Impact of Acute Pulmonary Embolization on Arterial Stiffening and Right Ventricular Function in Dogs

• Published in: Annals of biomedical engineering 2013-01, Vol.41 (1), p.195-204
• Main Authors: Bellofiore, Alessandro, Roldán-Alzate, Alejandro, Besse, Matthieu, Kellihan, Heidi B., Consigny, Daniel W., Francois, Christopher J., Chesler, Naomi C.
• Format: Article
• Language: English
• Subjects: Animals; Biochemistry; Biological and Medical Physics; Biomedical and Life Sciences; Biomedical Engineering and Bioengineering; Biomedicine; Biophysics; Blood Pressure; Classical Mechanics; Dogs; Female; Hypertension; Hypertension, Pulmonary - physiopathology; Magnetic Resonance Imaging; Pulmonary Artery - physiology; Pulmonary Embolism - physiopathology; Stroke Volume; Vascular Stiffness - physiology; Ventricular Function, Right - physiology
• ISSN: 0090-6964; 1573-9686; 1521-6047
• DOI: 10.1007/s10439-012-0635-z

Pulmonary hypertension (PH) can impact right ventricular (RV) function and alter pulmonary artery (PA) stiffness. The response of the RV to an acute increase in pulmonary pressure is unclear. In addition, the relation between total pulmonary arterial compliance and local PA stiffness has not been investigated. We used a combination of right heart catheterization (RHC) and magnetic resonance imaging (MRI) to assess PA stiffening and RV function in dogs before and after acute embolization. We hypothesized that in moderate, acute PH the RV is able to compensate for increased afterload, maintaining adequate coupling. Also, we hypothesized that in the absence of PA remodeling the relative area change in the proximal PA (RAC, a noninvasive index of local area strain) correlates with the total arterial compliance (stroke volume-to-pulse pressure ratio). Our results indicate that, after embolization, RV function is able to accommodate the demand for increased stroke work without uncoupling, albeit at the expense of a reduction of efficiency. In this acute model, RAC showed excellent correlation with total arterial compliance. We used this correlation to assess PA pulse pressure (PP) from noninvasive MRI measurements of stroke volume and RAC. We demonstrated that in acute pulmonary embolism MRI estimates of PP are remarkably close to measurements from RHC. These results, if confirmed in chronic PH and clinically, suggest that monitoring of PH progression by noninvasive methods may be possible.