Withdrawal Of Amiodarone Research Articles

Safety of implantation of a cardioverter-defibrillator without general anesthesia in an electrophysiology laboratory

Implantable cardioverter-defibrillators (ICDs) have conventionally been implanted in an operating room under general anesthesia. This study was performed to evaluate ICD implantation without general anesthesia by 2 electrophysiologists in an electrophysiology laboratory. Between February and September 1994, 27 consecutive patients (22 men and 5 women, mean age 59 +/- 15 years) who underwent ICD implantation by 2 electrophysiologists were included in this study. Fourteen patients received biphasic waveform ICDs, and the remaining 13 had monophasic waveform devices. All patients received local anesthesia and intravenous sedation for implantation. Implantation was successful in 23 of 27 patients at first attempt (11 of 11 with biphasic and 12 of 16 with monophasic waveform ICDs, respectively). Of 4 patients in whom implantation was initially unsuccessful, 3 subsequently received biphasic devices and 1 had improved defibrillation threshold ( < or = 26 J) on repeat testing after amiodarone withdrawal. Mean implantation time was 128 +/- 51 minutes, with 132 +/- 35 minutes under sedation. Patients who received biphasic versus monophasic waveform ICDs had no significant differences in mean sedation or implantation time. Minor complications occurred in 2 patients (7%): 1 minor abdominal pocket hematoma and 1 incision-site cellulitis. Mean time from implantation to discharge was 2.5 +/- 2.1 days. During late follow-up (n = 23; mean 12.4 +/- 5.8 weeks), all devices were functioning appropriately. In conclusion, this report demonstrates that ICD implantation can be successfully and safely performed by a team of 2 electrophysiologists using local anesthesia and intravenous sedation.(ABSTRACT TRUNCATED AT 250 WORDS)

798-3 A Comparison of Amiodarone versus Flecainide Using a Quinidine Standard in the Treatment of Resistant Chronic Atrial Fibrillation

Chronic atrial fibrillation (AF) is a ommon arrhythmia with significant morbidity and mortality. The antiarrhythmic effects of amiodarone (AM) and flecainide (FLEC) in patients with resistant chronic AF have been studied separately in several small clinical trials. This study compared AM to FLEC in maintaining normal sinus rhythm (NSR) in patients (pts) with resistant chronic AF. To facilitate the comparison, quinidine (QUIN) was used as the reference standard. Studies using AM or FLEC in the treatment of chronic AF refractory to either Class I AF drugs or sotalol were identified. The results of 6 trials of AM (200–400 mg/day; 315 pts) and 2 trials of FLEC (200–300 mg/day; 163 pts) were aggregated using meta-analysis in NSR at 3 and 12 mos for AM and FLEC were compared relative to corresponding results for QUIN, which were acquired from a meta-analysis of OUIN used as first-line therapy for AF. Duration of chronic AF ranged from 2 wks to 25 yrs. After 3 and 12 mos of treatment with AM, 217 of 299 (72.6%) and 64 of 107 (59.8%) pts, respectively, remained in NSR. These percentages were significantly greater (p &lt; 0.00011 when compared to OUIN at these time points (70% and 50%, respectively). After 3 and 12 mos of treatment with FLEC, the percentage of pts remaining in NSR were significantly lower (p &lt; 0.00011 than OUIN: 79 of 163 (48.5%) and 56 of 163 (34%) pts, respectively. The aggregated percentages of pts requiring withdrawal of AM and FLEC were 9.5% and 8.6%, respectively. Mortality and proarrhythmia could not be assessed. This analysis suggests that low-dose AM is more efficacious and equally well-tolerated when compared to FLEC in the management of chronic, drug-resistant AF.

A Case of Amiodarone-Induced Pulmonary Toxicity

Amiodarone is a potent antiarrythmic agent used in the treatment of refractory tachyarrythmias and premature ventricular contractions. Amiodarone may be responsible for the frequent and various side effects including corneal deposits, abnormal liver function test, hyperthyriodism or hypothyroidism, bluish discoloration of the skin, neuropathies, and the others. However, pulmonary toxicity is most serious adverse reaction limiting the clinical efficacy. Rescently, we experienced a case of pulmonary toxicity induced by low dose 10-month amiodarone treatment for atrial fibrilation with rapid ventricular response. Lung biopsy reveals interstitial inflammation, fibrosis, hyperplasia of pneumocytes, and foamy macrophages. Respiratory symptoms and abnormal chest X-ray findings were nearly complete cleared after using steroid and withdrawal of amiodarone. We report a case of amiodarone-induced pulmonary toxicity with literature review.

Amiodarone-induced thyrotoxicosis: clinical presentation and expanded indications for thyroidectomy.

Amiodarone-induced thyrotoxicosis (AIT) is a rare disorder that is frequently refractory to conventional pharmacologic therapy. An analysis of seven patients who underwent thyroidectomy for control of AIT between 1987 and 1993 was completed to examine the clinical manifestations and the indications for surgical therapy. Five men and two women, 53 to 72 years of age, had AIT after 3 to 55 months of amiodarone treatment (mean, 21 months). The primary manifestations of AIT were ventricular tachycardia (five), exacerbation of chronic pulmonary disease (one), and occult hyperthyroidism (one). Medical therapy included propylthiouracil in doses up to 1200 mg/day in five patients, a beta-receptor antagonist in three, and withdrawal of amiodarone in five. Near-total or total thyroidectomy resulted in resolution of thyrotoxicosis in all patients. Morbidity included pneumonia (one) and cardiac dysrhythmias (two). One patient died of ventricular dysrhythmias 4 months after thyroidectomy. The mean thyroid weight was 50 gm (range, 17 to 216 gm). Microscopic examination showed destructive follicular lesions with fibrosis in all patients. Associated thyroid pathologic condition included multinodular goiter in four patients and a follicular adenoma in one. AIT may be clinically occult or manifested by unusual symptoms requiring a high index of suspicion for diagnosis. Near-total thyroidectomy is safe and effective in producing rapid resolution of AIT and is indicated for the initial treatment of patients who present with a resurgence of life-threatening cardiac arrhythmias and for all patients with AIT refractory to medical therapy.

Low-dose amiodarone for atrial fibrillation

Concerns about proarrhythmia risk and inefficacy associated with class I antiarrhythmic drugs have revived interest in low-dose amiodarone (maintenance dose 200–400 mg/day) for suppression of atrial fibrillation. In nonrandomized trials of amiodarone for atrial fibrillation refractory to conventional agents, amiodarone has been successful in maintaining sinus rhythm in 53–79% of patients during a mean follow-up of 15–27 months. Intolerable side effects, including pulmonary toxicity, are in the range of 1–12% per year and resolve following amiodarone withdrawal in the majority of cases. Proarrhythmia risk associated with amiodarone, even in the setting of left ventricular dysfunction, is extremely low. In patients with congestive heart failure, in whom other pharmacologic options are limited by proarrhythmia risk and negative inotropism, preliminary experience with amiodarone is especially promising. Randomized trials are needed, directly comparing amiodarone to conventional antiarrhythmic therapy for atrial fibrillation suppression and comparing amiodarone to warfarin for thromboembolism prevention in patients with atrial fibrillation refractory to conventional antiarrhythmic drugs.

Amiodarone Pulmonary Toxicity

Amiodarone, a benzofuran derivative, has proven useful in the control of serious cardiac arrhythmias. We reviewed the English language medical literature to characterize clinical, radiographic, scintigraphic, pathologic, diagnostic, and prognostic data concerning amiodarone pulmonary toxicity. Our review showed that features consistent with amiodarone pulmonary toxicity include exertional dyspnea, fever, and high sedimentation rates, usually in patients taking larger maintenance doses. Positive findings on gallium scan, foamy alveolar macrophages on lung biopsy or bronchoalveolar lavage, and resolution of abnormal chest roentgenogram upon withdrawal of amiodarone and/or institution of corticosteroid therapy support a diagnosis of amiodarone pulmonary toxicity. Conversely, maintenance doses of 400 mg or less daily, normal lung diffusing capacity and bronchoalveolar lavage or lung biopsy specimens without foamy alveolar macrophages are features that make amiodarone pulmonary toxicity unlikely. Amiodarone pulmonary toxicity should be considered in any patient who has new or clinical worsening of respiratory symptoms and/or abnormalities on chest roentgenogram. Congestive heart failure is often present in these patients and must be excluded before a diagnosis of amiodarone pulmonary toxicity can be considered. Amiodarone pulmonary toxicity also needs to be distinguished from pulmonary infection. Therefore, amiodarone pulmonary toxicity remains a clinical diagnosis relying upon a composite of clinical, radiographic, and histopathologic findings.

Southwestern Internal Medicine Conference: Amiodarone Pulmonary Toxicity

Amiodarone is an effective antiarrhythmic agent whose utility is limited by many side-effects, the most problematic being pneumonitis. The pulmonary toxicity of amiodarone is thought to result from direct injury related to the intracellular accumulation of phospholipid and T cell-mediated hypersensitivity pneumonitis. The clinical and radiographic features of amiodarone-induced pulmonary toxicity are characteristic but nonspecific. The diagnosis depends on exclusion of other entities, such as heart failure, infection, and malignancy. While withdrawal of amiodarone leads to clinical improvement in majority of cases, this is not always possible or advisable. Dose reduction or concomitant steroid therapy may have a role in selected patients.

Toxicité neurologique de l'amiodarone. À propos de cinq observations

Five patients developed neurological adverse effects as they were treated with amiodarone for 2 to 18 months. The daily maintenance dose did not exceed 400 mg. The neurological manifestations included tremor, ataxia, peripheral neuropathy, dyskinesia, myoclonic jerks, extrapyramidal hypertony, and altered mental status. These side effects resolved within 3 days to 3 months after amiodarone withdrawal. Advanced age, renal failure, diabetes mellitus, and alcoholism seemed to be risk factors for development of amiodarone neurotoxicity. Both peripheral and central nervous systems are involved in these amiodarone-induced complications.

Bronchoalveolar Lavage Cell Data in Amiodarone-Associated Pneumonitis: Evaluation in 22 Patients

To assess the value of bronchoalveolar lavage (BAL) for diagnosis, understanding, and treatment of amiodarone-associated pneumonitis, we examined the results of BAL total and differential cell counts and phenotyping of lymphocytes in 22 patients with this lung disorder and in 33 normal subjects. Overall, the total cell count was found to be almost the same as that seen in control subjects; the macrophage population was significantly reduced, and the lymphocyte, neutrophil, and eosinophil populations were increased in absolute number and percentage. When results were analyzed individually, BAL data appeared to be distributed according to two patterns. In the first pattern, there was no abnormal lymphocytosis. In the second pattern a lymphocyte alveolitis was found in percentage and in absolute number. This lymphocyte alveolitis was present either alone or associated with neutrophil alveolitis or with eosinophil alveolitis. In the first pattern, despite the normal level of the lymphocyte population, the percentage of CD4 T-lymphocytes and the CD4:CD8 T-lymphocyte ratio were significantly lowered. In the second pattern the CD8 T-lymphocyte count was increased in absolute number and percentage, with a low CD4:CD8 ratio. In six patients relavaged two to four months after amiodarone withdrawal, there was a significant fall in alveolar lymphocytosis, but the progressive increase in the neutrophil population over time seemed to be associated with the seriousness and progression of the disease. Finally, these findings closely resembled those obtained in patients with hypersensitivity pneumonitis due to inhalation of organic dust and suggest that an underlying immunologic cell-mediated mechanism may play a role in this iatrogenic pulmonary disease.

Acute Polymyositis and Hyperthyroidism in a Patient on Long-Term Amiodarone Therapy

A 52-year-old male received continuous oral amiodarone therapy for 3 years for the management of ventricular tachycardia nonresponsive to other antiarrhythmics, after he sustained a Q wave anterior myocardial infarction. He developed pain and weakness in both thigh and shoulder muscles in addition to weight loss and profuse sweating. His investigations confirmed the diagnosis of acute polymyositis and hyperthyroidism. His symptoms disappeared and the abnormal biochemical tests returned to normal after the withdrawal of amiodarone. We have not been able to find any other such report and believe that these were adverse side-effects of this drug.

Photosensitivity and Hyperpigmentation in Amiodarone-Treated Patients: Incidence, Time Course, and Recovery

Amiodarone (AD) induces photosensitivity in 75% of the patients treated with this drug. Phototoxic reactions can be experimentally elicited with UVA but not with UVB. The UVA-MED is significantly reduced after 12 months of treatment. The development of photosensitivity depends on the total dose of AD; 40 g is the minimal cumulative dose requirement. Under the regimens commonly used, photosensitivity can be expected after 4 months of continuous AD treatment and appears to be unrelated to the skin type. Photosensitivity gradually decreases and returns to normal between 4 and 12 months after the withdrawal of AD. AD-related hyperpigmentation develops after an average of 20 months of continuous AD treatment and a minimal total dose of 160 g AD in about 8% of the patients (mainly of skin type I). Electron microscopic examination of the sun-exposed skin of patients without AD discoloration shows pigment deposits similar to those already described in patients with AD hyperpigmentation in exposed and non-exposed skin. Light and electronmicroscopic examination of sun-exposed skin of both clinically photosensitive and non-photosensitive patients reveals perivascular inflammation even in the absence of a clinical rash. Reduplications of vascular basal laminae occur in sun-exposed skin of both patients with and without UVA photosensitivity but are absent from non-exposed skin. In one patient, followed for 33 months after drug withdrawal, massive AD-induced hyperpigmentation was found to be reversible.

A Low Incidence of Proarrhythmia Using Low‐Dose Amiodarone

The incidence of proarrhythmia with antiarrhythmic agents is reported to be 2%‐23%, depending on the agent, definition of proarrhythmia, method of assessment, and severity of underlying rhythm disturbance. Several case reports of amiodarone‐induced proarrhythmia have appeared; however, its prevalence and clinical significance have not been adequately defined. In our series of 107 patients with potentially lethal ventricular arrhythmias, amiodarone was administered as a 5‐mg/kg bolus infusion, followed by 600–800 mg/day for 7–10 days. A mean daily maintenance dose of 270 mg/day was given for an average of 15 months (range &lt;57). Proarrhythmia was defined by the method of Morganroth as: (1) a three‐ to tenfold increase in VPC frequency, (2) a marked increase in VT rate, or (3) the development of new sustained VT/VF or torsade de pointes. Bradyarrhythmias, conduction delays, and out‐of‐hospital sudden death were not included by definition. Baseline 24‐hour‐Holter monitoring revealed 449 ± 685 VPCs/hr, 740 ± 584 couplets/24 hr, and 61 ± 685 episodes of nonsustained VT/24 hr. Proarrhythmia occurred in three patients (2.8%). Two of these episodes occurred during the first week of treatment and resolved without dosage adjustment. These episodes included a 4.7‐ and 5.1‐fold increase in VPC frequency. The other proarrhythmic event was a case of torsade de pointes that occurred after 12 months of treatment and required acute intervention and withdrawal of amiodarone. In conclusion, low‐dose amiodarone appears to have a low potential for proarrhythmia and compares favorably with other agents in this regard, perhaps owing to its unique electrophysiologic properties.

Atypical Pulmonary and Neurologic Complications of Amiodarone in the Same Patient

Atypical manifestations of pulmonary toxicity and previously unreported autonomic nervous system dysfunction complicating amiodarone therapy were observed in a patient being treated for sustained ventricular tachycardia. Pulmonary and hepatic nodules on computed tomographic scan masquerading as metastatic carcinoma were initially noted. Focal infiltrates and a large left pleural effusion mimicking infection, malignant neoplasm, or collagen vascular disease became manifest at a later stage. Autonomic dysfunction presented as incapacitating orthostatic hypotension and persisted for six weeks after amiodarone withdrawal. The pleuropulmonary toxic effects were reversible on discontinuation of amiodarone therapy, and resolution was hastened by short-course steroid treatment.

Amiodarone-induced thyroid gland dysfunction

Of a population of 400 patients treated with amiodarone, 97 underwent thyroid function evaluation. Of these, 20 patients proved to be thyrotoxic and 16 hypothyroid. In thyrotoxic patients, symptoms developed 2 to 36 months after starting treatment with amiodarone, the most specific laboratory finding being a high total T 3 (TT 3). No antithyroid treatment proved useful. Thyroid function returned to normal 3 to 7 months after stopping amiodarone therapy. In the hypothyrold group, a high thyroid-stimulating hormone was the most specific laboratory finding. These patients were treated with substitute therapy with or without withdrawal of amiodarone. The iodine content of the thyroid gland in part of this population taking amiodarone was measured by in vivo x-ray fluorescence. Patients in whom thyrotoxicosis developed showed especially high Iodine contents. During treatment with amiodarone, patients at high risk of thyrotoxocosis were recognized by increasing TT 3 values and higher iodine thyroid levels. A reduction in maintenance dose should be considered in this specific population.

AMIODARONE IODINE‐INDUCED HYPOTHYROIDISM: RISK FACTORS AND FOLLOW‐UP IN 28 CASES

Amiodarone, an iodine-rich drug widely used for the treatment of cardiac tachyarrhythmias, may induce either hyperthyroidism or hypothyroidism. Of 467 patients chronically treated with this drug referred to our institution, amiodarone iodine-induced hypothyroidism (AIIH) developed in 28 patients (6%). AIIH patients were subdivided into two groups according to the presence (group A) or absence (group B) of underlying thyroid abnormalities. Thyroid autoantibodies were present in 10 of 19 patients from group A and 0 of 9 patients from group B. The thyroid 24-h radioiodine uptake (RAIU) was evaluated in 15 patients: low values (less than 4%) were found in three patients and detectable values (7-50%) were observed in 12. Perchlorate discharge tests were positive in all four patients tested. Follow-up data were available in 20 patients (16 in group A and four in group B). Hypothyroidism was transient in 12 (60%) and persistent for several months after amiodarone withdrawal in eight (40%). While all patients in group B had transient hypothyroidism, 50% of patients with underlying thyroid abnormalities (group A) had persistent hypothyroidism. Thyroid autoantibodies were found in seven of eight patients with persistent hypothyroidism and in only three of 12 patients with transient hypothyroidism. Conversely, seven of 10 patients with positive thyroid autoantibodies had persistent hypothyroidism and 9 of 10 patients with undetectable thyroid autoantibodies had transient hypothyroidism. These data indicate that: (i) AIIH may develop in patients with or without underlying thyroid abnormalities; (ii) RAIU is inappropriately elevated in many patients with AIIH; (iii) intrathyroidal iodine is not organified; (iv) serum thyroid autoantibodies represent a risk factor for the development of AIIH; (v) AIIH spontaneously remits after amiodarone withdrawal in patients without thyroid abnormalities, but may persist in patients with concomitant thyroid disorders, especially those with circulating thyroid autoantibodies.

Amiodarone: a common source of iodine-induced thyrotoxicosis.

Amiodarone, a iodine-rich drug widely used in the treatment of tachyarrhythmias, represents one of the most common sources of iodine-induced thyrotoxicosis. The data concerning 58 patients with amiodarone-iodine-induced thyrotoxicosis (AIIT) were analyzed in the present study. Prevalence of AIIT was higher in males than in females (M/F = 1.23/l). Thyrotoxicosis occurred either during treatment with or at various intervals after withdrawal of amiodarone. AIIT developed not only in patients with underlying thyroid disorders, but also in subjects with apparently normal thyroid gland. Classical symptoms of thyrotoxicosis were often lacking, the main clinical feature being a worsening of cardiac disorders. Biochemical diagnosis of AIIT was established by the finding of elevated serum total and free triiodothyronine levels, since elevated serum total and free thyroxine could be found also in euthyroid amiodarone-treated subjects. Twenty-four-hour thyroid radioiodine uptake was very low or undetectable in AIIT patients with apparently normal thyroid glands, while it was inappropriately elevated in patients with underlying thyroid disorders, despite iodine contamination. The role of autoimmune phenomena in the pathogenesis of AIIT appeared to be limited, because circulating thyroid autoantibodies were undetectable in AIIT patients without underlying thyroid disorders or with nodular goiter. Conversely, humoral features of thyroid autoimmunity were mostly found in AIIT patients with diffuse goiter. Treatment of AIIT appeared to be a difficult challenge. Among the 11 patients given no treatment, thyrotoxicosis spontaneously subsided in the 5 patients with apparently normal thyroid gland, whereas the 6 patients with nodular or diffuse goiter were still hyperthyroid 6-9 months after discontinuation of the drug. The administration of high doses (40 mg/day) of methimazole alone proved to be ineffective in most (14/16) patients given this treatment. Twenty-seven patients were treated by methimazole combined with potassium perchlorate (1 g/day). With one exception, euthyroidism was restored within 15-90 days in all cases with underlying thyroid abnormalities, and within 6-55 days in subjects with apparently normal thyroid gland. Thus, the combined treatment appears to be the most effective one, but, due to the potential toxicity of potassium perchlorate, it should be reserved to patients with severe thyrotoxicosis and should be carefully monitored.

Kinetics of electrophysiologic changes during oral loading of amiodarone and after withdrawal of amiodarone in the unsedated dog.

We examined the temporal kinetics of onset and offset of the cardiac electrophysiologic effects of orally administered amiodarone in chronically instrumented, unsedated adult dogs (n = 8). Right atrial (RA), atrioventricular nodal (AVN), and right ventricular (RV) effective refractory period (ERP), and AVN functional refractory period (FRP), were determined daily for 21 days during amiodarone loading (24 mg/kg/day) and for 21 days after cessation of amiodarone. Left ventricular (LV) ERP was assessed in four of eight animals. Group mean RA-ERP peaked and plateaued early during amiodarone loading (time to reach one-half observed peak change [t1/2 onset] = 1.2 +/- 0.5 days) and rapidly returned toward baseline after cessation of drug (decay time to one-half peak value [t1/2 offset] = 2.0 +/- 1.7 days). Group mean RV-ERP rose in a linear manner throughout the loading period (t1/2 onset = 9.3 +/- 2.1 days) and remained elevated after cessation of drug (t1/2 offset greater than 21.0 days). Group mean AVN-ERP and FRP exhibited temporal kinetics intermediate between those of the RA-ERP and RV-ERP, both during amiodarone loading and after cessation of the drug. Group mean LV-ERP onset kinetics (assessed in a limited number of animals, n = 4) appeared to differ from RV-ERP onset kinetics (t1/2 onset = 2.5 +/- 2.5 days), whereas LV-ERP and RV-ERP offset kinetics appeared similar (t1/2 offset greater than 21 days). In summary, our findings demonstrate that during oral loading, the temporal sequence of onset of amiodarone-induced electrophysiologic effects is site dependent. Similarly, after cessation of amiodarone, the persistence of drug-induced electrophysiologic effects is both variable and site dependent.

Pneumonitis with pleural and pericardial effusion and neuropathy during amiodarone therapy

A patient with sinuatrial disease and implanted pacemaker was treated with amiodarone (maximum dose 1000 mg, maintenance dose 800 mg daily) for 10 months, for control of supraventricular tachyarrhythmias. He developed pneumonitis, pleural and pericardial effusions, and a predominantly proximal motor neuropathy. Immediate but gradual improvement followed withdrawal of amiodarone and treatment with prednisolone. Review of this and previously reported cases indicates the need for early diagnosis of amiodarone pneumonitis, immediate withdrawal of amiodarone, and prompt but continued steroid therapy to ensure full recovery.

Amiodarone-treated patients with suppressed TSH test are at risk of thyrotoxicosis.

Therapeutic use of the potent antiarrhythmic drug amiodarone requires early detection of impending hyperthyroidism, a potentially life-threatening adverse reaction in cardiac patients. Since amiodarone inhibits peripheral conversion of thyroxine (T4) to triiodothyronine (T3), serum T4 and T3 levels become unreliable parameters of thyroid function. In 44 patients treated with amiodarone for a median period of 7.3 months, up to seven TRH-TSH tests were performed. The TSH response to TRH was normal in 23 patients, partially suppressed in eight, totally suppressed in eight and overshooting in five patients. Two of the eight patients with suppressed TRH-TSH tests were clinically hyperthyroid, in four others thyrotoxicosis developed within 1 to 2 1/2 months after the first observation of a suppressed TSH response, while two patients remained euthyroid. In all patients with negative TRH-TSH tests. TSH response to TRH returned to normal between 2 and 29 months after withdrawal of amiodarone. We conclude that the TRH-TSH test, repeated at intervals, is a reliable tool for assessing thyroid function in patients on long-term treatment with amiodarone. Patients with a suppressed response under amiodarone therapy are at risk of developing thyrotoxicosis. Normalization of the TSH response indicates that this risk is over.

Polymorphous Ventricular Tachycardia Associated with a Marked Prolongation of the Q‐T Interval Induced by Amiodarone

We report the case of a patient who developed a life-threatening polymorphous ventricular tachycardia ( PVT ) after six weeks of treatment with amiodarone. The Q-T interval was markedly prolonged at 0.86 second. The drug induction of PVT was strongly suggested by the fact that PVT resolved four days after withdrawal of amiodarone when the Q-T interval had shortened to 0.60 second; the arrhythmia has not recurred in the nine months of follow-up since then. Amiodarone, though a very effective antiarrhythmic agent, may induce serious PVT .