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(Circulation. 2005;112:I-212 – I-218.)
© 2005 American Heart Association, Inc.

Myocardial Protection and Vascular Biology

Right Atrial and Ventricular Adaptation to Chronic Right Ventricular Pressure Overload

Sydney L. Gaynor, MD; Hersh S. Maniar, MD; Jeffrey B. Bloch; Paul Steendijk, PhD; Marc R. Moon, MD

From the Division of Cardiothoracic Surgery (S.L.G., H.S.M., J.B.B., M.R.M.), Washington University School of Medicine, St Louis, Mo; and the Department of Cardiology (P.S.), Leiden University Medical Center, the Netherlands.

Correspondence to Dr Marc R. Moon, Division of Cardiothoracic Surgery, Washington University School of Medicine, 3108 Queeny Tower, 1 Barnes-Jewish Plaza, St Louis, MO 63110-1013. E-mail moonm{at}msnotes.wustl.edu

Background— Increased mortality in patients with chronic pulmonary hypertension has been associated with elevated right atrial (RA) pressure. However, little is known about the effects of chronic right ventricular (RV) pressure overload on RA and RV dynamics or the adaptive response of the right atrium to maintain RV filling.

Methods and Results— In 7 dogs, RA and RV pressure and volume (conductance catheter) were recorded at baseline and after 3 months of progressive pulmonary artery banding. RA and RV elastance (contractility) and diastolic stiffness were calculated, and RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed versus open, respectively. With chronic pulmonary artery banding, systolic RV pressure increased from 34±7 to 70±17 mm Hg (P<0.001), but cardiac output did not change (P>0.78). RV elastance and stiffness both increased (P<0.05), suggesting preserved systolic function but impaired diastolic function. In response, RA contractility improved (elastance increased from 0.28±0.12 to 0.44±0.13 mm Hg/mL; P<0.04), and the atrium became more distensible, as evidenced by increased reservoir function (49±14% versus 72±8%) and decreased conduit function (51±14% versus 28±8%; P<0.002).

Conclusions— With chronic RV pressure overload, RV systolic function was preserved, but diastolic function was impaired. To compensate, RA contractility increased, and the atrium became more distensible to maintain filling of the stiffened ventricle. This compensatory response of the right atrium likely plays an important role in preventing clinical failure in chronic pulmonary hypertension.

Key Words: atrium • hypertension, pulmonary • pulmonary heart disease