Adenosine appears to be effective and safe for the pre-hospital treatment of PSVT.

Clinical, angiographic, echocardiographic and electrophysiologic data were examined in 101 patients with a history of sustained ventricular arrhythmia not associated with acute myocardial infarction. These patients included 66 survivors of out of hospital cardiac arrest and 35 patients presenting with hemodynamically well tolerated sustained ventricular tachycardia. On univariate analysis, patients in the cardiac arrest group had a lower incidence of previous myocardial infarction and left ventricular aneurysm and a higher ejection fraction compared with the ventricular tachycardia group. During electrophysiologic testing, the arrhythmia induced in the patients in the cardiac arrest group was fast and polymorphic and frequently degenerated into ventricular fibrillation. In contrast, in the ventricular tachycardia group, a slower, monomorphic and hemodynamically well tolerated ventricular tachycardia was commonly induced. On multivariate analysis, a polymorphic pattern of the induced ventricular arrhythmia was the only independent variable that distinguished the survivors of cardiac arrest from those presenting with sustained ventricular tachycardia. These results suggest that 1) the survivors of cardiac arrest and patients presenting with sustained well tolerated ventricular tachycardia are clinically distinct groups; and 2) the polymorphic tachycardia induced during programmed electrical stimulation in the survivors of cardiac arrest may indicate an unstable tachycardia mechanism. This may explain why these patients present with ventricular fibrillation and cardiac arrest, whereas others present with hemodynamically stable ventricular tachycardia.

The effectiveness and safety of oral flecainide for suppression of complex ventricular arrhythmias was tested in nine patients in a short-term (4 wk), single-blind, placebo-controlled experiment. The prevalence of multiform premature ventricular complexes (PVCs), couplets and nonsustained ventricular tachycardia (VT) (less than 3 PVCs at rate less than 100/min) was determined by 48-hr Holter monitoring on placebo and flecainide (200 to 300 mg b.i.d.) therapy. Multiform PVCs/hr were reduced by 96% in eight of nine patients (P less than 0.001). Couplets per 24-hr period were suppressed entirely in six patients (P less than 0.001). Couplets per 24-hr period were suppressed entirely in six patients (P less than 0.001) and reduced by 92% in the remaining two patients. VT runs per 24 hr were abolished in six patients (P less than 0.02) and reduced by 91% in one. As a group the frequency of PVCs per hour, couplets per 24 hr and VT per 24 hr was reduced by 96% (P less than 0.01) over than in the preceding placebo period. Flecainide (P less than 0.02) slowed heart rate by 10% and prolonged PR, QRS, and QTc intervals by 31%, 47% and 6%. No hematologic, hepatic, or renal abnormalities were found. Side effects were mild, transient, and central nervous system related; blurring of vision was the most frequent effect and was reported in four patients.

Bidirectional tachycardia is an uncommon and unique arrhythmia. It typically occurs in patients with digitalis toxicity, but it can also be associated with other causes. There has been controversy regarding the origin and the mechanism of bidirectional tachycardia. Treatment of bidirectional tachycardia involves the correction of reversible factors and the use of some antiarrhythmic medication.

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Eighty-two patients with drug-resistant ventricular tachycardia or fibrillation were treated with oral tocainide. Treatment in 54 patients, all with inducible ventricular tachycardia or fibrillation at baseline electrophysiologic testing, was based on the results of invasive electrophysiologic testing. Twenty-eight additional patients with frequent spontaneous ventricular tachycardia or no inducible arrhythmia during electrophysiologic testing were treated on the basis of the findings of electrocardiographic (ECG) Holter monitoring. Tocainide was effective in 7 (13%) and partially effective in 5 (8%) of the 54 patients in the electrophysiologic study group and was effective in 17 (61%) of the 28 patients in the ECG monitoring group. History of previous myocardial infarction and failure of response to lidocaine correlated with failure to respond to tocainide. Side effects were common both during initial therapy and during long-term treatment and necessitated discontinuation of tocainide therapy in 17% of the patients. At a mean follow-up period of 14 months, 13 patients are still receiving tocainide and are arrhythmia-free. In conclusion, the usefulness of oral tocainide in the management of drug-refractory sustained ventricular tachycardia or fibrillation is limited because of its low effectiveness and frequent side effects.

Introduction: Noncompaction cardiomyopathy is a rare, primary, genetic cardiomyopathy that results from intrauterine arrest of the compaction process. It commonly involves the apical area of the left ventricle, and uncommonly involves the right ventricle. Case Report: A 45yearold male presented to the hospital for heart failure. He was started on anticoagulation for the apical thrombus and later he suffered cerebrovascular accident. On careful evaluation he was found to have ventricular noncompaction both in right and left ventricles. Conclusion: Noncompaction cardiomyopathy should be considered in all refractory cases of heart failure. Anticoagulation is crucial in patients with decreased systolic function and atrial fibrillation.