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Pulmonary arterial hypertension causes an increase in the mechanical loading imposed on the right ventricle that results in progressive changes to its mechanics and function. Here, we quantify the mechanical changes associated with PAH by assimiliating clinical data consisting of reconstructed 3D geometry, pressure and volume waveforms as well as regional strains measured in PAH patients (n = 12) and controls (n = 6) within a computational modeling framework of the ventricles. Modeling parameters reflecting regional passive stiness and load-independent contractility as indexed by the tissue active tension were optimized so that simulation results matched the measurements The optimized parameters were compared with clinical metrics to and usable indicators associated with the underlying mechanical changes. Peak contractility of the RV free wall γ was found to be strongly correlated, and had an inverse relationship with the RV and left ventricle end-diastolic volume ratio (i.e., RVEDV/LVEDV) (γ=-0.13(RVEDV/LVEDV)+0.44, R=0.77). Correlation with RV ejection fraction (R=0.5) and end-diastolic volume index (R=0.4) were comparatively weaker. Patients with RVEDV/LVEDV≤1.5 had 18% higher γ (P = 0.09) than that of the control whereas those with RVEDV/LVEDV > 1.5 had 25% lower γ (P<0.05). On average, RVFW passive stiffness increased progressively with the degree of remodeling as indexed by RVEDV/LVEDV and RVFW myofiber stress was increased by 49% only in patients with RVEDV/LVEDV ≥ 1.5 (P = 0.14). These results provide the mechanical basis of using RVEDV/LVEDV as a clinical index for delineating disease severity and estimating RVFW contractility in PAH patients.
This article was published in the following journal.
Name: American journal of physiology. Heart and circulatory physiology
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The development and application of computational models of human pathophysiology that are individualized to patient-specific data.
A potentially lethal cardiac arrhythmia characterized by an extremely rapid, hemodynamically unstable ventricular tachycardia (150-300 beats/min) with a large oscillating sine-wave appearance. If untreated, ventricular flutter typically progresses to VENTRICULAR FIBRILLATION.
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An abnormally rapid ventricular rhythm usually in excess of 150 beats per minute. It is generated within the ventricle below the BUNDLE OF HIS, either as autonomic impulse formation or reentrant impulse conduction. Depending on the etiology, onset of ventricular tachycardia can be paroxysmal (sudden) or nonparoxysmal, its wide QRS complexes can be uniform or polymorphic, and the ventricular beating may be independent of the atrial beating (AV dissociation).
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