4.7 Article

Asleep blood pressure: significant prognostic marker of vascular risk and therapeutic target for prevention

期刊

EUROPEAN HEART JOURNAL
卷 39, 期 47, 页码 4159-+

出版社

OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehy475

关键词

Asleep blood pressure; Ambulatory blood pressure monitoring; Bedtime hypertension chronotherapy; Cardiovascular risk; Stroke

资金

  1. Ministerio de Ciencia e Innovacion, Spanish Goverment [SAF2009-7028-FEDER]
  2. Instituto de Salud Carlos III, Ministerio de Economia y Competitividad, Spanish Government [PI14-00205]
  3. Conselleria de Economia e Industria, Direccion Xeral de Investigacion e Desenvolvemento, Galician Regional Government [INCITE08-E1R-322063ES, INCITE09-E2R-322099ES, 09CSA018322PR, IN845B-2010/114]
  4. Conselleria de Cultura, Educacion e Ordenacion Universitaria, Galician Regional Government [CN2012/251, GPC2014/078]
  5. European Regional Development Fund (ERDF)
  6. Galician Regional Government
  7. Vicerrectorado de Investigacion, University of Vigo

向作者/读者索取更多资源

Aims Sleep-time blood pressure (BP) is a stronger risk factor for cardiovascular disease (CVD) events than awake and 24 h BP means, but the potential role of asleep BP as therapeutic target for diminishing CVD risk is uncertain. We investigated whether CVD risk reduction is most associated with progressive decrease of either office or ambulatory awake or asleep BP mean. Methods and results We prospectively evaluated 18 078 individuals with baseline ambulatory BP ranging from normotension to hypertension. At inclusion and at scheduled visits (mainly annually) during follow-up, ambulatory BP was measured for 48 consecutive hours. During the 5.1-year median follow-up, 2311 individuals had events, including 1209 experiencing the primary outcome (composite of CVD death, myocardial infarction, coronary revascularization, heart failure, and stroke). The asleep systolic blood pressure (SBP) mean was the most significant BP-derived risk factor for the primary outcome [hazard ratio 1.29 (95% CI) 1.22-1.35 per SD elevation, P < 0.001], regardless of office [1.03 (0.97-1.09), P = 0.32], and awake SBP [1.02 (0.94-1.10), P = 0.68]. Most important, the progressive attenuation of asleep SBP was the most significant marker of event-free survival [0.75 (95% CI 0.69-0.82) per SD decrease, P < 0.001], regardless of changes in office [1.07 (0.97-1.17), P = 0.18], or awake SBP mean [0.96 (0.85-1.08), P = 0.47] during follow-up. Conclusion Asleep SBP is the most significant BP-derived risk factor for CVD events. Furthermore, treatment-induced decrease of asleep, but not awake SBP, a novel hypertension therapeutic target requiring periodic patient evaluation by ambulatory monitoring, is associated with significantly lower risk for CVD morbidity and mortality.

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