Publications by authors named "Coe Y"

Article Synopsis
  • Pulmonary hypertension (PH) is caused by high blood pressure in the pulmonary artery and is often marked by distinctive sounds during heartbeats, particularly loud closures of the pulmonic valve.
  • This study aimed to investigate whether vibrations in pulmonary circulation produce sounds akin to those made by vocal cords in speech, specifically looking for unique sound signatures in patients with pulmonary artery hypertension (PAH) across four specific auscultation sites.
  • By using a digital stethoscope and analyzing heart sounds recorded during cardiac catheterization, researchers found that PAH subjects exhibited a notable reduction in sinusoid formant entropy, indicating a unique vowel-like sound pattern that could lead to non-invasive screening methods for PAH detection.
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Article Synopsis
  • Researchers investigated whether heart sounds in children with pulmonary artery hypertension (PAH) would show unique sound patterns due to vibrations from the pulmonary circulation.
  • They recorded and analyzed heart sounds from 27 subjects, separating them into two groups based on mean pulmonary artery pressure (mPAp) values.
  • Findings indicate that a significant reduction in the entropy of heart sound patterns correlates with higher mPAp, suggesting a possible noninvasive way to diagnose PAH in children.
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Article Synopsis
  • Pulmonary artery hypertension (PAH) is hard to detect, but digital stethoscopes might help improve diagnosis by analyzing heart sound frequencies.
  • The study involved 27 children, comparing those with normal pulmonary artery pressure to those with elevated pressure, using advanced sound analysis techniques.
  • Results showed that children with PAH had significantly lower heart sound power in the 21-22 Hz range, suggesting that frequency analysis could enhance PAH diagnosis and inform future auscultation methods.
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A case of percutaneous pulmonary valve implantation following a failed homograft in the pulmonary position is reported. A 16-year-old boy developed infective endocarditis of his pulmonary homograft, which was implanted four years earlier during a Ross procedure for congenital aortic stenosis. Following successful medical therapy, the boy was symptomatic due to pulmonary stenosis and regurgitation.

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Endothelin-1 (ET-1) is considered an intermediary in the constrictor response of the pulmonary vasculature to hypoxia and, by extension, is assigned a prime role in the pathogenesis of pulmonary hypertension. We report here the antihypertensive action in the conscious newborn lamb of two novel endothelin A receptor antagonists, sodium 2-benzo-[1,3]dioxol-5-yl-4- (4-methoxy-phenyl)-4-oxo-3-(3,4,5-trimethoxy-benzyl)-but-2- enoate (PD 156707) and 4-(7-ethyl-benzo[1,3]dioxol-5-yl)-1, 1-dioxo-2-(2-trifluoromethyl-phenyl)-1,2-dihydro-1l6-benzo-[e][1,2]thiazine-3-carboxylic acid potassium (PD 180988), differing in chemical properties and half-life within the body. PD 156707 and PD 180988, given in the right atrium as a bolus followed by infusion, had little or no effect on pulmonary and systemic hemodynamics under normoxia.

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Endothelin-1 (ET-1) is assigned a mediator role in the constrictor response of the pulmonary vasculature to hypoxia. Accordingly, a recently developed endothelin-A (ETA) antagonist, PD180988, was tested in the chronically instrumented newborn lamb to verify this possibility and, at the same time, to study a potential new treatment for pulmonary hypertension (PH). PD180988, given by infusion after a priming bolus, had an insignificant effect on the pulmonary circulation under normoxia, while it reversed the sustained pulmonary constriction caused by hypoxia.

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1. Using isolated pulmonary resistance vessels from mature fetal lamb and chronically instrumented lambs (8-17 days old), we have examined whether hypoxic pulmonary vasoconstriction is sustained by activation of a constrictor mechanism or suppression of a dilator mechanism. 2.

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Three hundred and seventy nine patients who had undergone mitral valve replacement using unstented antibiotic sterilised aortic homografts were followed up for 52 to 138 months (mean 102 months). Patients requiring additional aortic valve replacement were excluded. The commonest cause was rheumatic heart disease (321 patients).

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