Verapamil responsive incessant ventricular tachycardia resulting in severe ventricular dysfunction in a young child: successful management with oral verapamil.

In young children with incessant ventricular tachycardia and severe ventricular dysfunction, the management of tachycardia with conventional antiarrhythmic drugs remains a major therapeutic challenge because most of these drugs can further depress myocardial function. We report a four year old boy with verapamil responsive incessant ventricular tachycardia and severe ventricular dysfunction in whom oral verapamil treatment eliminated both the arrhythmia and the picture of dilated cardiomyopathy. On oral verapamil, the patient remains asymptomatic without recurrence of the ventricular tachycardia over a follow up period of 10 months.     

Hypertrophic cardiomyopathy with left ventricular dilatation

There is increasing interest in the notion that some patients with hypertrophic cardiomyopathy (HCM) progress to morphological and functional manifestations similar to those of dilated cardiomyopathy (DCM). From 165 consecutive patients with HCM, 20 patients with left ventricular dilatation (left ventricular end-diastolic diameter greater than or equal to 50 mm) were selected and designated as dilated HCM. The diagnosis of HCM was established in these patients either by detection of the classical form of HCM in family members, with 2-dimensional echocardiographic evidence of asymmetric septal hypertrophy (ASH; septal thickness greater than or equal to 15 mm and a ratio of septal to posterior wall thickness greater than or equal to 1.3); or by demonstrating myocardial fiber disarray in autopsy or biopsy samples. The clinical manifestations of these patients with dilated HCM were then compared with those of other forms of HCM without left ventricular dilatation; 1) 40 patients with hypertrophic obstructive cardiomyopathy (HOCM) who had resting intraventricular pressure gradients of 20 mmHg or more, 2) 80 patients with non-obstructive HCM, each of whom had ASH of the entire ventricular septum (typical ASH), and 3) 25 non-obstructive patients whose hypertrophy was localized to the apical region of the ventricular septum (apical ASH). Patients having apical hypertrophy with a spade-like configuration on the left ventriculogram were excluded from the study. Compared with HOCM and typical ASH groups, the patients with dilated HCM had family histories of significantly more frequent HCM and less frequent hypertension. The patients with dilated HCM also had significantly less fractional shortening (FS), decreased interventricular septal thickness, greater left ventricular end-diastolic pressure (LVEDP), and left ventricular dilatation. During the follow-up period (average: 3.5 years), seven patients (35%) with dilated HCM died; five from congestive heart failure (CHF), one suddenly, and one three days following mitral valve replacement. The other five patients had CHF at the time of their follow-up examination. The patients with apical ASH had clinical features similar to those of dilated HCM; a higher familial frequency, less marked septal hypertrophy, and higher LVEDP. They tended to develop left ventricular dilatation, associated with reduced fractional shortening, although left ventricular diameter at end-diastole did not exceed 50 mm. These findings suggested that dilated HCM is not a rare condition. It is observed in 12% of consecutive patients with HCM.(ABSTRACT TRUNCATED AT 400 WORDS)     

Efficacy of verapamil in exercise-induced ventricular tachycardia

The antiarrhythmic efficacy of verapamil was determined by serial treadmill testing in 16 patients with reproducible exercise-induced ventricular tachycardia (VT). Twelve of the 16 patients responded to verapamil, 0.2 mg/kg intravenously; in 8 of these 12 responders, an oral verapamil regimen of 160 to 320 mg given every 8 hours also prevented exercise-induced VT. Plasma verapamil concentration was significantly higher in the responders than in the nonresponders to intravenous verapamil, but levels were similar in responders and nonresponders to oral therapy. The 8 responders to the oral drug were followed up while receiving verapamil therapy for 6 to 22 months (mean 15), and exercise-induced VT did not recur in any patient. Five of the 8 responders also had concomitant spontaneous VT unrelated to exercise which verapamil suppressed initially as well: 4 remained free of spontaneous VT, while 1 patient had recurrence of spontaneous VT. Thus, in patients with exercise-induced VT, verapamil is a promising alternative therapy to beta-adrenergic blocking agents. The effectiveness of verapamil is consistent with a mechanism of arrhythmogenesis involving calcium channels.     

Isolated left ventricular non-compaction in association with ventricular tachycardia

A 32-year-old young male was found to have non-sustained, repetitive, monomorphic ventricular tachycardia of right bundle branch morphology during routine pre-anaesthetic evaluation for orthopaedic surgery. Echocardiography and left ventricular angiogram were suggestive of isolated non-compaction of left ventricular apex with systolic dysfunction. He was successfully managed with anti-arrhythmic drugs and had an uneventful 9-month follow-up. The index case is an unusual association of asymptomatic, non-sustained ventricular tachycardia with isolated ventricular non-compaction.     

Ventricular tachycardia during exercise treated by verapamil

The case history of two patients with symptomatic ventricular tachycardia is described. The first patient with systolic narrowing of a segment of the left anterior descending artery did not show any improvement on class I and III antiarrhythmic drugs. Oral verapamil suppressed the arrhythmia which showed some features of triggered activity. Cessation of the drug resulted in symptomatic recurrence. The second patient presented with a sustained ventricular tachycardia showing the morphology of right bundle branch block and left axis deviation. During electrophysiologic study the tachycardia was not inducible after oral verapamil. No definite conclusion on the mechanism of the arrhythmia could be drawn, nor on the mechanism of the antiarrhythmic action of verapamil in the first patient. Appropriate techniques to prove the efficacy of verapamil are needed in patients when it is given for chronic treatment of ventricular tachycardia.     

Successful treatment of stress-induced therapy refractory ventricular tachycardia with verapamil

A 51-year-old woman was admitted to the hospital for further elucidation of a syncope of unknown origin and exercise-induced tachycardias with broad QRS-complex. The tachycardia was induced by bicycle exercise stress testing, had a frequency of 165/min, showed an inferior axis and left bundle branch block. Organic heart disease was excluded by right and left heart catheterization and selective coronary angiography. A nodoventricular bundle or an atrio-ventricular bundle was excluded by an extensive electrophysiologic study, therefore the documented tachycardia was probably of ventricular origin. However, it was not possible to induce a ventricular tachycardia by programmed ventricular stimulation with up to three extrastimuli even after the infusion of isoprenaline. Sotalol (2 x 160 mg/die) and the combined treatment with mexiletine (2 x 360 mg/die) and disopyramide (2 x 250 mg/die) did not prevent the induction of the tachycardia by exercise testing. The combination of sotalol and flecainide (2 x 100 mg/die) evoked complex ventricular arrhythmias at rest not noted before, and it was therefore withdrawn as well. After all antiarrhythmic drugs were withdrawn verapamil was given in a dose of 3 x 120 mg and this therapy reproduceably prevented the induction of ventricular tachycardia by exercise testing.     

Hazards of intravenous verapamil for sustained ventricular tachycardia

In 11 of 25 patients (44%) with sustained ventricular tachycardia (VT) who received intravenous verapamil (5 to 10 mg), acute severe hypotension or loss of consciousness developed, necessitating immediate cardioversion. Comparison of these 11 patients with the 14 who did not have adverse effects after verapamil revealed no significant difference in age, heart disease, ejection fraction, blood pressure before verapamil administration, other oral or intravenous drugs use, verapamil dose or VT characteristics (rate and morphologic pattern). Although most patients with severe adverse effects after verapamil had prior myocardial infarction, deterioration also occurred in patients without coronary disease and in patients with a normal left ventricular ejection fraction. VT terminated after verapamil infusion in 6 patients. No single electrocardiographic morphologic pattern characterized these patients. A control group of 25 patients presenting with hemodynamically stable VT who received other antiarrhythmic agents was examined. Hypotension developed in only 1 patient during acute therapy and did not require emergency cardioversion. Thus, although verapamil may terminate VT, severe adverse effects occur much more often. Use of verapamil to differentiate supraventricular tachycardia with aberrant conduction from ventricular tachycardia is hazardous.     

Efficacy of verapamil in chronic, recurrent ventricular tachycardia

Verapamil, 0.25 mg/kg, was given to 24 patients with chronic, recurrent ventricular tachycardia (VT) whose clinical tachyarrhythmias were reproduced at electrophysiologic study. Seven patients (29%) responded acutely to verapamil: VT was not inducible in 5 and spontaneously terminated within 5 seconds of induction in 2 patients in whom it was previously sustained. Four of the 7 responders had no identifiable structural heart disease, and 3 had coronary artery disease. Responders were younger and had better left ventricular function than did nonresponders. Long-term therapy with verapamil, attempted in 5 of the 7 responders, was effective in 3, ineffective in 1, and of uncertain efficacy in 1. Verapamil therapy was discontinued because of worsened congestive heart failure in 2 patients.

The short-term efficacy of verapamil in these patients compares favorably with the efficacy of other antiarrhythmic agents against VT induction in patients with long-term, recurrent, drug-refractory VT. The short-term efficacy of verapamil correlated with its long-term efficacy. These observations provide preliminary evidence that verapamil may be useful in the treatment of some patients with recurrent VT. When standard drugs are not effective, verapamil should be given a trial, especially in young patients with good left ventricular function.     

Idiopathic recurrent sustained ventricular tachycardia responsive to verapamil

The role of i.v. verapamil in the management of atrioventricular (AV) nodal reentrant tachycardias is well established (Schamroth et al., 1980). Generally however the drug is not very effective in recurrent ventricular tachycardia (VT) (Singh et al., 1983). Verapamil was recently demonstrated to be successful in terminating VT induced by programmed stimulation in only 1 out of 8 patients tested (Wellens et al., 1980). Conversely a few recent cases of verapamil responsive VT, mostly occurring in young people without obvious organic heart disease, have been reported (Belhassen, 1984; Klein, 1984; Delise, 1985; Ward, 1984; Lin 1983; German, 1983; Mason, 1983; Wu, 1981). We describe 3 clinical examples of idiopathic recurrent sustained VT responsive to verapamil. A careful analysis of our cases support the hypothesis of different pathophysiologic mechanism involved in the genesis of this unique arrhythmic entity.     

伴右心室出口的左心室起源缺血性室性心动过速的标测和消融

目的折返性的缺血性室性心动过速（VT）绝大多数发生于左心室并表现为右束支阻滞（RBBB）图形。本文报道1组VT折返环位于左心室但出口在右心室且表现为左束支阻滞（LBBB）的病例。方法32例因陈旧性心肌梗死伴VT而接受电生理检查和射频消融的患者,其中4例临床有LBBB形态的VT。使用非接触等电位和虚拟单极标测判断VT起源,结合舒张中期电位（MDP）和拖带标测确定折返关键通路和消融靶点。用盐水冲洗电极导管在折返环的关键峡部行线性消融。结果全部32例患者中,4例临床有LBBB型VT者均成功被诱发,其中1例有两种LBBB型VT,1例同时有RBBB型VT但周长与LBBB型相同;另有1例共有6种形态的VT,包括RBBB和LBBB型。在右心室内的非接触式等电位标测可迅速确定VT在右心室的传出部位,该处的虚拟单极标测显示rS型提示左心室起源。3例在左心室成功拖带并消融成功,靶点均紧邻左心室间隔,其中1例位于下壁,1例在前壁,1例两种LBBB型VT分别在前壁和下壁间隔旁消融成功。随访1～4．2年,未服抗心律失常药无VT发作。而1例诱发出6种单形（包括RBBB和LBBB型）VT患者因巨大室壁瘤及心功能障碍不能耐受而中途放弃消融。结论紧邻室间隔的前壁和下壁心肌梗死后的左心室起源VT可能因在右心室有出口而表现为LBBB型,需要在标测和消融时予以注意。     

Surgery of ventricular tachycardia in post-infarction left ventricular aneurysm

The treatment of post-infarction ventricular tachycardias with antiarrhythmic drug therapy, implantable automatic defibrillators, radiofrequency ablation, also includes different surgical procedures such as endocardial resection of the infarct scar, encircling endocardial ventriculotomy and endocardial cryoablation or thermoexclusion by laser. These procedures may be extensive or limited, guided or not by preoperative mapping. The aim of this review of the literature is to update our knowledge of these different surgical techniques and to define their indications.     

Response of recurrent sustained ventricular tachycardia to verapamil.

A 28-year-old man is described with no demonstrable organic heart disease and recurrent paroxysmal attacks of sustained ventricular tachycardia. Lignocaine and ajmaline failed to terminate the first attack but a bolus infection of verapamil succeeded. This drug was subsequently successful on six more occasions. During electrophysiological study of the eighth attack, slow intravenous administration of verapamil significantly reduced the rate of the tachycardia and prevented its subsequent reinitiation by pacing. Two mechanisms are postulated to explain both the arrhythmia and the beneficial effects of verapamil in this case.     

Idiopathic verapamil-sensitive sustained left ventricular tachycardia

Idiopathic verapamil-sensitive left ventricular tachycardia (VT) has characteristic QRS configurations during VT: right bundle-branch block with either left axis or right axis (less common) deviation. QRS duration is relatively narrow (0.13-0.16s) and frequently endocardial activation prior to QRS is recorded during VT, which is the basis of its being called fascicular tachycardia. The mechanism is probably reentry, but the nature of the slow conduction necessary for the occurrence of reentry is quite different from that of other sustained monomorphic VT associated with structural heart disease. Chronic oral verapamil therapy is the drug of choice for alleviation of symptoms. Long-term prognosis is good.     

Ventricular tachycardia of left bundle branch block configuration in patients with isolated right ventricular dilatation. Clinical and electrophysiological features

Electrophysiological studies showed ventricular tachycardia in five patients (four male, one female) with isolated right ventricular dilatation. All had been asymptomatic before the onset of palpitation which had developed in adolescence or early adult life. Tachycardia had been associated with syncope in four patients, and three had been resuscitated from ventricular fibrillation before investigation. The electrocardiogram during ventricular tachycardia showed a left bundle branch block pattern, and endocardial mapping at electrophysiological study confirmed the right ventricular origin. The presenting tachycardia could be induced in all patients by programmed stimulation, and in three patients ventricular tachycardia of differing configuration could be induced, but the right ventricular origin and left bundle branch block pattern were maintained. In two patients ventricular tachycardia degenerated into ventricular fibrillation. Cineangiography, cross sectional echocardiography, and multigated radionuclide angiography confirmed the dilated abnormal right ventricle while indicating that left ventricular function was normal. On resting electrocardiograms T wave inversion over the right precordial leads was the sole abnormality. There were no signs of right heart failure and exercise tolerance was normal. Four patients have received maintenance treatment with antiarrhythmic drugs, and one had undergone operative mapping and ablative surgery. Thus ventricular tachycardia complicating right ventricular dilatation may be associated with serious symptoms and ventricular electrical instability; and in adults it may be suspected on clinical grounds by inverted T waves in the right precordial leads.