Right Ventricular Pacing in Pulmonary Arterial Hypertension

Summary

In pulmonary arterial hypertension (PAH), progressive pulmonary vascular remodeling leads to supraphysiologic right ventricular (RV) afterload. Pharmacologic trials have shown that aggressive upfront treatment reversing pulmonary vascular remodeling successfully increases RV function and improves survival. To date, however, there are no proven treatments that target RV contractile function. Echocardiographic studies of RV dysfunction in the setting of pressure overload have demonstrated intra and interventricular dyssynchrony even in the absence of overt right bundle branch block (RBBB). Electrophysiologic studies of patients with chronic thromboembolic disease (CTEPH) at the time of pulmonary endarterectomy have shown prolongation of action potential and slowed conduction in the right ventricle which has correlated with echocardiographic measures of dyssynchrony. Cardiac MRI measures of RV strain in patients with PAH demonstrated simultaneous initiation of RV and left ventricular (LV) contraction, but delayed peak RV strain suggesting that interventricular dyssynchrony is a mechanical rather than electrical phenomenon. Prior studies of RV dysfunction in an animal model, computer model, congenital heart disease, and CTEPH have suggested acute hemodynamic benefits of RV pacing. However, RV pacing has not been studied in patients with PAH. Furthermore, it remains unclear if pacing particular regions of the RV can achieve a hemodynamic benefit and what cost this hemodynamic improvement may incur with regards to myocardial energetics and wall stress. Therefore, the investigators propose to examine RV electrical activation in PAH, map the area of latest activation, and then evaluate the hemodynamic and energetic effects of RV pacing in these patients.

Eligibility

Inclusion Criteria:

* Patients referred for a clinically indicated right heart catheterization to either diagnose pulmonary arterial hypertension prior to initiating therapies or monitor response to ongoing therapies in patients with diagnosed pulmonary arterial hypertension.
* Patients with pulmonary arterial hypertension with or without significant right ventricular dysfunction as assessed by baseline echocardiography and standard of care right heart catheterization
* Functional class 2 or 3 symptoms
* Are able to undergo cardiac MRI, endocardial mapping, and pressure volume measurements
* English speaking
* All patients will be required to have evidence of right ventricular hypertrophy or conduction delay (QRS \> 130ms) on surface ECG

Exclusion Criteria:

* Preexisting left bundle branch block, current atrial fibrillation, or pacemaker/ defibrillators
* Functional class 4 symptoms
* Patients treated with parenteral or subcutaneous therapies for pulmonary hypertension
* Contraindication to right heart catheterization including significant thrombocytopenia (platelets \< 50,000), coagulopathy (INR \> 1.8), or pregnancy as determined by routine screening laboratory work
* Mean pulmonary artery pressure less than 25 mmHg as determined by the right heart catheterization on the day of the study procedure
* Pulmonary capillary wedge pressure greater than or equal to 15 mmHg as determined by the right heart catheterization on the day of the study procedure
* Severe tricuspid regurgitation as determined by baseline transthoracic echocardiogram.
* Left ventricular dysfunction (EF \< 50%) as determined by baseline transthoracic echocardiogram.
* Inability to complete cardiac MRI or transthoracic echocardiography
* Patients with confounding systemic disease specifically portopulmonary hypertension and scleroderma associated pulmonary hypertension
* Patients otherwise deemed not appropriate for the study as determined by the study investigators

Conditions3

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