Unusual Forms of Severe Ventricular Tachyarrhythmias: Their Relationships with the QT Interval and the Vago-Sympathetic Balance

Cardiac effects of sodium stibogluconate.

“…In this study of sodium stibogluconate the drug did not appear to influence PR interval, QRS duration or R wave height. In agreement with others however (Dempsey, 1965;Kaplan et al, 1978) (Coumel et al, 1980;Schwartz, 1980). This is of great importance during antimonial therapy as QT prolongation, malignant ventricular arrhythmias and even sudden death have been reported (Honey, 1960;Davis, 1961;Sommers & Rosanelli, 1962;Surawicz, 1970;Stemmer, 1976).…”

Malignant Purkinje ectopy induced by sodium channel blockers

“…21 ScPVCs were previously reported as an R-on-T phenomenon often initiating VF and described with different names in patients with apparently normal hearts. [12][13][14][15][16] The role of ScPVCs as a specific subset of IVF has been reported with an incidence varying from 6.6% 16 to 20%, 27 depending on the respective inclusion criteria. This arrhythmia was demonstrated to be responsive to quinidine.…”

“…5 Over the past decade, specific subtypes of IVF have been described. These were based on phenotypic characterization of the arrhythmia itself, for example, VF initiated by shortcoupled premature ventricular complexes (ScPVCs) [12][13][14][15][16] or based on the presence of subclinical myocardial alterations. 17 ScPVCs originating from the Purkinje system are the most common triggers of IVF and an effective ablation target for preventing VF recurrence.…”

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

“…Clinically, many authors stressed early afterdepolarizations in the genesis of torsade de pointes, because the first beat of such an episode usually interrupts terminal repolarization of a markedly prolonged QT interval when the heart rate slows [49,107]. However, subsequent experimental and clinical studies in patients with proarrhythmic QT prolongation favored both mechanism--dispersion of repolarization and early afterdepolarizations--to be a common cause of proarrhythmia due to the following criteria [225]: the initiating effect of a low heart rate [151,226], the effect of programmed stimulation [166], suppression by rapid pacing [119], the role of R-on-T phenomenon [227], the effect of hypokalemia [225], the effect of autonomic tone [41], or spontaneous termination of proarrhythmia [120].…”