Pulmonary arterial hypertension is a manifestation of a group of disorders leading to pulmonary vascular remodeling and increased pulmonary pressures. The right ventricular (RV) response to chronic pressure overload consists of myocardial remodeling, which is in many ways similar to that seen in left ventricular (LV) failure. Maladaptive myocardial remodeling often leads to intraventricular and interventricular dyssychrony, an observation that has led to cardiac resynchronization therapy (CRT) for LV failure. CRT has proven to be an effective treatment strategy in subsets of patients with LV failure resulting in improvement in LV function, heart failure symptoms, and survival. Current therapy for pulmonary arterial hypertension is based on decreasing pulmonary vascular resistance, and there is currently no effective therapy targeting the right ventricle or maladaptive ventricular remodeling in these patients. This review focuses on the RV response to chronic pressure overload, its effect on electromechanical coupling and synchrony, and how lessons learned from left ventricular cardiac resynchronization might be applied as therapy for RV dysfunction in the context of pulmonary arterial hypertension.Keywords: pulmonary hypertension, pulmonary arterial hypertension, right ventricular failure, dyssynchrony, cardiac resynchronization therapy. Pulmonary arterial hypertension is a manifestation of a group of disorders that cause pulmonary vascular remodeling, alterations in pulmonary vascular resistance, and reduced compliance. Ultimately, increased pulmonary pressures may induce alterations in right ventricular structure and function. Current therapy is largely based on targeting biochemical pathways to decrease pulmonary vascular resistance. Despite this, the final common pathway for many patients remains right ventricular failure and death. Although left ventricular (LV) failure has been well characterized, leading to multiple therapies with proven mortality benefit, less is known about the failing right ventricle (RV). In fact, early evaluation of the role of RV function in disease states (i.e., RV free wall infarction/ ablation, Fontan physiology, or lung transplantation) suggested that the RV was highly adaptable and perhaps superfluous to overall cardiac function in the absence of sustained pulmonary arterial hypertension. However, recent improvements in imaging and technology, including strain imaging, tissue Doppler imaging (TDI), and magnetic resonance imaging (MRI) have led to a better understanding of the adaptation of the RV to chronic pressure overload.Many similarities between RV and LV failure have been observed, including changes in mechanical function, RV global and myocyte structure and function, 2 myocardial blood flow, 3 and electrophysiologic properties. 4 In a limited number of mechanical interventions in the pulmonary circulation (lung transplantation and pulmonary artery endarterectomy), RV reverse remodeling has been noted, suggesting a reversible component to RV remodeling related t...