Volume 32, Issue 12 pp. 1762-1770
Original Investigation

Importance of End-Diastolic Rather than End-Systolic Right Atrial Size in Chronic Pulmonary Hypertension

Angel Lopez-Candales M.D.

Corresponding Author

Angel Lopez-Candales M.D.

Cardiovascular Medicine Division, University of Puerto Rico School of Medicine, San Juan, Puerto Rico

Address for correspondence and reprint requests: Angel López-Candales, M.D., F.A.C.C., F.A.S.E., Cardiovascular Medicine Division, University of Puerto Rico School of Medicine, Medical Sciences Building, PO Box 365067, San Juan 00936-5067, Puerto Rico. Fax: +787-754-1739

E-mail: [email protected]

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Denada S. Palm M.D.

Denada S. Palm M.D.

Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio

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Francisco R. Lopez M.D.

Francisco R. Lopez M.D.

UC Heart, Lung & Vascular Institute, University of Cincinnati College of Medicine, Cincinnati, Ohio

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Reynerio Perez M.D.

Reynerio Perez M.D.

Cardiovascular Medicine Division, University of Puerto Rico School of Medicine, San Juan, Puerto Rico

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Maria D. Candales M.S.

Maria D. Candales M.S.

University of Puerto Rico, Rio Piedras, Puerto Rico

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First published: 20 June 2015
Citations: 1
Role of Sponsors: There are no sponsor(s).

Abstract

Background

Right atrial (RA) enlargement has been associated with worse clinical outcomes in chronic pulmonary hypertension (cPH) patients. Even though current guidelines only recommend measurement of RA dimensions at the end of ventricular systole in these patients, there is paucity of information regarding the potential utility of RA dimensions obtained at the end of ventricular diastole.

Methods

In this retrospective study, standard echocardiographic data were collected from 80 studies. The population studied was divided into Group I that consisted of 35 patients (52 ± 10 years) without PH while Group II included 45 patients (56 ± 14 years; P = 0.2) with cPH. RA measurements were obtained not only at the end of ventricular systole, but also at the end of ventricular diastole to determine which RA measurement was more indicative of abnormal right ventricular afterload.

Results

Even though all RA measurements were abnormal, RA area (>8.4 cm2) measured at the end of ventricular diastole was the most useful RA variable to identify cPH patients with elevated pulmonary pressures (P < 0.0001) and with an abnormal pulmonary vascular resistance (P = 0.001).

Conclusions

Based on these results, it appears that isolated RA measurements made at the end of ventricular systole are insufficient to fully explain the hemodynamic load of cPH. Additional studies are now required to determine whether sequential monitoring of the composite change in RA dimensions that occur throughout the cardiac cycle over time correlates better with response to vasodilator therapy and overall clinical outcomes.

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