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Higher left ventricular mass–wall stress–heart rate product and outcome in aortic valve stenosis

OBJECTIVE: Whether increased myocardial oxygen demand could help explain the association of left ventricular (LV) hypertrophy with higher adverse event rate in patients with aortic valve stenosis (AS) is unknown. METHODS: Data from 1522 patients with asymptomatic mostly moderate AS participating in...

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Detalles Bibliográficos
Autores principales: Gerdts, Eva, Saeed, Sahrai, Midtbø, Helga, Rossebø, Anne, Chambers, John Boyd, Einarsen, Eigir, Bahlmann, Edda, Devereux, Richard
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BMJ Publishing Group 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6855785/
https://www.ncbi.nlm.nih.gov/pubmed/31154431
http://dx.doi.org/10.1136/heartjnl-2018-314462
Descripción
Sumario:OBJECTIVE: Whether increased myocardial oxygen demand could help explain the association of left ventricular (LV) hypertrophy with higher adverse event rate in patients with aortic valve stenosis (AS) is unknown. METHODS: Data from 1522 patients with asymptomatic mostly moderate AS participating in the Simvastatin-Ezetimibe in AS study followed for a median of 4.3 years was used. High LV mass–wall stress–heart rate product was identified as >upper 95% CI limit in normal subjects. The association of higher LV mass–wall stress–heart rate product with major cardiovascular (CV) events, combined CV death and hospitalised heart failure and all-cause mortality was tested in Cox regression analyses, and reported as HR and 95% CI. RESULTS: High LV mass–wall stress–heart rate product was found in 19% at baseline, and associated with male sex, higher body mass index, hypertension, LV hypertrophy, more severe AS and lower LV ejection fraction (all p<0.01). Adjusting for these confounders in time-varying Cox regression analysis, 1 SD higher LV mass–wall stress–heart rate product was associated with higher HR of major CV events (HR 1.16(95% CI 1.06 to 1.29)), combined CV death and hospitalised heart failure (HR 1.29(95% CI 1.09 to 1.54)) and all-cause mortality (HR 1.34(95% CI 1.13 to 1.58), all p<0.01). CONCLUSION: In patients with initially mild–moderate AS, higher LV mass–wall stress–heart rate product was associated with higher mortality and heart failure hospitalisation. Our results suggest that higher myocardial oxygen demand is contributing to the higher adverse event rate reported in AS patients with LV hypertrophy. TRIAL REGISTRATION NUMBER: NCT000092677; Post-results.