Torsades de Pointes: Occurrence in myocardial ischaemia as a separate entity. Multiform ventricular tachycardia or not?

Torsades de pointes (Tdp) were evaluated with respect to aetiology, morphology and response to treatment in 16 patients admitted to the CCU. Analysis was based on monitor strip charts and conventional 12 lead ECGs. Underlying disease was total AV block in four patients, acute myocardial ischaemia in nine patients, with acute ventricular aneurysms in four patients; one patient had chronic ventricular aneurysm, one idiopathic hypokalaemia, and one was on quinidine therapy. Heart rate was less than 30 beats min−1 in patients with total AV block and above 90 beats min−1 in six out of 12 patients with basic sinus rhythm. QT prolongation was not present in six patients with acute myocardial ischaemia. Tdp were always initiated by PVCs either falling on the downslope of the T wave of the preceding normal beat or shortly after it in the range of a U wave. Coupling intervals in a run of Tdp were variable in most patients, with an increase in eight patients and a decrease in five patients. In patients with total AV block Tdp could be controlled by increasing the heart rate through pacemaker stimulation. Patients in sinus rhythm (heart rate above 60 beats min−1) received antiarrhythmic drugs: propafenon was effective in 80% (eight out often patients). Ten patients were long-term survivors. Outcome of the acute stage of the disease seemed to be determined by underlying myocardial function. Differentiation between Tdp and multiform ventriadar tachycardia (i.e. VT with torsion of QRS complexes occurring in acute myocardial ischaemia) seems unnecessary to us, since morphological features were similar in both groups with the exception of QT prolongation, which was absent in six out of nine patients with acute myocardial ischaemia. Propafenon was active in patients without as well as with QT prolongation.