Mode of initiation and clinical significance of malignant rapid ventricular arrhythmias

Figure 1. Polymorphic ventricular tachycardia was initiated by premature ventricular contraction (↓) with short coupling interval (300 ms), which subsequently degenerated into ventricular fibrillation in a patient with chronic renal failure. The Q-T interval is normally 320 ms. Short-long-short sequences before polymorphic ventricular tachycardia precipitation were not observed.

Figure 2. Polymorphic ventricular tachycardia was initiated by premature ventricular contraction (↓) with very short coupling interval (240 ms) in a patient with no evidence of ischemic or structural cardiac disease. Each premature ventricular contraction fell on the ascending limb of the preceding sinus T wave. The Q-T interval is normal. Short-long-short sequences before polymorphic ventricular tachycardia precipitation were not observed.

Figure 3. Polymorphic ventricular tachycardia was initiated by premature ventricular contraction (↓) with short coupling interval (300 ms), which subsequently degenerated into ventricular fibrillation in a patient with Brugada syndrome. Each premature ventricular contraction fell on the peak of the preceding sinus T wave. Short-long-short sequences (—) before polymorphic ventricular tachycardia precipitation were always observed. The Q-T interval is normal.

Figure 4. Torsade de pointes was initiated by premature ventricular contraction (↓) with long coupling interval (600 ms), which subsequently degenerated into ventricular fibrillation in a patient with coronary heart disease, heart failure, and hypokalemia. Short-long-short sequences (—) before polymorphic ventricular tachycardia precipitation were always observed. The Q-T interval was significantly prolonged (620 ms).