FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1902610511> ?p ?o ?g. }

• W1902610511 endingPage "1912" @default.
• W1902610511 startingPage "1901" @default.
• W1902610511 abstract "Key points A hallmark of mitral stenosis (MS) is the markedly altered left ventricular (LV) loading. As most of the methods used to determine LV performance in MS patients are influenced by loading conditions, previous studies have shown conflicting results. The present study calculated LV elastance, which is a robust method to quantify LV function. We demonstrate that LV loading in MS patients is elevated but normalizes after valve repair and might be a result of reflex pathways. Additionally, we show that the LV in MS is less compliant than normal due to a combination of right ventricular loading and the valvular disease itself. Immediately after valve dilatation the increase in blood inflow into the LV results in even greater LV stiffness. Our findings enrich our understanding of heart function in MS patients and provide a simple reproducible way of assessing LV performance in MS. Abstract Left ventricular (LV) function in rheumatic mitral stenosis (MS) remains an issue of controversy, due to load dependency of previously employed assessment methods. We investigated LV performance in MS employing relatively load‐independent indices robust to the altered loading state. We studied 106 subjects (32 ± 8 years, 72% female) with severe MS (0.8 ± 0.2 cm 2 ) and 40 age‐matched controls. MS subjects underwent simultaneous bi‐ventricular catheterization and transthoracic echocardiography (TTE) before and immediately after percutaneous transvenous mitral commisurotomy (PTMC). Sphygmomanometric brachial artery pressures and TTE recordings were simultaneously acquired in controls. Single‐beat LV elastance ( E es ) was employed for LV contractility measurements. Effective arterial elastance ( E a ) and LV diastolic stiffness were measured. MS patients demonstrated significantly elevated afterload ( E a : 3.0 ± 1.3 vs . 1.5 ± 0.3 mmHg ml −1 ; P < 0.001) and LV contractility ( E es : 4.1 ± 1.6 vs . 2.4 ± 0.5 mmHg ml −1 ; P < 0.001) as compared to controls, with higher E a in subjects with smaller mitral valve area (≤ 0.8 cm 2 ) and pronounced subvalvular fusion. Stroke volume (49 ± 16 to 57 ± 17 ml; P < 0.001) and indexed LV end‐diastolic volume (LVEDV index : 57 ± 16 to 64 ± 16 ml m −2 ; P < 0.001) increased following PTMC while E es and E a returned to more normal levels. Elevated LV stiffness was demonstrated at baseline and increased further following PTMC. Our findings provide evidence of elevated LV contractility, increased arterial load and increased diastolic stiffness in severe MS. Following PTMC, both LV contractility and afterload tend to normalize." @default.
• W1902610511 created "2016-06-24" @default.
• W1902610511 creator A5000473191 @default.
• W1902610511 creator A5001699588 @default.
• W1902610511 creator A5007005415 @default.
• W1902610511 creator A5009778108 @default.
• W1902610511 creator A5018809373 @default.
• W1902610511 creator A5021857228 @default.
• W1902610511 creator A5025782461 @default.
• W1902610511 creator A5054886076 @default.
• W1902610511 creator A5065018814 @default.
• W1902610511 creator A5079926789 @default.
• W1902610511 creator A5085307118 @default.
• W1902610511 date "2015-02-09" @default.
• W1902610511 modified "2023-10-16" @default.
• W1902610511 title "The impact of arterial load on left ventricular performance: an invasive haemodynamic study in severe mitral stenosis" @default.
• W1902610511 cites W1576660560 @default.
• W1902610511 cites W1972918094 @default.
• W1902610511 cites W1974728007 @default.
• W1902610511 cites W1975104654 @default.
• W1902610511 cites W1978998322 @default.
• W1902610511 cites W1980745547 @default.
• W1902610511 cites W1982713568 @default.
• W1902610511 cites W1984623267 @default.
• W1902610511 cites W1987613101 @default.
• W1902610511 cites W1989338200 @default.
• W1902610511 cites W2006134444 @default.
• W1902610511 cites W2006413157 @default.
• W1902610511 cites W2014697620 @default.
• W1902610511 cites W2020252734 @default.
• W1902610511 cites W2030155811 @default.
• W1902610511 cites W2030372119 @default.
• W1902610511 cites W2035746156 @default.
• W1902610511 cites W2037624879 @default.
• W1902610511 cites W2039757279 @default.
• W1902610511 cites W2040026900 @default.
• W1902610511 cites W2044075776 @default.
• W1902610511 cites W2062316006 @default.
• W1902610511 cites W2082543306 @default.
• W1902610511 cites W2100924809 @default.
• W1902610511 cites W2101099004 @default.
• W1902610511 cites W2107836188 @default.
• W1902610511 cites W2111359734 @default.
• W1902610511 cites W2119229486 @default.
• W1902610511 cites W2145950740 @default.
• W1902610511 cites W2146589023 @default.
• W1902610511 cites W2150144941 @default.
• W1902610511 cites W2300337887 @default.
• W1902610511 cites W2337579201 @default.
• W1902610511 cites W2340731691 @default.
• W1902610511 cites W2398640998 @default.
• W1902610511 cites W2414105706 @default.
• W1902610511 cites W2427556123 @default.
• W1902610511 cites W2460559055 @default.
• W1902610511 doi "https://doi.org/10.1113/jphysiol.2014.280404" @default.
• W1902610511 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4405750" @default.
• W1902610511 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25630680" @default.
• W1902610511 hasPublicationYear "2015" @default.
• W1902610511 type Work @default.
• W1902610511 sameAs 1902610511 @default.
• W1902610511 citedByCount "8" @default.
• W1902610511 countsByYear W19026105112016 @default.
• W1902610511 countsByYear W19026105112017 @default.
• W1902610511 countsByYear W19026105112018 @default.
• W1902610511 countsByYear W19026105112020 @default.
• W1902610511 countsByYear W19026105112021 @default.
• W1902610511 crossrefType "journal-article" @default.
• W1902610511 hasAuthorship W1902610511A5000473191 @default.
• W1902610511 hasAuthorship W1902610511A5001699588 @default.
• W1902610511 hasAuthorship W1902610511A5007005415 @default.
• W1902610511 hasAuthorship W1902610511A5009778108 @default.
• W1902610511 hasAuthorship W1902610511A5018809373 @default.
• W1902610511 hasAuthorship W1902610511A5021857228 @default.
• W1902610511 hasAuthorship W1902610511A5025782461 @default.
• W1902610511 hasAuthorship W1902610511A5054886076 @default.
• W1902610511 hasAuthorship W1902610511A5065018814 @default.
• W1902610511 hasAuthorship W1902610511A5079926789 @default.
• W1902610511 hasAuthorship W1902610511A5085307118 @default.
• W1902610511 hasBestOaLocation W19026105111 @default.
• W1902610511 hasConcept C126322002 @default.
• W1902610511 hasConcept C164705383 @default.
• W1902610511 hasConcept C178853913 @default.
• W1902610511 hasConcept C2777543888 @default.
• W1902610511 hasConcept C2780007028 @default.
• W1902610511 hasConcept C39133596 @default.
• W1902610511 hasConcept C71924100 @default.
• W1902610511 hasConceptScore W1902610511C126322002 @default.
• W1902610511 hasConceptScore W1902610511C164705383 @default.
• W1902610511 hasConceptScore W1902610511C178853913 @default.
• W1902610511 hasConceptScore W1902610511C2777543888 @default.
• W1902610511 hasConceptScore W1902610511C2780007028 @default.
• W1902610511 hasConceptScore W1902610511C39133596 @default.
• W1902610511 hasConceptScore W1902610511C71924100 @default.
• W1902610511 hasIssue "8" @default.
• W1902610511 hasLocation W19026105111 @default.
• W1902610511 hasLocation W19026105112 @default.
• W1902610511 hasLocation W19026105113 @default.
• W1902610511 hasOpenAccess W1902610511 @default.

• next