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.