Association of accelerated idioventricular rhythm and paroxysmal ventricular tachycardia in acute myocardial infarction

Although previous studies have suggested that accelerated idioventricular rhythm rarely coexists with paroxysmal ventricular tachycardia, this relation has not been systematically evaluated in acute myocardial infarction. To examine this relation, the frequency and characteristics of the two arrhythmias were analyzed by performing 24 hour Holter monitoring during the initial 24 hours of acute myocardial infarction in 52 successive patients. Twenty-four of these patients had documented accelerated idioventricular rhythm; 28 patients did not. Paroxysmal ventricular tachycardia occurred in 83 percent of patients with accelerated idioventricular rhythm but in only 18 percent of patients without this arrhythmia (P < 0.001). The results remained at the same level of significance whether paroxysmal ventricular tachycardia was defined by rates greater than 100, 120 or 140 beats/min. These findings suggest that accelerated idioventricular rhythm complicating acute myocardial infarction is not always benign and is frequently associated with more serious forms of ventricular arrhythmia.     

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.     

Endocardial, intramural, and epicardial activation patterns during sustained monomorphic ventricular tachycardia in late canine myocardial infarction

Thirteen dogs in whom at least one morphologically distinct sustained ventricular tachycardia (VT) could be reproducibly initiated by programmed cardiac stimulation 18 +/- 3 days following experimental myocardial infarction were placed on total cardiopulmonary bypass for detailed study of the endocardial and epicardial activation during VT under hemodynamically stable conditions. Thirteen morphologically distinct monomorphic VTs were investigated by simultaneous epicardial, endocardial, and intramural bipolar recordings. Local electrograms were used to generate computer-assisted isochronous-activation sequence maps. A complete reentry circuit could be mapped on the epicardial surface in 4 animals and on the endocardial surface in one other animal. In the remaining 8 animals, there was a gap period lasting 43-62 msec in the cardiac cycle during which no endocardial or epicardial activity was observed. In 6 of the 8 animals, bipolar intramural recordings from sites closely associated with regions of endocardial and epicardial conduction block showed intramural activity progressing slowly during the gap period. In these 6 animals, a reentry circuit could be completed by incorporating the local electrograms recorded from the intramural sites. VT could be reproducibly terminated by selectively rendering only these intramural sites refractory by critically timed extrastimuli that failed to result in global ventricular capture. VT could be terminated by epicardial cooling in 2 of the 4 animals with epicardial reentry. By contrast, epicardial cryoablation did not effect intramural reentry and failed to interrupt VT. In this study, intramural pathways constituted an integral part of the reentry circuit in a large proportion of the VTs.     

Sinus rhythm mapping in healed experimental myocardial infarction: contrasting activation patterns for inducing ventricular tachycardia versus fibrillation

The inducibility of ventricular tachycardia (VT) and fibrillation (VF) is variable in healed myocardial infarction (MI) in the dog. To better understand the electrophysiologic basis for these arrhythmias, MI was produced in dogs by ligating the left anterior descending artery. One week later, epicardial mapping was performed with the dog in sinus rhythm using a hand-held bipolar electrode. Transmural mapping was performed with the dog in sinus rhythm with 4 pairs of bipolar electrodes mounted on a #14 needle. Ventricular arrhythmias were induced by the S₁S₂S₃ technique or 3- to 5-beat burst pacing at twice diastolic threshold. Only VF could be induced in 11 dogs, while sustained VT was induced in 6 dogs. Significantly more marked and more extensive delay in activation was seen both in the epicardium and transmurally in dogs with VT than in dogs with VF. In addition, dogs with VT had morphologic evidence of a large transmural MI, whereas dogs with VF had only a subendocardial MI. It is concluded that inducible sustained VT in the dog is usually associated with a large transmural MI and an activation sequence in sinus rhythm characterized by an extensive area of marked delay in activation. This activation pattern in sinus rhythm presumably is necessary to provide the underlying electrophysiologic milieu for sustained reentry.     

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.     

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.     

Prognostic significance of sustained monomorphic ventricular tachycardia induced by programmed ventricular stimulation using up to triple extrastimuli in survivors of acute myocardial infarction

The prognostic significance of sustained monomorphic ventricular tachycardia (VT) induced by programmed ventricular stimulation using up to 3 extrastimuli was evaluated in 133 consecutive survivors of acute myocardial infarction (AMI) at a mean interval of 1.8 +/- 1.1 months after onset. This was compared with hemodynamic and angiographic abnormalities shown by cardiac catheterization and ventricular ectopic activity detected by Holter monitoring. Sustained monomorphic VT was induced in 25 (19%) patients, sustained polymorphic VT in 11 (8%) patients, nonsustained monomorphic VT (greater than or equal to 10 beats) in 12 patients (9%) and nonsustained polymorphic VT in 9 patients (7%). Multivariate logistic regression analysis of clinical, angiographic, hemodynamic and electrocardiographic variables showed that the presence of a left ventricular aneurysm (p = 0.005) and Lown grade 4B ventricular ectopic activity (p less than 0.001) were independent predictors of inducibility of sustained monomorphic VT. During a mean follow-up of 21 +/- 13 months, there were 8 (6%) sudden cardiac deaths and 3 (2.3%) spontaneous occurrences of life-threatening sustained VT. The 2-year probability of freedom from sudden cardiac death or sustained ventricular tachyarrhythmias was 53 +/- 13% for patients with inducible sustained monomorphic VT, 70 +/- 10% for those with a left ventricular ejection fraction less than 40% and 58 +/- 13% for those with Lown grade 4B ventricular ectopic activity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pacemaker-induced ventricular tachycardia in patients with acute inferior myocardial infarction

We analysed a group of 35 consecutive patients with acute myocardial infarction—23 of the inferior, 12 of the anterior wall—who needed temporary pacing for bradycardiac arrhythmias. We observed in three patients ventricular tachycardias induced by pacemaker stimuli falling onto the vulnerable part of the cardiac cycle due to improper sensing. All three had an inferior myocardial infarction involving the right ventricle. Because the pacemaker electrode in this condition lies in the vicinity of the infarcted myocardium sensing problems occur more frequently and re-entry tachy-cardias can be triggered more easily. It represents a possible risk of pacemaker treatment in this group of patients who, on the other hand, often need cardiac pacing in the acute phase following the development of transient AV-block.     

Incessant ventricular tachycardia complicating acute myocardial infarction: treatment by map-guided infarctectomy

A 58-year-old man developed incessant ventricular tachycardia on the fourth and fifth days following acute anterior myocardial infarction. The tachycardia was resistant to antiarrhythmic drugs, cardioversion and pacing. Preoperative and intraoperative mapping suggested a subendocardial origin, and successful infarctectomy was performed on the fifth day of the infarction.     

Catheter ablation of monomorphic ventricular tachycardia

PURPOSE OF REVIEW: Patients with ventricular tachycardia are subject to frequent recurrences and antiarrhythmic drug therapy has been disappointing. Catheter ablation offers an alternative means of controlling ventricular tachycardia. RECENT FINDINGS: The origin and pathophysiology of ventricular tachycardia are being defined for newly recognized types of ventricular tachycardia as well as scar-related ventricular tachycardias. The approach to mapping and ablation of ventricular tachycardia depends on the nature of the arrhythmia substrate, which is largely determined by the underlying heart disease. Focal origin ventricular tachycardias often occur in patients without structural heart disease. The right ventricular and left ventricular outflow tracts are common locations. Ablation is usually successful unless the focus is epicardial in location or in close proximity to the ostia of a coronary artery. The reentry path for idiopathic left ventricular reentrant ventricular tachycardia is now defined. In patients with heart disease, most ventricular tachycardias are scar related, with areas of fibrous tissue forming the border for reentry paths. Substrate mapping defines areas of scar, abnormal conduction, and reentry circuit exits during sinus rhythm. Ablation of multiple ventricular tachycardias and unstable ventricular tachycardias performed largely during sinus rhythm is often possible. Ablation is usually adjunctive therapy to an ICD in these patients. Epicardial mapping and ablation are needed in some patients. SUMMARY: Ablation is a reasonable alternative to antiarrhythmic drug therapy for controlling frequent ventricular tachycardia episodes in many patients. Further technological advances can be anticipated.     

Helicoid ventricular tachycardia, torsade de pointes, in acute myocardial infarction

Helicoidal ventricular tachycardia (Torsades de Pointe), (HVT) is an arrhythmia with peculiar characteristics and therefore should be individualized. The occurrence of HVT during acute myocardial evolution has been denied by many authors. In this paper, the possibility that this association may be not only coincidental is analyzed. A group of 1,307 patients with acute myocardial infarction was studied, in 29 of them this arrhythmia was detected in the first 72 hours and these patients didn't have an associated disease and/or treatment related to HVT. This represents an incidence of 2.22% in this group. The helicoidal ventricular tachycardia had a peculiar behavior, different to the one found in HVT of other etiologies. It was triggered by early premature ventricular beats, it was found even in cases with supraventricular tachycardia and acute atrio--ventricular heart block, very seldom is autolimited and usually degenerates into ventricular fibrillation, the most important factor in association with this arrhythmia is QT prolongation. Intracavitary pacing is the treatment of choice.     

Valsalva termination of ventricular tachycardia in myocardial infarction

A 66-yr-old patient with recurrent monomorphic ventricular tachycardias subsequent to a previous myocardial infarction is reported. The tachycardia could repeatedly be terminated by the Valsalva manoeuvre. Procainamide, infused shortly before, possibly had an additional effect. As far as we know, this is the first report of ventricular tachycardias, as a result of an old myocardial infarction, that could be terminated by the Valsalva manoeuvre.