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CLINICAL RESEARCH: PULMONARY HYPERTENSION

Interventricular Mechanical Asynchrony in Pulmonary Arterial Hypertension

Left-to-Right Delay in Peak Shortening Is Related to Right Ventricular Overload and Left Ventricular Underfilling

J. Tim Marcus, PhD^_*,_*, C. Tji-Joong Gan, MSc^,1, Jaco J.M. Zwanenburg, PhD^,2, Anco Boonstra, MD, PhD, Cor P. Allaart, MD, PhD, Marco J.W. Götte, MD, PhD and Anton Vonk-Noordegraaf, MD, PhD

^_* Department of Physics and Medical Technology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, the Netherlands
Department of Pulmonary Diseases, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, the Netherlands
Department of Cardiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, the Netherlands
Image Sciences Institute, University Medical Center Utrecht, Utrecht, the Netherlands.

Manuscript received August 8, 2006; revised manuscript received October 10, 2007, accepted October 22, 2007.

^_* Reprint requests and correspondence: Dr. J. Tim Marcus, Department of Physics and Medical Technology, VU University Medical Center, P.O. Box 7057, 1007 MB Amsterdam, the Netherlands. (Email: jt.marcus{at}vumc.nl).

Objectives: The purpose of this study was to explore in pulmonary arterial hypertension (PAH) whether the cause of interventricular asynchrony lies in onset of shortening or duration of shortening.

Background: In PAH, leftward ventricular septal bowing (LVSB) is probably caused by a left-to-right (L-R) delay in myocardial shortening.

Methods: In 21 PAH patients (mean pulmonary arterial pressure 55 ± 13 mm Hg and electrocardiogram–QRS width 100 ± 16 ms), magnetic resonance imaging myocardial tagging (14 ms temporal resolution) was applied. For the left ventricular (LV) free wall, septum, and right ventricular (RV) free wall, the onset time (T_onset) and peak time (T_peak) of circumferential shortening were calculated. The RV wall tension was estimated by the Laplace law.

Results: The T_onset was 51 ± 23 ms, 65 ± 4 ms, and 52 ± 22 ms for LV, septum, and RV, respectively. The T_peak was 293 ± 58 ms, 267 ± 22 ms, and 387 ± 50 ms for LV, septum, and RV, respectively. Maximum LVSB was at 395 ± 45 ms, coinciding with septal overstretch and RV T_peak. The L-R delay in T_onset was –1 ± 16 ms (p = 0.84), and the L-R delay in T_peak was 94 ± 41 ms (p < 0.001). The L-R delay in T_peak was not related to the QRS width but was associated with RV wall tension (p < 0.05). The L-R delay in T_peak correlated with leftward septal curvature (p < 0.05) and correlated negatively with LV end-diastolic volume (p < 0.05) and stroke volume (p < 0.05).

Conclusions: In PAH, the L-R delay in myocardial peak shortening is caused by lengthening of the duration of RV shortening. This L-R delay is related to LVSB, decreased LV filling, and decreased stroke volume.

Abbreviations and Acronyms   BSA = body surface area   ECG = electrocardiogram   EDV = end-diastolic volume   L-R delay = left-to-right ventricular delay in circumferential shortening   LV = left ventricle/ventricular   LVSB = leftward ventricular septal bowing   MRI = magnetic resonance imaging   PAH = pulmonary arterial hypertension   PAP = pulmonary arterial pressure   RBBB = right bundle branch block   RV = right ventricle/ventricular   Tonset = time to onset of circumferential shortening   Tpeak = time to peak of circumferential shortening

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