Left ventricular underfilling and not septal bulging dominates abnormal left ventricular filling hemodynamics in chronic thromboembolic pulmonary hypertension

Abstract

Chronic thromboembolic pulmonary hypertension (CTEPH) is associated with abnormal left ventricular (LV) filling hemodynamics [mitral early passive filling wave velocity/late active filling wave velocity (E/A) < 1]. Pulmonary endarterectomy (PEA) acutely reduces pulmonary vascular resistance, resulting in an increase of mitral E/A. The abolishment of leftward septal bulging and an increase in right ventricular (RV) output are thought to be responsible for the increase of mitral E/A. In this study, we quantified the separate effects of leftward septal bulging and RV output on LV hemodynamics. In 39 CTEPH patients who underwent PEA, transmitral flow velocities and RV hemodynamic data were obtained pre- and postoperatively. A mathematical model describing the mechanics of ventricular interaction was fitted to the preoperative average values of cardiac output (CO; 4.4 l/min), mean pulmonary artery pressure (mPAP; 50 mmHg), mitral E/A (0.74), and mean left atrial pressure (mLAP; 9.8 mmHg). Starting from this preoperative reference state with leftward septal bulging, PEA was simulated by changing mPAP and CO to average postoperative values (28 mmHg and 5.7 l/min, respectively). Simulated and postoperatively measured data on E/A (1.27 vs. 1.48), mLAP (12.6 vs. 11.5 mmHg), and septal curvature (both rightward) were consistent. When an exclusive decrease of mPAP was simulated, mitral E/A increased 26%, mLAP decreased 16%, and septal curvature became rightward. When an exclusive increase of CO was simulated, mitral E/A increased 53% and mLAP increased 62%, whereas leftward septal bulging persisted. Thus, our simulations suggest that the increase of mitral E/A with PEA is caused two-thirds by an increase of RV output and one-third by the abolishment of leftward septal bulging.

Modeling Cardiac Electromechanics and Mechanoelectrical Coupling in Dyssynchronous and Failing Hearts

“…Indeed, in this model, the first steps toward patient-specific modeling in PAH have led to a better understanding of left ventricular inflow patterns in PAH as well as to the interesting observation that right ventricular pacing in PAH might be beneficial [47, 48]. Computation times are limited thanks to the geometric simplicity of the model.…”

Assessment of left atrial volume before and after pulmonary thromboendarterectomy in chronic thromboembolic pulmonary hypertension

“…The results suggested that that the abnormal E/A pattern was in large part due to decreased LV preload [6]. These findings were supported by Lumens et al using a computer-generated model that could separate the influences of septal bulging vs. LV filling on transmitral Doppler flow patterns pre- and post-PTE [7]. Gurudevan also reported that early diastolic mitral annular velocity (E’) was abnormally low in CTEPH but increased after PTE.…”

“…More recent studies, however, have supported the theory of decreased RV output and relative LV underfilling as the primary cause of the perceived LV diastolic impairment in CTEPH [5-7]. If this is correct, one might hypothesize that left atrial volume would increase after successful pulmonary thromboendarterectomy (PTE) and potentially correlate with improvements in right heart catheterization measurements.…”

Patient-specific modeling of dyssynchronous heart failure: A case study

“…In the Windkessel model the circulatory system is a large compliant compartment (representing the major arteries) and a peripheral resistance (representing the capillaries) that opposes the blood flow. The arterial walls are considered rigid, and two parameters are not sufficient to account for high-frequency components of the pressure-volume relationship in non-rigid, compliant, wave propagating medium (Lumens et al, 2010; Stergiopulos et al, 1999). Therefore this model lacks the detail to generate realistic waveforms of the human circulatory system.…”