title: Differential modulation of right ventricular strain and right atrial mechanics in mild vs. severe pressure overload.
abstract: Increased right atrial (RA) and ventricular (RV) chamber volumes are a late maladaptive response to chronic pulmonary hypertension. The purpose of the current investigation was to characterize the early compensatory changes that occur in the right heart during chronic RV pressure overload before the development of chamber dilation. Magnetic resonance imaging with radiofrequency tissue tagging was performed on dogs at baseline and after 10 wk of pulmonary artery banding to yield either mild RV pressure overload (36% rise in RV pressure; n = 5) or severe overload (250% rise in RV pressure; n = 4). The RV free wall was divided into three segments within a midventricular plane, and circumferential myocardial strain was calculated for each segment, the septum, and the left ventricle. Chamber volumes were calculated from stacked MRI images, and RA mechanics were characterized by calculating the RA reservoir, conduit, and pump contribution to RV filling. With mild RV overload, there were no changes in RV strain or RA function. With severe RV overload, RV circumferential strain diminished by 62% anterior (P = 0.04), 42% inferior (P = 0.03), and 50% in the septum (P = 0.02), with no change in the left ventricle (P = 0.12). RV filling became more dependent on RA conduit function, which increased from 30 ± 9 to 43 ± 13% (P = 0.01), than on RA reservoir function, which decreased from 47 ± 6 to 33 ± 4% (P = 0.04), with no change in RA pump function (P = 0.94). RA and RV volumes and RV ejection fraction were unchanged from baseline during either mild (P > 0.10) or severe RV pressure overload (P > 0.53). In response to severe RV pressure overload, RV myocardial strain is segmentally diminished and RV filling becomes more dependent on RA conduit rather than reservoir function. These compensatory mechanisms of the right heart occur early in chronic RV pressure overload before chamber dilation develops.
authors.affiliation: Division of Cardiothoracic Surgery, Washington University School of Medicine, Saint Louis, Missouri, USA.
authors.forename: Rochus K
authors.initials: RK
authors.lastname: Voeller
authors.forename: Abdulhameed
authors.initials: A
authors.lastname: Aziz
authors.forename: Hersh S
authors.initials: HS
authors.lastname: Maniar
authors.forename: Nneka N
authors.initials: NN
authors.lastname: Ufere
authors.forename: Ajay K
authors.initials: AK
authors.lastname: Taggar
authors.forename: Noel J
authors.initials: NJ
authors.lastname: Bernabe
authors.forename: Brian P
authors.initials: BP
authors.lastname: Cupps
authors.forename: Marc R
authors.initials: MR
authors.lastname: Moon
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D016280:Atrial Function, Right; D001696:Biomechanical Phenomena; D001794:Blood Pressure; D003250:Constriction; D004195:Disease Models, Animal; D004285:Dogs; D065627:Familial Primary Pulmonary Hypertension; D006976:Hypertension, Pulmonary / Q000150:complications* / Q000503:physiopathology; D017380:Hypertrophy, Right Ventricular / Q000209:etiology / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D011651:Pulmonary Artery / Q000503:physiopathology / Q000601:surgery; D012720:Severity of Illness Index; D013314:Stress, Mechanical; D013318:Stroke Volume; D013997:Time Factors; D018497:Ventricular Dysfunction, Right / Q000209:etiology* / Q000503:physiopathology; D016278:Ventricular Function, Right; D017725:Ventricular Pressure