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(Chest. 2001;119:1761-1765.)
© 2001 American College of Chest Physicians

Impaired Left Ventricular Filling Due to Right Ventricular Pressure Overload in Primary Pulmonary Hypertension*

Noninvasive Monitoring Using MRI

J. Tim Marcus, PhD; Anton Vonk Noordegraaf, MD, PhD; Roald J. Roeleveld, MD; Pieter E. Postmus, MD, PhD, FCCP; Rob M. Heethaar, PhD; Albert C. Van Rossum, MD, PhD and Anco Boonstra, MD, PhD

* From the Departments of Clinical Physics and Informatics (Drs. Marcus and Heethaar), Pulmonary Medicine (Drs. Vonk Noordegraaf, Roeleveld, Postmus, and Boonstra), and Cardiology (Dr. Van Rossum), ICaR-VU, University Hospital Vrije Universiteit, Amsterdam, The Netherlands.

Correspondence to: J. Tim Marcus, PhD, Department of Clinical Physics and Informatics, University Hospital, Vrije Universiteit, PO Box 7057, Boelelaan 1117, 1007 MB Amsterdam, The Netherlands; e-mail: jt.marcus{at}azvu.nl

Objective: To analyze the effect of primary pulmonary hypertension (PPH) on cardiac function using MRI.

Methods: In 12 patients (9 women; age range, 30 to 56 years), the diagnosis of PPH had been established by catheterization (mean ± SD pulmonary artery pressure [PAP] was 56 ± 8 mm Hg). With breath-hold cine MRI, a series of short-axis images was acquired covering the whole left ventricle (LV) and right ventricle (RV). The curvature, defined as 1 divided by the radius of curvature in centimeters, was calculated for the septum and the LV free wall in early diastole. Leftward ventricular septal bowing (LVSB) is denoted by a negative curvature. For the LV and the RV, the end-diastolic volume (EDV), stroke volume (SV), and volumetric filling rate were calculated. The control subjects were all healthy (n = 14; 11 women; age range, 20 to 57 years).

Results: In the patients, LVSB was quantified in early diastole by the septal curvature of - 0.14 ± 0.07 cm-1, and the septal to free-wall curvature ratio of - 0.42 ± 0.21. LV EDV and LV SV correlated negatively with diastolic PAP (p = 0.004 and p = 0.04, respectively). In patients vs control subjects, RV SV was reduced (52 ± 12 mL vs 82 ± 11 mL, p < 0.0001); LV peak filling rate was smaller (2.2 ± 0.7 EDV/s vs 3.3 ± 0.5 EDV/s, p < 0.001); LV EDV was smaller (81 ± 23 mL vs 117 ± 19 mL, p = 0.001); and LV SV was smaller (49 ± 18 mL vs 83 ± 13 mL, p < 0.0001).

Conclusion: In PPH, RV pressure overload leads to LVSB and reduced RV output. By decreased blood delivery, LV filling is reduced, which results in decreased LV SV by the Frank-Starling mechanism.

Key Words: diastole • heart failure • hypertension • pulmonary • pulmonary heart disease • ventricles




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