Novel left ventricular mechanical index in pulmonary arterial hypertension

Author:

Ichimura Kenzo123ORCID,Santana Everton J.45ORCID,Kuznetsova Tatiana5,Cauwenberghs Nicholas5,Sabovčik František5,Chun Lindsey3,Francisco Nadia L. C.3,Kheyfets Vitaly O.6,Salerno Michael4,Zamanian Roham T.12,Spiekerkoetter Edda123,Haddad Francois234

Affiliation:

1. Department of Medicine, Division of Pulmonary, Allergy and Critical Care Stanford University Stanford California USA

2. Vera Moulton Wall Center of Pulmonary Vascular Disease Stanford School of Medicine Stanford California USA

3. Cardiovascular Institute Stanford University Stanford California USA

4. Department of Medicine, Division of Cardiovascular Medicine Stanford University Stanford California USA

5. Research Unit Hypertension and Cardiovascular Epidemiology, Department of Cardiovascular Sciences University of Leuven Leuven Belgium

6. Pediatric Critical Care Medicine; Developmental Lung Biology and CVP Research Laboratories, School of Medicine University of Colorado Aurora Colorado USA

Abstract

AbstractVentricular interdependence plays an important role in pulmonary arterial hypertension (PAH). It can decrease left ventricular (LV) longitudinal strain (LVLS) and lead to a leftward displacement (“transverse shortening”) of the interventricular septum (sTS). For this study, we hypothesized the ratio of LVLS/sTS would be a sensitive marker of systolic ventricular interactions in PAH. In a cross‐sectional cohort of patients with PAH (n = 57) and matched controls (n = 57), we quantified LVLS and septal TS in the amplitude and time domain. We then characterized LV phenotypes using upset plots, ventricular interactions using network analysis, and longitudinal analysis in a representative cohort of 45 patients. We also measured LV metrics in mice subjected to pulmonary arterial banding (PAB) using a 7 T magnetic resonance imaging at baseline, Week 1, and Week 7 post‐PAB (N = 9). Patients with PAH had significantly reduced absolute LVLS (15.4 ± 3.4 vs. 20.1 ± 2.3%, p < 0.0001), higher sTS (53.0 ± 12.2 vs. 28.0 ± 6.2%, p < 0.0001) and lower LVLS/sTS (0.30 ± 0.09 vs. 0.75 ± 0.16, p < 0.0001) compared to controls. Reduced LVLS/sTS was observed in 89.5% of patients, while diastolic dysfunction, impaired LVLS (<16%), and LV atrophy were observed in 73.7%, 52.6%, and 15.8%, respectively. In the longitudinal cohort, changes in LVLS/sTS were closely associated with changes in N‐terminal pro B‐type natriuretic peptide (r = 0.73, p < 0.0001) as well as survival. Mice subjected to PAB showed significant RV systolic dysfunction and decreased LVLS/sTS compared to sham animals. We conclude that in PAH, LVLV/sTS is a simple ratio that can reflect ventricular systolic interactions.

Funder

U.S. Department of Defense

American Heart Association

National Heart, Lung, and Blood Institute

Actelion Pharmaceuticals

National Institutes of Health

Publisher

Wiley

Subject

Pulmonary and Respiratory Medicine

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