Search

To further define the relation between changing adrenergic tone, beta-blocker therapy, and clinical ventricular tachycardia (VT), we evaluated these factors in 35 patients with VT unrelated to coronary artery disease or ventricular dysfunction. Testing included Holter monitoring (91% had VT), exercise test (69% had VT), Adrenergic responsiveness of VT was graded according to diurnal variation, response to exercise, isoproterenol infusion, and response to beta-blockers. beta-Blockers were effective and well tolerated in this population. There was also a predictable relation between changing adrenergic tone and the arrhythmia response to beta-blocker therapy.

Adenosine has become the preferred treatment for common types of supraventricular tachycardia because it is extremely effective and rarely associated with with serious side effects. It has also been advocated as an intervention for diagnostic use to assess uncommon types of tachycardia. Evidence is shown in this report that adenosine was associated with dangerous worsening of arrhythmia in patients with atrial flutter. In two patients, adenosine precipitated acceleration of ventricular response, in one case necessitating emergent cardioversion. Both patients had atrial flutter with 2 to 1 atrioventricular block that evolved into 1 to 1 atrioventricular conduction. In three other patients, adenosine was associated with prolonged bradyasystole and hypotension. In each of the five patients, adenosine was given in a standard fashion (6 or 12 mg). In summary, adenosine should be recognized as a potentially dangerous intervention in patients with atrial flutter. If it is used for diagnostic purposes, resuscitative equipment should be readily available.

We studied 41 patients with clinically symptomatic ventricular tachycardia in the absence of coronary artery disease or left ventricular dysfunction to define the extent of right and left heart derangement and their relation to electrophysiologic and clinical data. Individual echocardiographic measurements as well as global assessment scores of the right and left heart demonstrated a wide spectrum of right heart echocardiographic abnormalities. There was much less variation in the left heart, with the majority of patients being close to normal. There was an association between the right heart score, the clinical presentation of arrhythmia, the response to programmed electrical stimulation, and the recurrence of arrhythmia (p < 0.05). Thus echocardiographic findings demonstrate the whole spectrum of right heart involvement in patients with apparent idiopathic ventricular tachycardia and can give insight into clinical history, arrhythmia inducibility, and prognosis.

Thirty-seven patients with symptomatic ventricular tachyarrhythmia and no apparent structural heart disease were evaluated with multiple cardiovascular tests to establish the relationship between the results of programmed electric stimulation and other clinical and arrhythmia variables. Of 37 patients, 12 (32%) had inducible sustained ventricular tachycardia. Factors associated with the results of programmed electric stimulation included a history of ventricular tachycardia > or = 30 seconds requiring intervention for termination and global right heart abnormality documented by echocardiography. During treatment for a mean follow-up of 50 months, 29 patients did well, 6 patients had recurrences of major arrhythmia symptoms, 1 was lost to follow-up and 1 had a noncardiac death. Those patients with an adverse outcome were more likely to have inducible ventricular tachycardia. Thus certain clinical and echocardiographic data are associated with the results of programmed electric stimulation, which in turn have important prognostic value in this group of patients. Sustained ventricular tachycardia is unlikely to be induced in patients with no evidence of structural heart disease and clinical nonsustained ventricular tachycardia.

Inducible ventricular tachycardia frequently persists despite solitary class I antiarrhythmic drug therapy. To determine the effect of metoprolol as adjuvant therapy, 19 patients with clinical ventricular tachycardia with baseline inducible sustained monomorphic ventricular tachycardia and persistently inducible ventricular tachycardia despite class I drugs were evaluated. Eight of 19 patients (42%) became noninducible when metoprolol was added to class I drug therapy. Sixteen of 19 patients (84%) were harder to induce or noninducible on a regimen of adjuvant metoprolol therapy. In evaluating the clinical characteristics of the 19 patients, no significant differences were found between patients who were persistently inducible and those rendered noninducible. In evaluating the electrophysiologic characteristics, the group eventually rendered noninducible had a significantly shorter baseline induced cycle length (259 +/- 27 vs 305 +/- 53 msec). Combination class I drug and metoprolol therapy significantly lengthened the ventricular effective refractory period in both groups compared with baseline. The long-term follow-up was excellent in all patients remaining on metoprolol in the noninducible group. Therefore adjuvant metoprolol therapy creates a significant improvement in a number of patients with persistently inducible ventricular tachycardia despite class I drug therapy.

Previous reports have suggested that patients with heart failure and coexistent ventricular tachyarrhythmias have a 1-year mortality of 40% to 60%. To assess whether an antiarrhythmic management program could reduce mortality, we studied 20 consecutive patients with ventricular fibrillation (12) or ventricular tachycardia (eight) and heart failure. Coronary disease was the most common underlying cardiac disorder (85%). Heart failure was managed with digoxin (16), diuretics (16), and vasodilators (seven). All patients received antiarrhythmic drug therapy guided by both noninvasive and invasive studies. This included single (10) or combination drug therapy (10). Beta blockers were used alone or in combination for arrhythmia control in 11 patients. One-year survival was 89%. We conclude that an effective program can be developed for patients with life-threatening ventricular tachyarrhythmias and heart failure. Combination antiarrhythmic drug therapy is often required. Despite impaired left ventricular function, beta-blocking drugs can be used, and may be important.

The results of exercise treadmill stress testing were analyzed in 64 consecutive patients presenting with either ventricular fibrillation (42%) or hemodynamically significant ventricular tachycardia (58%). Underlying diseases included coronary artery disease (55%), dilated cardiomyopathy (16%), and miscellaneous disorders (29%). Patients were additionally studied with ambulatory electrocardiographic monitoring and programmed stimulation. During exercise testing, 22 patients (34%) had nonsustained and five (8%) had sustained ventricular tachycardia. No patient experienced ventricular fibrillation or a major complication during exercise testing. Patients with a history of ventricular fibrillation were significantly less likely to have exercise-induced ventricular tachycardia than those with a history of ventricular tachycardia. Other clinical factors were not associated with the results of exercise testing. The results of programmed stimulation did not correlate with the results of exercise testing. Ventricular tachycardia was commonly documented during ambulatory monitoring (72%), but this was not predictive of ventricular tachycardia during exercise. However, patients who did not have ventricular tachycardia during ambulatory monitoring were predictably unlikely to have it during exercise testing (p less than 0.002). Thus exercise testing is safe and can provoke ventricular tachycardia in a significant proportion of patients with life-threatening arrhythmias.

Although several studies suggest beta blockers (BB) are effective in suppressing ventricular arrhythmias, less is known about their role in the treatment of patients with ventricular tachyarrhythmias associated with impaired left ventricular function. To assess the tolerance and efficacy of these agents, 32 patients presenting with either ventricular fibrillation (18) or sustained ventricular tachycardia (14) were studied during BB therapy. Left ventricular dysfunction (mean ejection fraction 29%) was present as a consequence of coronary artery disease (26) or cardiomyopathy (6). Baseline arrhythmia assessment revealed recurrent ventricular tachycardia in all patients. Antiarrhythmic drug therapy including BB was guided by programmed stimulation (10), exercise testing (8), ambulatory monitoring (12), or was given empirically (2). Beta blockers were well tolerated, as measured by exercise duration, which improved significantly, and by long-term maintenance, which continued in 23 of 32 (72%) patients. Over a mean follow-up of 668 days, patients treated with BB had a relatively low incidence of both sudden (3%) and nonsudden (9%) death. Thus, BB can be effective and well tolerated adjunct therapy in patients with a history of ventricular tachyarrhythmias in the setting of impaired left ventricular function.

The combined occurrence of impaired left ventricular function and ventricular tachyarrhythmias portend a high annual mortality. Although antiarrhythmic drugs can reduce ventricular arrhythmias, the prognosis may be unchanged. We administered propafenone to 12 patients with ventricular tachyarrhythmias and left ventricular ejection fractions less than 40%. Propafenone significantly reduced isolated ventricular premature depolarizations, couplets, and ventricular tachycardia on ambulatory monitoring. Propafenone eliminated all exercise provocable ventricular tachycardia. Propafenone additionally abolished ventricular tachycardia inducible by programmed stimulation in five of six patients. In eight patients studied before and during therapy, there was no significant change in left ventricular ejection fraction determined by nuclear ventriculography. Propafenone was discontinued in three patients due to side effects. All patients remain alive and without recurrence of clinically significant arrhythmia over a mean follow-up period of 14 months. Propafenone is an effective drug for the management of ventricular tachyarrhythmias, and may be used in patients with impaired left ventricular function.

To assess the efficacy and predictability of solitary beta-adrenergic blocker (BB) therapy for ventricular tachyarrhythmia (VT), 30 patients (16 men and 14 women) with a mean age of 55 years, who initially had sustained ventricular tachycardia (70%) or ventricular fibrillation (30%), were studied. Results of baseline arrhythmia tests showed VT on ECG monitoring in 57% of the patients, during exercise in 50%, induced by programmed stimulation in 69%, increasing to 86% during isoproterenol. BB therapy prevented inducible VT during programmed stimulation in 37% of the patients, prevented VT on ECG monitoring in 54%, and prevented VT during exercise in 83%. Long-term BB therapy was given to 24 of 30 patients, whereas six other patients with hemodynamically unstable VT during BB therapy received other long-term treatment. During a mean follow-up of 824 days, 6 of 24 patients had recurrent VT. BB therapy was discontinued in two patients because of side effects. Long-term success was predicted by left ventricular ejection fraction greater than 45%, absence of coronary disease, and age less than 60 years (all p less than 0.02). Neither suppression of arrhythmia during exercise testing, nor results of programmed stimulation or ECG monitoring were predictive of outcome. Thus beta-adrenergic blockers can be effective as solitary antiarrhythmic therapy in selected patients with VT.