Author + information
- Karl Mischke, MD⁎ (, )
- Markus Zarse, MD,
- Thomas Schimpf, MD,
- Martina Baranowski, MD,
- Christian Knackstedt, MD,
- Jurgita Plisiene, MD and
- Patrick Schauerte, MD
- ↵⁎Department of Cardiology, RWTH Aachen University, 52074 Aachen, Germany
To the Editor:Despite great efforts and success in terminating ventricular tachycardia (VT) by methods like cardioversion and overdrive stimulation, there are situations in which VTs are ongoing (incessant VT) despite aggressive therapy. We assessed a stimulation technique for hemodynamic stabilization during VT.
A ventricular extrasystole occurring shortly after the effective ventricular refractory period generates a postextrasystolic pause and leads to an augmentation of the arterial pressure wave initiated by the next spontaneous beat. This phenomenon was originally described by Langendorff (1). We speculated that single premature ventricular beats during an ongoing VT might have a similar effect. The premature beats would be introduced with coupling intervals longer than the ventricular refractory period but shorter than the VT cycle length. The subsequent postextrasystolic pause should prolong the diastolic filling time, resulting in an augmented pressure wave initiated by the next spontaneous VT beat. Postextrasystolic potentiation of contractile force should contribute to hemodynamic stabilization during VT.
In 22 patients (70 ± 8 years, ejection fraction 38 ± 14%) with a history of spontaneous VT (n = 21) or ventricular fibrillation (VF) (n = 1) and inducible sustained VT during an electrophysiological study (n = 16) or ablation procedure (n = 6), paired ventricular stimulation (PST) was delivered. Patients suffered from ischemic heart disease (n = 17), dilated cardiomyopathy (n = 3), or idiopathic VT (n = 2). Programmed ventricular stimulation was performed with up to three extrastimuli. Arterial blood pressure was recorded via a femoral sheath. If sustained VT occurred, PST was delivered with ventricular extrastimuli from the right ventricular apex coupled to each spontaneous VT beat at four times the diastolic pacing threshold. The coupling interval was decreased by 10 ms until capture was lost. Ventricular capture was confirmed by changes of the QRS morphology in the surface electrocardiogram. The shortest coupling interval at which conducted ventricular beats occurred was chosen for hemodynamic evaluation because it has been shown to produce the largest postextrasystolic potentiation (2). The VT was then terminated by antitachycardiac pacing. Thereafter, VT was reinduced and arterial pressure was recorded during 30-s periods with and without PST. Pressure measurements were averaged for the respective time intervals. For individual comparisons, paired Student ttests were applied.
The mean VT cycle length was 402 ± 92 ms, with fast VTs (>170/min) being present in eight patients. Paired stimuli were introduced during VT at a coupling interval of 241 ± 36 ms. The resulting postpacing interval was 539 ± 125 ms.
Figure 1shows the hemodynamic benefit during PST. The PST significantly increased (paired ttest) systolic, mean, and diastolic pressure during VT. Overall, a 30 ± 17% increase of systolic and 17 ± 13% increase of mean arterial pressure was obtained (Fig. 2).The effect started almost immediately after PST initiation and declined rapidly after PST cessation. No correlation (Pearson) between pressure increase and VT cycle length or ejection fraction was found. In four patients, PST during VT was maintained for 1 h without loss of the positive inotropic effect.
Slowing of the pulse rate during VT by paired stimulation in dogs was described by Braunwald et al. (3) in 1964. Coupled ventricular stimulation during sinus rhythm has also been suggested as a means to increase ventricular inotropy in heart failure (3). Yamada et al. (4) showed in an animal model that coupled pacing might decrease the ventricular rate during atrial fibrillation and improve cardiac efficiency. Despite these mostly experimental findings, PST has never gained clinical application because of the increased oxygen demand and possible arrhythmogenic effects. However, proarrhythmia did not occur during PST in the present study. This is remarkable in a patient population with reduced left ventricular function and may be attributable to the fact that the clinical arrhythmia was VT in all but one patient. In addition, six patients were hospitalized for incessant VT, which typically persists rather stably for a long time without degenerating into VF.
Each paired stimulus produced a mechanical contraction. The magnitude of left ventricular pressure increase, however, was so little that the pressure level either did not or hardly exceeded aortic pressure. Thus, in some patients, the pressure curve did not show any systolic wave associated with the paired stimulus, whereas in others a very small systolic “hump” was present. In addition, analysis of the 12-lead electrogram showed that the tail end of the paced QRS complex sometimes fused with the next VT beat, especially when longer coupling intervals were applied. The supposed (small) re-entrant circuit of the VT origin, however, could not excite most of the ventricular tissue as this was still refractory because of the previous stimulus.
With regard to possible mechanisms, a prolongation of the diastolic interval may be operative: the postpacing cycle length was longer than the VT cycle length, thereby prolonging the ventricular filling time and augmenting the pressure wave elicited by the next VT beat. However, other factors are likely to contribute: when comparing ventricular pacing with ventricular pacing at higher rates but with interpolated paired stimuli so that both stimulation algorithms result in the same rate of arterial pressure waves, paired stimulation increased systolic pressure (3). In addition, after termination of coupled stimulation in dogs (3) and in our study the pressure effect persisted for several beats. This may be because of an elevated myoplasmic calcium concentration contributing to a postextrasystolic potentiation of contractile force, probably attributable to an increased calcium release from the sarcoplasmic reticulum (5).
Possible limitation of PST may include an increase in myocardial oxygen consumption. A supposedly higher oxygen demand, however, may be compensated by an increased coronary perfusion pressure during PST.
We did not evaluate cardiac output, thus we could not assess any potential contribution of the peripheral vascular resistance to the hemodynamic effect of PST. Because most patients reported subjective improvement of symptoms (dizziness, shortness of breath) during PST, this may be taken as some evidence for an improved cardiac output and clinical status.
We do not know whether PST will be effective and safe during spontaneous VT or for longer than 1 h. Although the mean cycle length of induced VTs was rather long, PST was also effective in eight patients with fast VTs. Still, a major challenge of the algorithm if applied during fast incessant VT will be to prevent VT detection breakdown because of necessary blanking periods.
In conclusion, PST during VT significantly augments systolic and mean arterial blood pressure. In patients with a high risk of VT, short-term PST up to 1 h did not accelerate VT or induce VF. The algorithm may help to hemodynamically stabilize patients with refractory or incessant VT.
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