Polymorphous Ventricular Tachycardia and Atrioventricular Block

Abstract

Nine patients are presented who had polymorphous ventricular tachycardia (PMVT) occurring during atrioventricular (AV) block. There were five men and four women with a mean age of 80 +/- 9 years. Five patients had organic heart disease and the remaining four had primary conduction disease (bundle branch block). AV block was complete in four patients (2:1 in three, and paroxysmal in two). The mean ventricular cycle length (of the AV block rhythm) was 1567 +/- 203 ms. The mean QT interval was 0.64 +/- 0.09 s and the mean QTc was 0.51 +/- 0.06 s. When compared to a similar control group with AV block but without PMVT, the ventricular cycle length was similar but the QT and QTc were significantly longer. PMVT was usually of short duration (eight beats to 12 s) and in seven of these nine patients, frequent premature ventricular beats (PVBs) were recorded at various times from the occurrence of PMVT. This is in contrast to the control patients in whom PVBs were detected in one patient only. In conclusion, patients with AV block who develop PMVT usually have longer QT intervals and have detectable PVBs on routine ECGs, unlike similar patients with AV block but without PMVT. In a patient with AV block, a QT interval above 0.60 s and PVBs on the ECG seem to indicate an increased risk for the development of PMVT.

Drug-Induced Long QT Syndrome

“…Although this association was first described over 40 years ago (Dessertenne, 1966), remarkably little is known about the ECG predictors of this potentially lethal complication of bradyarrhythmias (Strasberg et al, 1986;Kurita et al, 1992). Indeed, the "short-long-short" series of cycles before TdP discussed below is so characteristic of diLQTS that lack of a "pause" before onset calls into question the diagnosis.…”

Long QT Syndrome Complicating Atrioventricular Block

“…18 Yet, during AVB, different patients develop different degrees of QT prolongation in response to similar degrees of bradycardia, 8 and it is the magnitude of this QT prolongation in response to bradycardia, rather than the bradycardia per se, that determines the risk of TdP. [6][7][8] Here, we describe how cardiac memory plays a critical role in promoting QT prolongation.…”

“…2 Yet, despite extensive experimental data explaining the pathophysiology of QT prolongation in animal models of AVB, [3][4][5] current understanding of predictors of TdP in humans is limited. [6][7][8] Although it is well established that QT prolongation, [6][7][8] particularly when accompanied by T-wave abnormalities, 8 is a requisite for TdP during AVB, we do not know why some patients develop more QT prolongation than others, despite similar bradycardia. 8 …”

Atrio-Ventricular Block-Induced Torsades de Pointes: An Update

“…Kurita et al have reported that patients with bradycardia-induced torsades de pointes have abnormally long QT intervals at slow heart rates, compared with patients with bradycardia but no tachyarrhythmia (Kurita, 1992). Strasberg et al compared patients with atrioventricular block with torsades de pointes to those without torsades de pointes, and mentioned that the QT interval in patients with torsades de pointes was longer than in those without torsades de pointes, whereas heart rate and QRS interval during the escape rhythm were not significantly different (Strasberg, 1986). Moreover, they reported that QT interval above 600 ms and premature ventricular beats on electrocardiogram appear to indicate an increased risk for the development of polymorphic ventricular tachycardia in a patient with atrio-ventricular block.…”