- Oral presentation
- Open Access
Combined CMR and catheterization data in determining right ventricular-arterial coupling in children and adolescents with pulmonary arterial hypertension
© Truong et al.; licensee BioMed Central Ltd. 2014
- Published: 16 January 2014
- Pulmonary Arterial Hypertension
- Cardiac Magnetic Resonance
- Pulmonary Capillary Wedge Pressure
- Vascular Reactivity
- Receive Operating Characteristic Curve Analysis
Pulmonary arterial hypertension (PAH) remains a disease with high morbidity/mortality in pediatrics. Understanding ventricular-arterial coupling, a measure of how well matched the ventricular and vascular function is, may elucidate the pathway leading to right heart failure.
This retrospective study included subjects with PAH who a cardiac magnetic resonance (CMR) study within 14 days of cardiac catheterization between January 2009-August 2013. The effective elastance (Ea, index of arterial load) and right ventricular maximal end-systolic elastance (Emax, index of contractility) were determined by a combination of CMR and hemodynamic data. Ea is defined as (mean pulmonary arterial pressure minus pulmonary capillary wedge pressure)/stroke volume. Emax is defined as mean pulmonary arterial pressure/end systolic volume. Ea/Emax ratio was derived. Additionally, a measure of non-invasive ventricular arterial coupling (assuming PWCP is insignificant, making Ea/Emax = end systolic volume/stroke volume) was derived from only CMR. Pulmonary vascular resistance indexed (PVRi) and pulmonary vascular reactivity, as defined by Barst criteria (decrease in mean pulmonary artery pressure of > 20%, unchanged/increased cardiac index, and decreased/unchanged pulmonary to systemic vascular resistance ratio), were also determined. Pearson correlation coefficients were calculated between PVRi and Ea, Emax, and Ea/Emax. Receiving operating characteristic (ROC) curve analysis determined the diagnostic value of Ea/Emax in predicting vascular reactivity.
Measurement of ventricular arterial coupling, Ea/Emax, in pediatrics is feasible. Pulmonary vascular non-reactivity may be due to ventricular-arterial decoupling in which ventricular contractility fails to parallel increasing afterload in severe PAH. Use of Ea/Emax may have significant prognostic implication.
This work was supported by UL1 TR000154 from NCATS/NIH, 5R01HL114753 from NHLBI/NIH, as well as K25-094749 and K24-081506.
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