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Right-to-left ventricular diastolic delay in chronic thromboembolic pulmonary hypertension is associated with activation delay and action potential prolongation in right ventricle
Circulation: Arrhythmia and Electrophysiology, 08/06/09

Hardziyenka M et al. – Additive effects of electrophysiologic changes in right ventricle (RV), notably, conduction slowing and action potential prolongation, assessed by epicardial activation-recovery interval, contribute to diastolic interventricular delay in chronic thromboembolic hypertension (CTEPH) pts.

Methods

Study of whether RV electrophysiologic remodeling, notably, conduction slowing and action potential prolongation, contribute to loss of synchrony between left ventricle (LV) and RV
Epicardial mapping during pulmonary endarterectomy in 26 CTEPH pts
Comparison of findings with clinical, hemodynamic, and echocardiographic variables
Consecutive placement of a multi-electrode grid on epicardium of RV free wall and LV lateral wall
Correspondence of regions to RV and LV areas of echocardiographic Doppler sample volumes to measure RV-to-LV diastolic interventricular delay (DIVD)

Results

RV and LV epicardial action potential duration was assessed by measuring activation-recovery interval (ARI)
Onset of diastolic relaxation of RV free wall vs LV lateral wall (DIVD): delayed by 38 ± 31 ms in CTEPH pts vs -12 ± 13 ms in controls
In CTEPH pts, RV completed electrical activation later than LV and epicardial action potential duration by ARI measurement, was longer in RV free wall than in LV lateral wall

Exclusive Author Commentary
Hardziyenka M, 08/07/09

Recent studies in patients with chronic thromboembolic pulmonary hypertension and other forms of pulmonary arterial hypertension demonstrated delay in peak shortening of right ventricle with respect to the interventricular septum and left ventricle. This right-to-left diastolic interventricular delay (DIVD) is associated with diminished efficacy of right ventricle contraction, leftward interventricular septum bowing during early diastole, impaired left ventricle filling, and culminates in reduced cardiac output. We demonstrated that DIVD is explained, at least in part, by electrophysiologic remodeling of right ventricle, notably conduction slowing and prolongation of action potential duration.

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