Compression induced by RV pressure overload decreases regional coronary blood flow in anesthetized dogs

Abstract

Pulmonary artery constriction (PAC), a model of right ventricular (RV) pressure overload, flattens or inverts the septum and may flatten the left ventricular (LV) free wall. Finite element (FE) analysis predicts that such deformations may cause substantial compression. This study tests the hypothesis that deformation-induced myocardial compressive stress impedes coronary blood flow (CBF). Colored microspheres (∼2 × 106) were injected into the left atrium of 13 open-chest, anesthetized dogs under control conditions and during PAC, which decreased the end-diastolic transseptal pressure gradient (LV − RV) from 1.6 ± 1.3 to −3.4 ± 1.7 mmHg. Septal and LV deformation was assessed with the use of two-dimensional echocardiography, and by FE analysis, the hydrostatic component of stress was assessed. Postmortem, a 2.5-cm wide, LV equatorial ring was divided into 16 endocardial and epicardial samples. PAC decreased CBF in the FE-predicted compression zones, areas with the greatest compression having the greatest reductions in CBF. During PAC, compression reached a maximum of 25.3 ± 1.8 mmHg on the (LV) endocardial sides of the RV insertion points, areas that saw CBF decrease from 1.05 ± 0.08 to 0.68 ± 0.05 ml·min−1·g−1 ( P < 0.001), more than 30%. CBF decreased (from 1.08 ± 0.07 to 0.81 ± 0.07 ml·min−1·g−1; P < 0.001) on the RV side of the midseptum, an area with as much as 16.0 ± 1.0 mmHg of compression. Overall, average compressions of 10 mmHg decreased CBF by ∼30%. We conclude that acute RV pressure overload deforms the septum and LV and induces compressive stresses that reduce CBF substantially. This may help explain why some patients with pulmonary hypertension and no critical coronary disease have chest discomfort indistinguishable from angina pectoris.