ABSTRACT
A 65-year-old man with arterial hypertension received oral treatment with Ketanserin, a new drug, during a period of five months. He developed marked QT interval prolongation and have several Stokes-Adams attacks. A Holter recording obtained during one of these episodes showed torsade de pointes ventricular tachycardia. The arrhythmias occurred during maximum QT interval prolongation. The correlation between Ketanserin and QT interval prolongation was evaluated by using several Holter studies during administration and withdrawal of the drug. The effect of Ketanserin on the QTc interval was analyzed retrospectively in six patients who had been taking the drug orally. Following a period of four to eight months, the QTc interval was prolonged by the drug (5 to 31%, mean 17%) in five patients. We conclude that torsade de pointes is a potential hazard of long-term treatment with Ketanserin.
Subject(s)
Arrhythmias, Cardiac/chemically induced , Ketanserin/adverse effects , Long QT Syndrome/chemically induced , Tachycardia/chemically induced , Adult , Aged , Electrocardiography , Female , Humans , Male , Middle AgedABSTRACT
We studied 12 patients with ventricular parasystole in whom pacemaker activity could be modulated by nonparasystolic beats (NPBs). In six patients (group 1) in whom the intrinsic parasystolic cycle length (XX interval) was obtained without interposed NPBs, we found that NPBs falling during the first half of the cycle prolonged the XRX interval (containing one NPB) and that NPBs falling during the second half of the cycle abbreviated the XRX interval; both effects were maximal when NPBs fell close to the middle of the cycle and were separated by a reversal point. However, because of mutual interference between parasystolic beats and NPBs, only 13.2-43.4% of the parasystolic cycle could be effectively scanned. We also found that the XRX and RX intervals were linearly related. This relationship served to establish that in six patients in whom the XX interval was not obtained (group 2), modulation showed a similar behavior, although neither the reversal point nor the sense of the modulation could be determined. In this report, we suggest diagnostic criteria of parasystolic modulation.
Subject(s)
Arrhythmias, Cardiac/physiopathology , Arrhythmias, Cardiac/diagnosis , Electrocardiography , HumansABSTRACT
Exit block from a parasystolic focus is recognized when automatic discharges fail to become manifest during the excitable phase of the ventricular cycle. In the present study, an apparently complete exit block and a persistently concealed ventricular parasystole (VP) resulted from an exit refractory period (ExRP) longer than the sinus cycle length. Slowing of the heart rate caused the concealed VP to become apparent in the form of ventricular escapes of variable coupling and as an idioventricular rhythm that failed to show initial "warming up." These features reflect the fact that the automatic focus is protected from activity of the sinus impulses, which, however, can induce a prolonged ExRP. Seven cases of concealed VP are discussed. In two, concealment occurred spontaneously during the follow-up of a typical VP; in three, it was provoked by conduction-depressing drugs; and in two, ventricular escapes of varying coupling were shown to represent the manifestation of a concealed and previously unrecognized VP. In two cases, isoproterenol caused reappearance of typical VP, probably through a shortening of the ExRP. While isoproterenol may be useful for uncovering a concealed VP, conduction-depressing drugs may be used to provoke or increase exit block. Total extinction of the VP seemed to occur in two patients during follow-up studies.
