Right Heart Mechanics
Right heart dysfunction is common throughout the clinical progression from preclinical disease to overt heart failure (Figure 1). Almost half of patients with HFpEF have right heart dysfunction as assessed by RV longitudinal strain 38. HFpEF patients with prominent right heart dysfunction may represent a particularly high risk phenotype40. Although far less data examining right heart deformation in HFpEF are currently available, recommendations for the standardization of right heart deformation imaging have been published26 and future study will further our understanding of right heart dysfunction.
Intact structure, function, and geometry of the interventricular septum is of upmost importance in preserving RV function. Shearing forces of the oblique interventricular septal fibers result in systolic twisting of the base toward the apex, leading to RV longitudinal motion. Interventricular septal mechanics are normally responsible for approximately 80% of RV systolic function. Circumferential compression of the transversely oriented fibers of the RV free wall result in a bellows motion, which normally contributes approximately 20% of RV systolic function41,42. RV dysfunction initially involves reduced longitudinal performance with a compensatory increase in circumferential motion, therefore RV longitudinal strain may serve as a sensitive tool for identifying early dysfunction.
Asymptomatic patients with metabolic disease commonly exhibit mild reductions in RV longitudinal strain 43,44. With disease progression into symptomatic heart failure, almost half of HFpEF patients have RV dysfunction by deformation indices 38(Figure 2). RV longitudinal strain and global longitudinal early-diastolic strain rate (RV-SRe) are both more significantly impaired in patients with symptoms than in those with preclinical disease 45. Right heart dysfunction may occur as a result of resting pulmonary hypertension or exercise-induced pulmonary hypertension. However, in some patients LV GLS may be a more important predictor of impaired RV longitudinal function than pulmonary arterial systolic pressure 45, suggesting a global myocardial process as the driver of dysfunction as opposed to pulmonary hypertension alone. Nonetheless, indices incorporating simultaneous RV function and afterload provide a measure of RV performance and pulmonary circulation coupling. Among patients with HFpEF, the ratio of RV longitudinal strain to pulmonary artery systolic pressure independently predicted the composite endpoint of all-cause death and HF hospitalization, even after multivariate adjustment46.
Impairment of right atrial deformation has also been appreciated in HFpEF patients 47. Pulmonary hypertension is associated with a decrement in right atrial strain48. Right atrial mechanics may prove an indicator of systemic venous congestion and related cardiorenal dysfunction. A distinct HFpEF phenogroup characterized by extensive cardiac remodeling with prominent pulmonary hypertension and right heart failure exists40. This phenogroup more often includes elderly patients with chronic kidney disease and appears to be at particularly high risk.