Paroxysmal Sustained Ventricular Tachycardia Research Articles

Diagnosis and treatment of idiopathic ventricular tachycardia.

Idiopathic ventricular tachycardia in patients with an anatomically normal heart is a distinct entity whose management and prognosis differs from ventricular tachycardia associated with structural heart disease. The tachycardia's QRS morphology on surface electrocardiogram (ECG) predicts the site of origin and is commonly classified as right ventricular tachycardia or left ventricular tachycardia. The tachycardia is further characterized by clinical features such as repetitive monomorphic ventricular tachycardia (VT), paroxysmal sustained VT, or catecholamine dependent VT. The responsiveness of VT to adenosine or verapamil is useful in differentiating the mechanism, which may be reentry or triggered activity. Patients generally tolerate the tachycardia but may present with dizziness, syncope, or palpitations. Sudden cardiac death is rare in this patient population. Patient work-up should include 12-lead ECG, signal-averaged ECG, ambulatory ECG recording, stress testing, and tests to rule out structural heart disease such as echocardiography, cardiac angiography, endomyocardial biopsy, or magnetic resonance imaging. Treatment options include pharmacotherapy or catheter ablation. Although the prognosis of these patients remains excellent, they should continue to have periodic cardiac follow-up to rule out latent progressive heart disease such as arrhythmogenic right ventricular dysplasia or cardiomyopathy or other forms of cardiomyopathies.

CATHETER ABLATION OF VENTRICULAR TACHYCARDIA - LONG-TERM RESULTS

Ventricular tachycardia represents life-threatening cardiac rhythm disturbance and catheter ablation using radiofrequency current provides powerful means for definitive cure of almost all monomorphic tachyarrhythmias. Presence and extent of underlying structural heart disease is important for further prognosis of the patients, who undergo catheter ablation of ventricular tachycardia. Long-term results of catheter ablation for ventricular tachycarida in patients with and without structural heart disease are presented. Patients and results: Twenty three patients (9 females) aged 49.1 ± 15.6 (18–72) years underwent catheter ablation for monomorphic (resp. polymorphic in one patient) ventricular tqachycardia in 30 ablation procedures. Patients with structural heart disease: Seven patients (2 females) aged 54.2 ± 19.8 (21–72) years had structural heart disease (5 patients – post myocardial infarction, 1 patient – arrhythmogenic right ventricular dysplasia, 1 patient – surgically corrected transposition of great arteries). All sustained monomorphic ventricular tachycardias were eliminated during the catheter ablation and no ventricular tachycardia recurred during the follow-up period in 4 patients. In two patients sustained monomorphic ventricular tachycardia was not eliminated with radiofrequency current. One of the patients remains free of ventricular tachycardia and one patient experienced one recurrence of slowed ventricular tachycardia. Thus long-term clinical success was achieved in 4 patients and some clinical benefit probably also in the latter two patients. A different ablation strategy targeting large arrhythmogenic area at the border of postmyocardial infarction scar was employed in the last patient with frequent ICD discharges for polymorphic ventricular tachycardia associated with hemodynamic deterioration. This procedure brought immediate and long-term significant reduction of ICD shocks and rehospitalizations and probably was life-saving. Patients without structural heart disease: In sixteen patients (7 females) aged 44.2 ± 12.8 (18–66) years no structural heart disease was found. These patients presented with documented ventricular ectopy in different forms from incessant ventricular premature beats through repetitive nonsustained ventricular tachycardia to paroxysmal sustained ventricular tachycardia. The arrhythmia originated in the right ventricle in 11 patients (right ventricular outflow tract in 10 patients and basolateral wall in 1 patient) and in the left ventricle in 5 patients (inferoapicoseptal region in 4 patients and basoinferoseptal region in 1 patient). Eleven patients (68.7 %) had the arrhythmia eliminated or markedly suppressed during the ablation procedure and remain free of palpitations and antiarrhythmic drugs. Two patients with partial suppression of the ectopic rhythm are less symptomatic and the antiarrhythmic drugs could be reduced. In one patient one ventricular tachycardia morphology from the right ventricular outflow tract was eliminated while the second ventricular tachycardia morphology was not targeted (and was suppressed by antiarrhythmic drug) for close vicinity of the arrhythmogenic focus to the left anterior descending artery. Thus the clinical benefit of the ablation procedure is enhanced to 14 (87.5 %) patients. Ablation completely failed in two patients. Conclusion: Radiofrequency catheter ablation of ventricular tachycardia is highly effective and safe and results in long-term arrhythmia elimination. In patients with underlying structural heart disease it should be currently viewed as a adjunctive therapy to a complex management of the patient, while in otherwise healthy patients it can be considered a method for permanent cure.

Surgical correction of idiopathic paroxysmal ventricular tachycardia possibly related to left ventricular false tendon

Ventricular tachycardia (VT) can occur in healthy subjects. 1,2 We have reported a high prevalence of the coexistence of left ventricular false tendons or fibromuscular bands in the left ventricular cavity, and ventricular arrhythmias in apparently healthy subjects. 3,4 In this report, we describe a patient with paroxysmal sustained VT, which indicates a QRS morphology of right bundle branch block and left axis deviation. It has been completely suppressed by the surgical resection of the false tendon and the partial cryocoagulation of the left ventricular myocardium where the false tendon was attached.

A case of nonobstructive hypertrophic cardiomyopathy with paroxysmal sustained ventricular tachycardia

A case of nonobstructive hypertrophic cardiomyopathy with paroxysmal sustained ventricular tachycardia

Initial and long-term outpatient experience with lorcainide for suppression of malignant and potentially malignant ventricular arrhythmias

There is a need for effective, well-tolerated antiarrhythmic agents, particularly those effective by both intravenous and oral routes. Lorcainide, a new antiarrhythmic drug with such properties, was given long-term orally to 24 patients controlled initially with intravenous therapy—19 with frequent (>1/min) complex premature ventricular complexes (PVCs) on a baseline 24-hour Holter monitor and five with ongoing sustained ventricular tachycardia (VT) or frequent paroxysmal sustained VT, for a mean of 13 months (range 0.03 to 39.4 months). Long-term lorcainide was given in divided doses of 200 to 800 mg/day (median 260, mean 269 ± 90 mg/day). Response to long-term lorcainide therapy was assessed at a mean of both 26 days and 12.2 months. Frequency of PVCs on baseline averaged 13,490/24 hours (median 10,578, range 2,115 to 61,716); couplets averaged 309/24 hours (median 166, range 0 to 5,686), and runs averaged 33/24 hours (median 30, range 0 to 2,951). Median frequency of PVCs decreased by 94% (p ≪ 0.001) and 97% (p ≪ 0.01) at the first and second lorcainide efficacy assessments, respectively. Couplets decreased by a median of 99% (p ≪ 0.001) and 100% (p < 0.005) at the first and second assessments, respectively. Runs were suppressed by a median of 100% at both evaluations (p ≪ 0.001). Only three (16%) of the patients with complex PVCs failed to respond to therapy. No recurrence during lorcainide has been noted in the five patients with ongoing sustained VT or recurrent episodes of VT. Three continued on therapy, one could be discontinued after corrective cardiac surgery (coronary bypass grafting with aneurysmectomy), and one was discontinued because of side effects (dizziness, bitter taste). ECG PR and QRS intervals increased mildly but significantly (by 0.02 and 0.01 second, respectively) during therapy (p < 0.001). Adverse effects were frequent, however, and led to drug discontinuation in six (25%)-because of severe insomia in two; dizziness and metallic taste, impotence, arrhythmia exacerbation, and heart failure in one each. In summary, lorcainide is an effective antiarrhythmic long-term agent in patients initially responding to intravenous therapy, but is associated with a rather high incidence of adverse effects.

Lack of effectiveness of oral mexiletine in patients with drug-refractory paroxysmal sustained ventricular tachycardia: A study utilizing programmed stimulation

Recent studies indicate that oral administration of mexiletine is useful in the therapy of recurrent ventricular tachycardia (VT). To further define the clinical usefulness of this drug, mexiletine was administered to 13 men and 4 women with a mean age ± standard deviation of 62 ± 8 years who had drug-refractory paroxysmal sustained VT associated with chronic ischemic heart disease in 14, valvular heart disease in 1, and primary myocardial disease in 1. One patient had no heart disease. All 17 patients had inducible sustained VT during the control electrophysiologic study and during serial electrophysiologic study on conventional drugs. Eleven patients tolerated a mean maximal daily dose of 1,073 ± 149 mg of mexiletine and underwent programmed ventricular stimulation; sustained VT was inducible in 10 patients and nonsustained VT in 1. in 10 patients with inducible sustained VT on mexiletine, the VT cycle length was longer during mexiletine therapy than during control (mean ± standard error of the mean, 342 ± 22 versus 268 ± 14 ms, respectively) (p < 0.005). Programmed stimulation was not possible in 1 patient with severe neurologic side effects and in 5 patients with mexiletine-related worsening of ventricular arrhythmia. Seven other patients had severe neurologic or gastrointestinal side effects, necessitating dose reduction in 5. This 47 % incidence of noncardiovascular side effects is similar to that in previous reports, but the 29 % incidence of arrhythmia potentiation by mexiletine is unexpectedly higher. Limited follow-up reveals recurrence of VT in 3 of 4 patients treated with oral mexiletine on a long-term basis. In conclusion, oral mexiletine does not appear useful in the therapy of patients with drug-refractory, paroxysmal sustained VT. In addition, its use is associated with a high incidence of adverse effects, cardiovascular (arrhythmic) and noncardiovascular, some of which can be serious and life-threatening.

Prediction of response to class I antiarrhythmic drugs during electrophysiologic study of ventricular tachycardia

We have retrospectively examined data from 41 patients studied in our laboratory for symptomatic ventricular arrhythmia in order to test whether any clinical or electrophysiologic variables could be identified which would predict the patient's response to class I antiarrhythmic drugs. All patients had (1) clinically documented paroxysmal sustained ventricular tachycardia (VT) or ventricular fibrillation remote from acute myocardial infarction, (2) inducible sustained VT during control electrophysiologic study (EPS), and (3) EPS after one or more of the following class I antiarrhythmic drugs: intravenous procainamide (36 patients), oral quinidine (30 patients), and oral disopyramide (36 patients). Initially, patients were divided into those who had noninducible or only nonsustained VT after any of the tested drugs (responders), and those who continued to have inducible sustained VT after all tested drugs (nonresponders). A logistic regression technique demonstrated no independent contribution to drug response by any of the following variables: sex, arteriosclerotic heart disease, cardiomegaly, age, time since the initial episode of VT, and cycle length of VT during control study. The number of antiarrhythmic drugs the patient had received prior to study was found to be a significant independent contributor ( p < 0.03), with responders having received an average of 2.5 drugs compared with 4.2 for nonresponders. In addition to the logistic regression, 12 other clinical and electrophysiologic variables were not predictors of drug response. The question was also asked, “Does response or nonresponse to one class I drug predict response or nonresponse to the others?” Significant concordance of response and nonresponse was demonstrated for procainamide and quinidine, but not for either of these drugs and disopyramide. Drug therapy for inducible sustained VT therefore remains empiric.

Ventricular tachycardia: Prediction of response to oral aprindine with intravenous aprindine

Aprindine was administered both intravenously and orally to 25 patients with ventricular tachycardia refractory to conventional antiarrhythmic agents to test the hypothesis that the response to intravenous aprindine predicts the response to oral aprindine. Ten patients had incessant ventricular tachycardia and 15 had paroxysmal sustained inducible ventricular tachycardia. Eleven patients (43 percent) had conversion to sinus rhythm with intravenous aprindine (nine with incessant and two with paroxysmal sustained ventricular tachycardia). Thirteen patients (all with paroxysmal sustained ventricular tachycardia) manifested slowing of the tachycardia without conversion, whereas in one patient with incessant ventricular tachycardia, the tachycardia became less frequent and nonsustained after intravenous aprindine. All 11 patients who had conversion to sinus rhythm with intravenous aprindine remained free of ventricular tachycardia during oral treatment with aprindine (at 2 weeks) and for a follow-up period of 2 to 38 months (mean 16 ± 13). Of the 14 patients who did not have conversion to sinus rhythm with intravenous aprindine, 12 had spontaneous or inducible ventricular tachycardia, or both, at evaluation 1 to 2 weeks after initiation of oral aprindine. In conclusion, administration of intravenous aprindine to patients with ventricular tachycardia is helpful in predicting the subsequent response to oral aprindine. In addition, the pattern of ventricular tachycardia predicted the response to aprindine; patients with incessant ventricular tachycardia tended to respond, and those with paroxysmal sustained ventricular tachycardia tended not to respond.

Lack of effectiveness of bretylium in paroxysmal sustained ventricular tachycardia

Lack of effectiveness of bretylium in paroxysmal sustained ventricular tachycardia