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Systolic excursion of the leaflets of the truncal valve: An unusual mechanism for pulmonary stenosis in common arterial trunk.

ABSTRACT: Background:Pulmonary stenosis in patients with common arterial trunk protects the pulmonary vasculature. In our recently published prospective study of common arterial trunk, some patients with sinusal origin of the pulmonary arterial segment had pulmonary stenosis induced by systolic excursion of a truncal valvar leaflet. We aimed to determine the detailed morphologic characteristics of this unusual finding. Methods and Results:All 70 patients underwent echocardiography and computed tomographic angiography as per predefined study protocol. In selected cases, we also performed cardiac catheterization. Among 27 patients with aortic dominance, we found sinusal origin of the pulmonary arterial segment. In 5 of these patients, pulmonary stenosis was induced by systolic excursion of a truncal valvar leaflet. In all these patients, the truncal valve was trisinusate, albeit with asymmetric sinuses. The pulmonary arterial segment arose from the largest left sinus with its relatively large leaflet obstructing the pulmonary orifice during systole. In the remaining 22 patients, without pulmonary stenosis but with sinusal origin of pulmonary arterial segment, the truncal valve was quadrisinusate in 7, bisinusate in 2, and trisinusate in 13. None of the patients with quadrisinusate and bisinusate truncal valves had pulmonary stenosis. Among the 13 patients with trisinusate valves, the sinuses of the truncal valve were symmetrical in 6, while in 7, the pulmonary orifice originated from a smaller asymmetric sinus. Conclusion:Pulmonary stenosis, produced by a relatively large leaflet of an asymmetric truncal sinus, may prevent early development of pulmonary vascular disease. Timely recognition of this unusual mechanism of pulmonary stenosis is important for optimal management.

SUBMITTER: Gupta SK

PROVIDER: S-EPMC7437627 | biostudies-literature | 2020 Jul-Sep

REPOSITORIES: biostudies-literature

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Systolic excursion of the leaflets of the truncal valve: An unusual mechanism for pulmonary stenosis in common arterial trunk.

Gupta Saurabh Kumar SK Aggarwal Abhinav A Gulati Gurpreet S GS Ramakrishnan Sivasubramanian S Kothari Shyam S SS Saxena Anita A Sharma Sanjiv S Airan Balram B Anderson Robert H RH

Annals of pediatric cardiology 20200629 3

<h4>Background</h4>Pulmonary stenosis in patients with common arterial trunk protects the pulmonary vasculature. In our recently published prospective study of common arterial trunk, some patients with sinusal origin of the pulmonary arterial segment had pulmonary stenosis induced by systolic excursion of a truncal valvar leaflet. We aimed to determine the detailed morphologic characteristics of this unusual finding.<h4>Methods and results</h4>All 70 patients underwent echocardiography and compu ...[more]

PMID: 32863653

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Project description:Progressive superior shift of the mitral valve (MV) during systole is associated with abnormal papillary muscle (PM) superior shift in late systolic MV prolapse (MVP). The causal relation of these superior shifts remains unclarified. We hypothesized that the MV superior shift is related to augmented MV superiorly pushing force by systolic left ventricular pressure due to MV annular dilatation, which can be corrected by surgical MV plasty, leading to postoperative disappearance of these superior shifts. In 35 controls, 28 patients with holosystolic MVP, and 28 patients with late systolic MVP, the MV coaptation depth from the MV annulus was measured at early and late systole by two-dimensional echocardiography. The PM tip superior shift was monitored by echocardiographic speckle tracking. MV superiorly pushing force was obtained as MV annular area × (systolic blood pressure - 10). Measurements were repeated after MV plasty in 14 patients with late systolic MVP. Compared with controls and patients with holosystolic MVP, MV and PM superior shifts and MV superiorly pushing force were greater in patients with late systolic MVP [1.3 (0.5) vs. 0.9 (0.6) vs. 3.9 (1.0) mm/m2, 1.3 (0.5) vs. 1.2 (1.0) vs. 3.3 (1.3) mm/m2, and 487 (90) vs. 606 (167) vs. 742 (177) mmHg·cm2·m-2, respectively, means (SD), P < 0.001]. MV superior shift was correlated with PM superior shift ( P < 0.001), which was further related to augmented MV superiorly pushing force ( P < 0.001). MV and PM superior shift disappeared after surgical MV plasty for late systolic MVP. These data suggest that MV annulus dilatation augmenting MV superiorly pushing force may promote secondary superior shift of the MV (equal to late systolic MVP) that causes subvalvular PM traction in patients with late systolic MVP. NEW & NOTEWORTHY Late systolic mitral valve prolapse (MVP) is associated with mitral valve (MV) and papillary muscle (PM) abnormal superior shifts during systole, but the causal relation remains unclarified. MV and PM superior shifts were correlated with augmented MV superiorly pushing force by annular dilatation and disappeared after surgical MV plasty with annulus size and MV superiorly pushing force reduction. This suggests that MV annulus dilatation may promote secondary superior shifts of the MV (late systolic MVP) that cause subvalvular PM traction.

Project description:BACKGROUND:The ratios of tricuspid annular plane systolic excursion (TAPSE)/echocardiographically measured systolic pulmonary artery pressure (PASP), fractional area change/invasively measured mean pulmonary artery pressure, right ventricular (RV) area change/end-systolic area, TAPSE/pulmonary artery acceleration time, and stroke volume/end-systolic area have been proposed as surrogates of RV-arterial coupling. The relationship of these surrogates with the gold standard measure of RV-arterial coupling (invasive pressure-volume loop-derived end-systolic/arterial elastance [Ees/Ea] ratio) and RV diastolic stiffness (end-diastolic elastance) in pulmonary hypertension remains incompletely understood. We evaluated the relationship of these surrogates with invasive pressure-volume loop-derived Ees/Ea and end-diastolic elastance in pulmonary hypertension. METHODS:We performed right heart echocardiography and cardiac magnetic resonance imaging 1 day before invasive measurement of pulmonary hemodynamics and single-beat RV pressure-volume loops in 52 patients with pulmonary arterial hypertension or chronic thromboembolic pulmonary hypertension. The relationships of the proposed surrogates with Ees/Ea and end-diastolic elastance were evaluated by Spearman correlation, multivariate logistic regression, and receiver operating characteristic analyses. Associations with prognosis were evaluated by Kaplan-Meier analysis. RESULTS:TAPSE/PASP, fractional area change/mean pulmonary artery pressure, RV area change/end-systolic area, and stroke volume/end-systolic area but not TAPSE/pulmonary artery acceleration time were correlated with Ees/Ea and end-diastolic elastance. Of the surrogates, only TAPSE/PASP emerged as an independent predictor of Ees/Ea (multivariate odds ratio: 18.6; 95% CI, 0.8-96.1; P=0.08). In receiver operating characteristic analysis, a TAPSE/PASP cutoff of 0.31 mm/mm?Hg (sensitivity: 87.5% and specificity: 75.9%) discriminated RV-arterial uncoupling (Ees/Ea <0.805). Patients with TAPSE/PASP <0.31 mm/mm?Hg had a significantly worse prognosis than those with higher TAPSE/PASP. CONCLUSIONS:Echocardiographically determined TAPSE/PASP is a straightforward noninvasive measure of RV-arterial coupling and is affected by RV diastolic stiffness in severe pulmonary hypertension. CLINICAL TRIAL REGISTRATION:URL: https://www.clinicaltrials.gov. Unique identifier: NCT03403868.

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Systolic excursion of the leaflets of the truncal valve: An unusual mechanism for pulmonary stenosis in common arterial trunk.

Publications

Systolic excursion of the leaflets of the truncal valve: An unusual mechanism for pulmonary stenosis in common arterial trunk.

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