The Association between Left Ventricular Diastolic Dysfunction and Increased Aortic Stiffness Can Be Explained by Possible Neurohumoral Mechanisms

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dc.contributor.authorSurucu, Huseyin
dc.contributor.authorTatli, Ersan
dc.contributor.authorBoz, Hakki
dc.contributor.authorMeric, Mehmet
dc.date.accessioned2024-06-12T11:07:36Z
dc.date.available2024-06-12T11:07:36Z
dc.date.issued2010
dc.departmentTrakya Üniversitesien_US
dc.description.abstractObjective: In our study, we tried to find an answer to the question How could the association between left ventricular diastolic dysfunction (LVDDF) and increased aortic stiffness (IAS) be explained? Methods: Cases without coronary artery disease (CAD) were divided into three groups according to their left ventricular (LV) inflow patterns and their LV basal-lateral annulus pulsed-wave tissue Doppler imaging (pw-TDI). Group 1 (n = 38) represented the normal LV inflow pattern while Group 2 (n = 54) represented impaired LV relaxation and Group 3 (n = 18) represented pseudonormalization. Aortic diameters were measured by using M-mode at a level that is 3 cm above the aortic valve. Aortic strain (AS) and aortic distensibility (AD) were calculated by using aortic diameters and pulse pressure. Results: In Group 3, AS was lower compared to Groups 1 and 2 (respectively P < 0.001, P = 0.040). AS was also lower in Group 2 compared to Group 1 (P = 0.012). AD was higher in Group 1 compared to Groups 2 and 3 (respectively P = 0.01, P < 0.001). Early diastolic velocity of aortic pw-TDI was higher in normal LV inflow compared to Groups 2 and 3 (respectively P = 0.022, P = 0.050). Unfortunately, none of echocardiographic parameters that evaluate LV and aortic functions together (stroke volume, pulse pressure/stroke volume, pulse pressure/stroke volume index) were different among the groups. Conclusion: The results of our study clearly showed the association between LVDDF and IAS in cases without CAD. Additionally, it was concluded that this togetherness could be explained not by hemodynamic factors but by possible neurohumeral mechanisms. (Echocardiography 2010;27:275-281).en_US
dc.identifier.doi10.1111/j.1540-8175.2009.01017.x
dc.identifier.endpage281en_US
dc.identifier.issn0742-2822
dc.identifier.issue3en_US
dc.identifier.pmid20070360en_US
dc.identifier.scopus2-s2.0-77949666174en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage275en_US
dc.identifier.urihttps://doi.org/10.1111/j.1540-8175.2009.01017.x
dc.identifier.urihttps://hdl.handle.net/20.500.14551/22094
dc.identifier.volume27en_US
dc.identifier.wosWOS:000275757300010en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWiley-Blackwell Publishing, Incen_US
dc.relation.ispartofEchocardiography-A Journal Of Cardiovascular Ultrasound And Allied Techniquesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectLeft Ventricular Diastolic Dysfunctionen_US
dc.subjectIncreased Aortic Stiffnessen_US
dc.subjectCoronary-Artery-Diseaseen_US
dc.subjectPressure-Diameter Relationen_US
dc.subjectPulse-Wave Velocityen_US
dc.subjectElastic Propertiesen_US
dc.subjectHeart-Failureen_US
dc.subjectHypertensive Patientsen_US
dc.subjectCardiovascular Risken_US
dc.subjectDiabetes-Mellitusen_US
dc.subjectAscending Aortaen_US
dc.subjectDistensibilityen_US
dc.titleThe Association between Left Ventricular Diastolic Dysfunction and Increased Aortic Stiffness Can Be Explained by Possible Neurohumoral Mechanismsen_US
dc.typeArticleen_US

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