Harry A. Kopelman

Irrigated Radiofrequency Catheter Ablation Guided by Electroanatomic Mapping for Recurrent Ventricular Tachycardia After Myocardial Infarction The Multicenter Thermocool Ventricular Tachycardia Ablation Trial

Background— Recurrent ventricular tachycardia (VT) is an important cause of mortality and morbidity late after myocardial infarction. With frequent use of implantable cardioverter-defibrillators, these VTs are often poorly defined and not tolerated for mapping, factors previously viewed as relative contraindications to ablation. This observational multicenter study assessed the outcome of VT ablation with a saline-irrigated catheter combined with an electroanatomic mapping system. Methods and Results— Two hundred thirty-one patients (median LV ejection fraction, 0.25; heart failure in 62%) with recurrent episodes of monomorphic VT (median, 11 in the preceding 6 months) caused by prior myocardial infarction were enrolled. All inducible monomorphic VTs with a rate approximating or slower than any spontaneous VTs were targeted for ablation guided by electroanatomic mapping during sinus rhythm and/or VT. Patients were not excluded for multiple VTs (median, 3 per patient) or unmappable VT (present in 69% of patients). Ablation abolished all inducible VTs in 49% of patients. The primary end point of freedom from recurrent incessant VT or intermittent VT after 6 months of follow-up was achieved for 123 patients (53%). In 142 patients with implantable cardioverter-defibrillators before and after ablation for intermittent VT who survived 6 months, VT episodes were reduced from a median of 11.5 to 0 (P<0.0001). The 1-year mortality rate was 18%, with 72.5% of deaths attributed to ventricular arrhythmias or heart failure. The procedure mortality rate was 3%, with no strokes. Conclusions— Catheter ablation is a reasonable option to reduce episodes of recurrent VT in patients with prior myocardial infarction, even when multiple and/or unmappable VTs are present. This population remains at high risk for death, warranting surveillance and further study.

Randomized, Double-Blind Comparison of Intravenous Amiodarone and Bretylium in the Treatment of Patients With Recurrent, Hemodynamically Destabilizing Ventricular Tachycardia or Fibrillation

Background After several days of loading, oral amiodarone, a class III antiarrhythmic, is highly effective in controlling ventricular tachyarrhythmias; however, the delay in onset of activity is not acceptable in patients with immediately life-threatening arrhythmias. Therefore, an intravenous form of therapy is advantageous. This study was designed to compare the safety and efficacy of a high and a low dose of intravenous amiodarone with bretylium, the only approved class III antiarrhythmic agent. Methods and Results A total of 302 patients with refractory, hemodynamically destabilizing ventricular tachycardia or ventricular fibrillation were enrolled in this double-blind trial at 82 medical centers in the United States. They were randomly assigned to therapy with intravenous bretylium (4.7 g) or intravenous amiodarone administered in a high dose (1.8 g) or a low dose (0.2 g). The primary analysis, arrhythmia event rate during the first 48 hours of therapy, showed comparable efficacy between the bretyliu...

Dose-ranging Study of Intravenous Amiodarone in Patients With Life-threatening Ventricular Tachyarrhythmias

Background Oral amiodarone effectively suppresses ventricular arrhythmias; however, full activity may take days or weeks. In patients with frequent, life-threatening ventricular arrhythmias, this delay is not acceptable. Thus, in these patients, the speed and dosing accuracy of an intravenous formulation would be beneficial. The goal of this study was to demonstrate the efficacy of intravenous amiodarone in patients with refractory, recurrent hemodynamically destabilizing ventricular tachycardia or ventricular fibrillation by determining a dose response among three regimens. Methods and Results A total of 342 patients were enrolled at 46 medical centers in the United States. Patients received one of three randomized, double-blind dose regimens delivering 125, 500, or 1000 mg during the first 24 hours. Supplemental infusions (150 mg) of intravenous amiodarone could be given to treat breakthrough ventricular arrhythmias. The key efficacy end points were the arrhythmia event rate, time to first arrhythmic ev...

Reduction of infarct size with intracoronary perfluorochemical in a canine preparation of reperfusion.

The effect of low-dose (15 ml/kg) intracoronary perfluorochemical (Fluosol-DA) on infarct size, regional myocardial blood flow, and ventricular function was studied in 20 anesthetized closed-chest dogs subjected to 11/2 hr of proximal left anterior descending occlusion. In this preparation reperfusion was simulated with fibrinolytic therapy. The animals were randomly assigned one of two treatment groups and given 15 ml/kg of either oxygenated intracoronary perfluorochemical (n = 9) or saline (n = 11). Contrast ventriculograms were obtained at baseline, 1 hr after occlusion, and at 24 hr after reperfusion and were analyzed with a radial fractional shortening method. Regional myocardial blood flow was measured with radioactive microspheres. At 24 hr the area at risk was defined in vivo with monastryl blue staining and the area of necrosis was estimated after incubation of left ventricular slices with triphenyltetrazolium chloride. No significant changes were noted in heart rate, blood pressure, pulmonary capillary wedge pressure, or dP/dt during the experimental protocol. Infarct size was significantly reduced (p less than .02) in the perfluorochemical-treated group, both when expressed as a percentage of the total left ventricular mass (7.9 +/- 1.7% vs 14.7 +/- 2.5%) and as a percentage of the area at risk (20.1 +/- 5.0% vs 46.8 +/- 8.5%). This was associated with significant improvement in fractional shortening in the jeopardized zone at 24 hr after reperfusion. Although endocardial blood flow was significantly greater in the central ischemic zone and lateral region at risk immediately after reperfusion in the perfluorochemical-treated group, no difference was found 1 hr after reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Determinants of left ventricular aneurysm formation after anterior myocardial infarction: a clinical and angiographic study.

To determine factors involved in left ventricular aneurysm formation after transmural anterior myocardial infarction, 79 patients with a first myocardial infarction who underwent cardiac catheterization within 6 months of infarction were evaluated. Patients who had received thrombolytic therapy were excluded. Patients were divided into four groups depending on the status of the left anterior descending artery and the presence or absence of a left ventricular aneurysm: Group I (n = 25): aneurysm with occluded left anterior descending artery; Group II (n = 27): no aneurysm and occluded left anterior descending artery; Group III (n = 23): no aneurysm and patent left anterior descending artery; and Group IV (n = 4): aneurysm with patent left anterior descending artery. Single vessel disease was more common in Group I (aneurysm) compared with Groups II and III (no aneurysm) (chi 2(4) = 12.8; probability value equal to 0.012). Collateral blood supply in the presence of an occluded left anterior descending artery was significantly less in Group I (aneurysm) compared with Group II (no aneurysm) (0.9 versus 2.4, p less than 0.001). The extent of coronary artery disease and collateral blood supply in Groups I and II were directly related (p = 0.012). Neither age, sex nor risk factors for coronary disease correlated with aneurysm formation. At a mean follow-up of 48 months, no differences were observed in the incidence of recurrent angina, new myocardial infarction, embolic events or sudden death. More patients in Group II underwent coronary artery bypass surgery. Total occlusion of the left anterior descending artery in association with inherent poor collateral blood supply is a significant determinant of aneurysm formation after anterior myocardial infarction. Multivessel disease with either good collateral circulation or a patent left anterior descending artery is uncommonly associated with the development of left ventricular aneurysm.

Electrocardiographic changes associated with isolated right ventricular infarction

Isolated infarction of the right ventricle is an extremely rare entity. A patient is described with diffuse interstitial lung disease who developed ST segment elevation in inferior and anterior leads on a routine electrocardiogram and at autopsy was found to have an isolated right ventricular infarct involving approximately 70% of the right ventricular circumference without involvement of the left ventricle and septum. This case illustrates that isolated right ventricular infarction in the presence of cor pulmonale and right ventricular hypertrophy can produce an injury current in the limb and precordial leads of the electrocardiogram which mimics that seen in typical transmural infarction of the left ventricle.

Right ventricular myocardial infarction in patients with chronic lung disease: possible role of right ventricular hypertrophy.

To determine the relation between right ventricular hypertrophy and right ventricular myocardial infarction in patients with chronic lung disease, the records of 28 patients with chronic lung disease, inferior myocardial infarction and significant coronary artery disease (group I) and 20 patients with right ventricular hypertrophy, chronic lung disease without inferior myocardial infarction or significant coronary artery disease (group II) were reviewed. Chronic lung disease was diagnosed by clinical criteria, chest radiographs and pulmonary function tests. All patients had postmortem examinations. Patients in group I were classified into two subgroups: group Ia (without right ventricular hypertrophy) and group Ib (with right ventricular hypertrophy). Right ventricular wall thickness was 3.3 mm ± 0.5 in group la, 6.0 mm ± 1.1 in group Ib and 8.8 mm ± 2.4 in group II (group Ia versus Ib, p Patients with right ventricular hypertrophy as a result of chronic lung disease are prone to right ventricular myocardial infarction in the setting of inferior myocardial infarction. Isolated right ventricular myocardial infarction may occur in patients with chronic lung disease, right ventricular hypertrophy and insignificant coronary artery disease. Both increased myocardial oxygen demand and a decreased supply may play a role in this relation.

Cardiac sarcoidosis with sudden death: Treatment with the automatic implantable cardioverter defibrillator

variability found in our stroke distance measurements and was equally diagnostic.* However, the Exerdop equipment allows relatively inexperienced operators to obtain good signals quickly and the dedicated software allows rapid analysis and diagnosis. Thus this method should provide a powerful adjunct to the conventional methods of the diagnosis of broad complex tachycardias, especially in an emergency. It appears to be specific in diagnosing ventricular tachycardia, although it cannot distinguish ventricular tachycardia with 1: 1 retrograde conduction from supraventricular tachycardia.

Electrophysiologic effects of intravenous and oral sotalol for sustained ventricular tachycardia secondary to coronary artery disease

The electrophysiologic effects of intravenous sotalol (1.5 mg/kg load followed by 0.008 mg/kg maintenance, mean dose 150 +/- 23 mg) and oral sotalol (mean dose 583 +/- 204 mg daily) were prospectively evaluated in 16 patients undergoing electrophysiologic evaluation for sustained ventricular tachycardia (VT) secondary to coronary artery disease. Electrocardiographic intervals, indexes of sinus and atrioventricular node function and indexes of atrial and ventricular function were assessed. Inducibility or noninducibility of sustained VT and characteristics of the induced arrhythmia were also evaluated. Intravenous and oral sotalol exerted similar beta-blocking effects, which included significant prolongation of sinus cycle length (baseline 820 +/- 165 ms, intravenous sotalol 1,077 +/- 206 ms, oral sotalol 1,141 +/- 306 ms), AH interval (baseline 126 +/- 43, intravenous sotalol 169 +/- 42, oral sotalol 197 +/- 55 ms) and Wenckebach cycle length (baseline 375 +/- 70, intravenous sotalol 460 +/- 84, oral sotalol 449 +/- 68 ms). Both intravenous and oral sotalol also prolonged repolarization and refractoriness including significant increases in QT interval (baseline 338 +/- 47, intravenous sotalol 417 +/- 35, oral sotalol 450 +/- 70 ms), atrial effective refractory period (baseline 240 +/- 38, intravenous sotalol 330 +/- 71, oral sotalol 299 +/- 26 ms) and right ventricular effective refractory period (baseline 241 +/- 16, intravenous sotalol 289 +/- 35, oral sotalol 291 +/- 22 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Right ventricular hypertrophy is an important determinant of right ventricular infarction complicating acute inferior left ventricular infarction

To explore the role of right ventricular hypertrophy and chronic obstructive pulmonary disease in the pathogenesis of right ventricular infarction, 27 consecutive patients with a first inferior left ventricular infarction were prospectively studied. Right ventricular infarction was diagnosed using established hemodynamic criteria. Right ventricular hypertrophy was defined as right ventricular free wall thickness greater than or equal to 5 mm. Patients were classified into two groups: Group I patients with right ventricular infarction (n = 15), and Group II patients without right ventricular infarction (n = 12). The ratio of forced expiratory volume over forced vital capacity (FEV1/FVC) and forced expiratory flow between 25 and 75% expired volume (FEF) as a percent of predicted values were significantly reduced in Group I versus Group II (90 +/- 5 versus 105 +/- 6% and 63 +/- 13 versus 103 +/- 15%, respectively; p less than 0.05). This was associated with increased right ventricular wall thickness (Group I 5.5 +/- 0.3 mm versus Group II 3.9 +/- 0.2 mm, p less than 0.001). Multiple logistic regression analysis demonstrated that right ventricular wall thickness was the strongest predictor of right ventricular infarction (p less than 0.0005). No significant difference was found in the site of right coronary occlusion, collateral blood supply or extent of coronary artery disease between the two groups. These findings suggest that right ventricular hypertrophy predisposes patients with acute inferior myocardial infarction to right ventricular infarction independent of the site or extent of coronary artery disease.