Frequency and significance of induced sustained ventricular tachycardia or fibrillation two weeks after acute myocardial infarction

Electrophysiologic study, 24-hour ambulatory electrocardiographic monitoring, treadmill exercise test and angiographic evaluations were performed in 45 patients 14 +/- 3 days (mean +/- standard deviation) after acute myocardial infarction. Electrophysiologic study protocol included burst ventricular pacing and 1 to 3 ventricular extrastimuli at 2 cycle lengths from right ventricular apex, right ventricular outflow and left ventricle. Sustained monomorphic ventricular tachycardia (VT) (13 patients) or ventricular fibrillation (VF) (7 patients) was induced in 20 patients (44%) (group I). In these 20 patients, VT/VF was inducible with 2 extrastimuli in 10 patients, 3 extrastimuli in 9 patients and burst pacing in 1 patient. In the remaining 25 patients (56%), induction of no fewer than 7 ventricular beats were noted (group II). Severe left ventricular (LV) wall motion abnormalities occurred in 70% of group I patients and 22% of group II patients (p less than 0.005). There was no difference in the site of infarction, frequency and grade of ventricular ectopic rhythm on ambulatory electrocardiographic monitoring, double product on submaximal exercise, LV ejection fraction, and number of obstructed coronary arteries (70% or greater) (p greater than 0.1) between group I and group II patients. During a mean follow-up of 10 +/- 3 months, 1 patient in each group died suddenly, and in 1 group I patient spontaneous sustained VT developed which was identical in morphologic configuration to that induced during electrophysiologic study. In conclusion, electrical induction of sustained VT or VF during electrophysiologic study is common in patients 2 weeks after acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

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)     

Polymorphous ventricular tachycardia in acute myocardial infarction

Polymorphous ventricular tachycardia (VT) is thought to be uncommon in acute coronary heart disease, but its prevalence has not been determined. Seven hundred seventy-one consecutive patients admitted with acute myocardial infarction (MI) were reviewed for the occurrence of this arrhythmia. Nine patients (1.2%) had polymorphous VT. No patient had any of the predisposing factors previously associated with polymorphous VT. The arrhythmia was resistant to multiple drugs, and repeated cardioversion was effective in only 3 patients. Overdrive pacing was ineffective in the 3 patients in whom it was attempted. Verapamil was effective in 3 of 4 patients in whom it was tried. Six patients with polymorphous VT died during hospitalization; the remaining 3 died within 6 months of discharge. It is concluded that, when compared with regular VT, polymorphous VT in MI carries a poor prognosis. When the arrhythmia occurs in the context of acute ischemia, it appears to be more difficult to treat compared with its occurrence due to other predisposing factors. Verapamil, not usually indicated for ventricular arrhythmias, should be tested in a therapeutic trial.     

Early sustained ventricular arrhythmias complicating acute myocardial infarction

Objective

Sustained ventricular arrhythmias complicate 2% to 20% of acute myocardial infarctions (MIs) and are associated with increased in-hospital mortality. However, it remains unclear whether successful mechanical revascularization improves outcomes in these patients. The objective of this analysis was to identify predictors of sustained ventricular arrhythmias after acute MI and to determine the influence of successful revascularization on in-hospital mortality.

Methods

We conducted a retrospective cohort study of all patients who underwent percutaneous coronary intervention for acute MI in New York State between 1997 and 1999.

Results

Of the 9015 patients who underwent percutaneous coronary intervention for acute MI, 472 (5.2%) developed sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) before revascularization. After multivariable adjustment, independent predictors of sustained VT/VF included cardiogenic shock (odds ratio [OR], 4.10; 95% confidence interval [CI], 3.20-5.58; P <.001), heart failure (OR, 2.86; 95% CI, 2.24-3.67: P <.001), chronic kidney disease (OR, 2.58; 95% CI, 1.27-5.23; P = .009), and presentation within 6 hours of symptom onset (OR, 1.46; 95% CI, 1.18-1.81; P = .001). Patients with sustained VT/VF had greater in-hospital mortality (16.3% vs 3.7%, P <.001). Although successful percutaneous coronary intervention was associated with decreased in-hospital mortality in patients with VT/VF (P <.001), patients with sustained VT/VF and successful revascularization experienced increased mortality compared with patients without sustained ventricular arrhythmias (P <.001).

Conclusion

Among patients undergoing percutaneous coronary intervention for acute MI, sustained VT/VF remains a significant complication associated with a 4-fold increased risk of in-hospital mortality. Early mortality is reduced after successful percutaneous coronary intervention, but remains elevated in this high-risk group.     

Polymorphous ventricular tachycardia associated with acute myocardial infarction

BACKGROUND. During a 2.9-year period, 11 patients developed polymorphous ventricular tachycardia 1-13 days after acute anterior (seven patients) or inferior (four patients) myocardial infarction. None of the 11 patients had sinus bradycardia (mean heart rate, 90 +/- 23 beats/min), but three had a sinus pause immediately before the onset of polymorphous ventricular tachycardia. In all 11 patients, the QT interval and corrected QT interval (QTc) were normal or minimally prolonged (QT, 385 +/- 34 msec; QTc, 442 +/- 40 msec). None had significant hypokalemia (mean serum potassium concentration, 4.3 +/- 0.5 meq/l) or a grossly abnormal serum magnesium or calcium concentration (2.1 +/- 0.4 and 8.9 +/- 0.7 mg/dl, respectively). METHODS AND RESULTS. Immediately before the onset of polymorphous ventricular tachycardia, symptoms and/or electrocardiographic changes consistent with recurrent myocardial ischemia occurred in nine of 11 patients. One patient died before drug therapy could be initiated. Lidocaine was used in 10 patients and proved to be effective in only one. Intravenous procainamide was used in six patients: one improved, and five had recurrence of polymorphous ventricular tachycardia. Bretylium was used in five patients and was ineffective in all cases. Overdrive pacing was used in four patients and failed to suppress recurrent arrhythmias in all cases. Four patients with persistent polymorphous ventricular tachycardia unresponsive to lidocaine, procainamide, or bretylium responded to intravenous amiodarone. One patient with polymorphous ventricular tachycardia that was consistently preceded by ST segment elevation responded to intravenous nitroglycerin. Two patients with persistent polymorphous ventricular tachycardia and obvious recurrent ischemia unresponsive to pharmacological intervention responded to emergency coronary revascularization. A third patient who experienced recurrent angina and polymorphous tachycardia was initially stabilized with pharmacological therapy but subsequently underwent elective revascularization and has remained stable without antiarrhythmic therapy. CONCLUSIONS. Post-myocardial infarction polymorphous ventricular tachycardia is not consistently related to an abnormally long QT interval, sinus bradycardia, preceding sinus pauses, or electrolyte abnormalities. This arrhythmia has a variable response to class I antiarrhythmics but may be suppressed by intravenous amiodarone therapy. It is often associated with signs or symptoms of recurrent myocardial ischemia. Furthermore, coronary revascularization appears to be effective in preventing the recurrence of polymorphous ventricular tachycardia when associated with recurrent postinfarction angina.     

Identification of patients at high risk for recurrence of sustained ventricular tachycardia after healing of acute myocardial infarction.

A prognostic index for nonfatal recurrences of ventricular tachycardia (VT) was developed using a retrospective analysis of a group of 206 patients with sustained monomorphic VT or ventricular fibrillation (VF) after healing of acute myocardial infarction. 74 patients (36%) (64 with VT and 10 with VF) had recurrences of sustained monomorphic VT during 3.4 +/- 9 years of follow-up. Three clinical variables were selected and weighted by stepwise logistic discriminant analysis of the study group. They were coded as follows: interval of myocardial infarction to arrhythmia (less than 2 months = 1; 2 to 6 months = 2; greater than 6 months = 3), drug therapy with or without sotalol (with = 1, without = 2), and VT or VF as the presenting arrhythmia (VT = 1, VF = 2). The prognostic index was: 3.41 - (0.56 x interval) - (1.94 x therapy) + (0.86 x arrhythmia). This index was validated prospectively in a test group of 158 consecutive patients with VT or VF after healing of acute myocardial infarction. Patients were allocated into different classes with decreasing prognostic index values associated with increasing risk for recurrences of VT. In the test group, 27 of 158 (17%) patients (22 with VT and 5 with VF) had recurrences of VT (follow-up of 2 +/- 2 years). Two risk classes of patients were identified: high risk for recurrences of VT (61%) corresponding to patients with a negative index; and low risk (4%) consisting of those with a positive index. Thus, using O as the cutoff point, the sensitivity, specificity, and positive and negative predictive values were 81, 89, 62 and 96%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of end points of serial drug testing in patients with sustained ventricular tachycardia after healing of acute myocardial infarction

Serial electrophysiologic drug testing was used to guide antiarrhythmic therapy in a consecutive series of 150 patients with clinical sustained ventricular tachycardia (VT) or cardiac arrest and inducible monomorphic VT. All patients had coronary artery disease and a history of myocardial infarction. For patients with clinical sustained VT, drug responders and partial drug responders (VT slowed by drug to rate <150 beats/min, with systolic blood pressure ≥90 mm Hg) had similar total mortality rates (2-year actuarial survival 100% and 94%, P = NS), which were statistically different from that or patients with drug inefficacy (2-year survival 67%). Partial drug responders had high arrhythmia recurrence rates, similar to those of patients with drug inefficacy. For cardiac arrest survivors, the results of electrophysiologically guided drug testing did not predict prognosis. Patients with a change in mode or VT induction during antiarrhythmic therapy had a favorable prognosis (no deaths during follow-up).     

心肌梗塞后室性心动过速的微波消融

目的　比较射频消融与微波消融对心肌梗塞后室性心动过速 (室速 )的疗效。　方法　 2 7只健康成年犬 ,开胸。用 Harris二期阻闭加再灌注法造成心肌梗塞模型 ,用程序电刺激或毒毛旋花子甙 K(毒K)诱发持续性室速。将能诱发出持续性室速存活的 2 0只犬随机分成 2组 : 组为射频消融组 , 组为微波消融组 ,每组各 1 0只。射频消融组与微波消融组能量与放电时间均为 4 0× 1 2 0 Ws。　结果　射频消融组中被诱发出的 4 0次 (2 3次为程序电刺激诱发 ,1 7次为毒 K诱发 )持续性室速中 ,有 1 6次 (1 5次为毒 K诱发 ,1次为程序电刺激诱发 )被射频消融终止 ,分属 4只犬 ,在 3只犬术后未能再诱发出室速 ,成功率 3 0 %。微波消融组诱发出 2 8次 (1 7次为程序电刺激诱发 ,1 1次为毒 K诱发 )持续性室速 ,2 8次均被微波消融终止 ,1 0只犬术后未能再诱发出室速 ,成功率 1 0 0 %。　结论　微波消融比射频消融对心肌梗塞后室速可能具有更好的疗效。     

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。     

Correlation between inducibility of sustained ventricular tachycardia and QRS duration

Some studies provide a link between the width of QRS complexesand late potentials occurring at the end of the QRS complexin signal-averaged recordings. The purpose of this study wasto compare three methods of QRS duration measurement: the conventional12 lead ECG. the Frank vectorcardiogram (VCG) and the signal-averagedelectrocardiogram. The recordings were made at a similar timein 121 consecutive patients with the Cardionics PC-based system(ECG and VCG) and the ardionics high resolution ECG, based onmethods described by Simson. Patients with bundle branch blockwere excluded. All patients had presented a myocardial infarctionand were studied either for spontaneous ventricular arrhythmiasor systematically 3 to 6 weeks after an acute myocardial infarction. The signal-averaged ECG and VCG QRS durations were similar in41 patients without inducible ventricular arrhythmias and withnormal signal-averaged ECG but were longer (P<0·001)than the conventional ECG QRS duration. In 36 patients withspontaneous and inducible ventricular tachyarrhythmias, theQRS duration was significantly longer on signal-averaged ECGthan on VCG (P<0·05) and longer on VCG than on conventionalECG (P<0·05). The QRS duration was also significantly(P<0·001) longer with the three techniques in patientswith spontaneous ventricular tachycardia (VT) than in patientswithout spontaneous and inducible VT. A QRS duration on VCG 110 ms and on conventional ECG 100 ms had a sensitivity of93% and 77% and a specificity of 83% and 85% respectively forpredicting an abnormal signal-averaged ECG. In conclusion, the measurement of QRS duration with the conventionalECG, VCG or the signal-averaged ECG could be a simple methodto detect the patients with myocardial infarction prone to VT.     

Prognostic features of ventricular tachycardia complicating acute myocardial infarction

Prognostic features of 115 patients with ventricular tachycardia complicating acute myocardial infarction were analyzed. Age, sex, infarct location and peak CPK levels were not significantly different when comparing survivors (S) and non-survivors (NS). Highly significant clinical characteristics of NS compared to S were: heart rate, presence of cardiogenic shock and a poor response to lidocaine therapy (P<0.0001, 0.0003 and 0.001 respectively). Electrocardiographic features distinguishing S and NS were: coupling intervals (S=522.9, NS=389.9, P<0.004), prematurity index (S=1.36, NS=1.04, P<0.001), ventricular tachycardia rate (S=132, NS=174, P<0.0013) and number of episodes of ventricular tachycardia (S=4.04, NS=6.75, P<0.0058). These findings have importance for the evaluation of newer active and prophylactic therapies.     

Return to full normal activities including work at two weeks after acute myocardial infarction

Patients are generally advised to return to full normal activities, including work, 6 to 8 weeks after acute myocardial infarction (AMI). We assessed the outcomes of early return to normal activities, including work at 2 weeks, after AMI in patients who were stratified to be at a low risk for future cardiac events. Patients were considered for randomization before discharge if they had no angina, had left ventricular ejection fraction >40%, a negative result from a symptom-limited exercise stress test for ischemia (<2 mm ST depression) at 1 week, and achieved >7 METs. Patients with left ventricular ejection fraction <40% were included only if they did not have inducible ventricular tachycardia at electrophysiologic studies. Seventy-two patients were randomized to return to normal activities at 2 weeks and 70 patients to undergo standard cardiac rehabilitation and return to normal activities at 6 weeks after AMI. There were no deaths or heart failure in either group. There was no significant difference in the incidence of reinfarction, revascularization, left ventricular function, lipids, body mass index, smoking, or exercise test results at 6 months. In conclusion, return to full normal activities, including work at 2 weeks, after AMI appears to be safe in patients who are stratified to a low-risk group. This should have significant medical and socioeconomic implications.     

Late fields of the magnetocardiographic QRS complex as indicators of propensity to sustained ventricular tachycardia after myocardial infarction

INTRODUCTION: Magnetocardiographic (MCG) mapping is a new method to record cardiac signals. This study examined the association of MCG late fields with the propensity to sustained ventricular tachycardia (VT) after myocardial infarction (MI). METHODS AND RESULTS: One hundred patients with remote MI were studied, 38 with and 62 without history of VT. High-resolution MCG and signal-averaged ECG (SAECG) as a comparative method were recorded. Time-domain parameters describing the abnormal low-amplitude end QRS activity, MCG late fields, and SAECG late potentials were analyzed. Late field parameters differed significantly between the patient groups: filtered QRS duration was 137 +/- 26 msec in the VT group and 110 +/- 18 msec in the control group (P < 0.001), and root mean square amplitude of the last 40 msec was 260 +/- 170 and 510 +/- 360 fT (P < 0.001), respectively. The optimal MCG parameter combination yielded a sensitivity of 92% and a specificity of 61% in classification to the VT group, whereas those for SAECG were 63% and 66%. In a subgroup of 63 patients with marked left ventricular dysfunction and comparable stage of coronary heart disease, only MCG (sensitivity 73%, specificity 67%) but not SAECG could assign a patient to the VT group. CONCLUSION: Late fields of the MCG QRS complex indicate propensity to life-threatening arrhythmias in post-MI patients. This discriminative ability persists in the presence of severe left ventricular dysfunction where ECG late potentials lose their informative value. MCG late field analysis is a potential new method for noninvasive risk assessment in post-MI patients.     

Predictors of sustained ventricular tachycardia inducibility in patients with nonsustained ventricular tachycardia and chronic coronary artery disease

To assess the likelihood of inducing sustained ventricular tachycardia, we analyzed a cohort of 58 retrospective and 18 prospective patients with chronic coronary artery disease who underwent electrophysiologic study because of spontaneous nonsustained ventricular tachycardia (three or more beats, lasting less than 30 seconds, at a rate greater than 100/min). In 24 of the 58 retrospective patients (41%) sustained ventricular tachycardia was inducible. Stepwise logistic regression identified two "major" variables--left ventricular aneurysm/dyskinesis/akinesis (p = 0.0001; relative risk = 11.88) and ejection fraction less than 40% (p = 0.0002; relative risk = 9.69)--and one "minor" variable--nonsustained ventricular tachycardia longer than 10 beats (p = 0.0151; relative risk = 4.21)--as significant predictors of inducibility. Nineteen patients with both major variables had a high probability of inducibility (greater than 90%). Nineteen patients with neither major variable had a low probability of inducibility (less than 5%). The remaining 20 patients with only one of the major variables had an intermediate probability of inducibility (14% to 75%). The significance of the third minor factor, nonsustained ventricular tachycardia longer than 10 beats, was confined to this intermediate group, in which it could be used to segregate relatively high (65% to 75%) and relatively low (14% to 20%) probability of inducibility. Prospective application of the predictor function stratified 18 additional patients into three groups with high (six patients), intermediate (seven patients), and low (five patients) probability of inducibility. The observed rate of inducibility in each group was 5 of 6 (83%), 2 of 7 (29%), and 0 of 5 (0%), respectively. These data suggest that patients with nonsustained ventricular tachycardia and chronic coronary artery disease can be stratified into subgroups with high, intermediate, and low probability of inducibility of sustained ventricular tachycardia on the basis of ejection fraction and regional ventricular wall motion defects alone.     

Frequency and significance of occult late potentials on the signal-averaged electrocardiogram in sustained ventricular tachycardia after healing of acute myocardial infarction

The quantitative and morphologic characteristics and significance of late potentials on the signal-averaged electrocardiographic QRS complex remain unknown. To assess this, the signal-averaged electrocardiogram of 48 patients (mean age +/- standard deviation 62 +/- 9 years) with sustained ventricular tachycardia (VT) after healing of acute myocardial infarction and late potentials were analyzed. Late potentials could be classified into 3 morphologic subtypes: type I late potentials (19 patients, 40%) occurred in the terminal 40 ms of the QRS complex; type II late potentials (16 patients, 33%) started before the end of the QRS complex and extended 30 +/- 17 ms into the ST segment; type III late potentials (13 patients, 27%) started after the end of the QRS complex in the ST segment and ended 67 +/- 27 ms after the end of the QRS complex. The amplitude of the late potentials in type III, when compared with types I and II, was significantly lower, whereas the QRS duration on the electrocardiogram in type I, when compared with types II and III, was significantly longer. Computer algorithm based on noise failed to identify most type III late potentials. No difference was noted in age, sex, site of the myocardial infarction, and rate of induced VT among the 3 types.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relation between the transmural extent of acute myocardial infarction and associated myocardial contractility two weeks after infarction

To characterize the relation between the transmural extent of acute myocardial infarction (AMI) and associated regional contractility after recovery from ischemia, 11 mongrel dogs underwent occlusion of the proximal left anterior descending coronary artery and were evaluated 2 weeks after infarction. Occlusion was permanent in 5 dogs, and reperfusion was allowed after 2 hours of occlusion in 6 dogs. All dogs had computer-assisted quantitative wall-thickening analysis by 2-dimensional echocardiography and infarct localization by the triphenyl-tetrazolium chloride technique. Percent systolic wall thickening was correlated with the transmural extent of AMI in 40 regions of interest, each measuring approximately 60 arc degrees in circumference. In 11 non-infarct-containing regions, the mean wall thickening was 59 +/- 16% (+/- standard deviation). In 29 infarct-containing segments (with transmural extent of infarction 11 to 100%) systolic wall thickening ranged from -4% to 47%. Wall thickening and transmural extent of AMI were inversely related. Least-squares regression analysis found the relation to be best described by the logarithmic function, percent wall thickening = 61 - 26 log (percent transmural extent of infarction +1), r = -0.87. The nature of this relation between structure and function suggests that salvage of small amounts of myocardium (transmural extent less than 30 to 40%) by coronary reperfusion or other means may have little effect on systolic myocardial function when compared with the function of transmural infarcts. Alternatively, salvage of more than 40% of the jeopardized myocardium should be expected to appreciably augment myocardial function.