Abstract 17447: Decreasing LV Torsion Rate Causes Inter-Ventricular Mechanical De-coupling and Thereby Disrupts RV Function in Pediatric Pulmonary Hypertension

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Abstract

Introduction: Pulmonary Arterial Hypertension (PAH) is a disease characterized by progressively declining RV function. While RV contraction relies on mechanical energy transferred from the left ventricle (LV), little research has been devoted to the role of the LV in RV functional decline.

Hypothesis: (1) LV torsion-rate is significantly decreased in children with PAH, which is correlated with decreasing RV contractility; and (2) decreased LV torsion-rate is a cause of decreased RV contractility.

Methods: To address the first objective, tagged MRI of 19 pediatric PAH patients and 15 age-matched controls were prospectively obtained to measure LV torsion-rate in systole. For the PAH cohort, right heart catheterization was acquired within 2 days of MRI to measure RV contractility (as end-systolic elastance) using the single-beat method. To address the second objective, a bi-ventricular computational model was developed to assess the impact of LV torsion-rate on RV contractile function if the RV was passive during systole. A total of 4 simulations were executed for the duration of time that the pulmonic valve remains open. Fig 1d explains the conditions of each simulation.

Results: LV torsion-rate is significantly decreased in children with PAH compared to controls (Fig. 1a). Within the PAH cohort, the decrease in LV torsion-rate is significantly associated with a decrease in RV contractility (Fig. 1b). Bi-ventricular model (Fig. 1c) simulations show that when the RV is completely passive, increasing LV torsion-rate causes more rapid RV ejection, thus transferring more kinetic energy to the blood (Fig. 1d).

Conclusions: LV torsion-rate is decreased in PAH, which disrupts mechanical energy transfer to the RV. This could be contributing to RV functional decline and cardio-pulmonary decoupling during the progression of PAH.

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