineteen patients with drug-refractory ventricular tachycardia (VT) underwent mapping-guided subendocardial resection for control of their arrhythmias from 3 weeks to 10 years after acute myocardial infarction (AMI). Patients were separated into 2 groups: those treated early (within 4 months, group I) and those treated later (after 1 year, group II) after AMI. There were 32 patients in group I and 72 patients in group II. Both groups of patients had similar clinical, angiographic and hemodynamic characteristics. Patients in group I had VT with a shorter mean cycle length than patients in group II (322 +/- 71 vs 349 +/- 88 ms, p less than 0.05). The groups did not differ with respect to operative mortality (12% vs 7%), late mortality (31% vs 33%, mean follow-up 23 months), or frequency with which subendocardial resection without any adjunctive therapy prevented postoperative spontaneous or inducible VT (21% vs 34%). Group I was further separated into patients who underwent subendocardial resection within 1 month of AMI (n = 7) and those who underwent subendocardial resection with 2 months of AMI (n = 14). Although patients in group I were characterized by having more spontaneous morphologically distinct tachycardias, their operative mortality, total mortality and surgical success rates were comparable to those of patients in group II.(ABSTRACT TRUNCATED AT 250 WORDS)