Ramón C Hermida1, Juan J Crespo1,2, Alfonso Otero3, Manuel Domínguez-Sardiña2, Ana Moyá4, María T Ríos1,2, María C Castiñeira1,5, Pedro A Callejas1,2, Lorenzo Pousa1,2, Elvira Sineiro1,4, José L Salgado1,2, Carmen Durán2, Juan J Sánchez1,6, José R Fernández1, Artemio Mojón1, Diana E Ayala1. 1. Bioengineering & Chronobiology Laboratories, Atlantic Research Center for Information and Communication Technologies (AtlantTIC), University of Vigo, Vigo, Spain. 2. Estructura de Gestión Integrada de Vigo, Servicio Galego de Saúde (SERGAS), Vigo, Spain. 3. Servicio de Nefrología, Complejo Hospitalario Universitario, Estructura de Gestión Integrada de Ourense, Verín y O Barco de Valdeorras, Servicio Galego de Saúde (SERGAS), Ourense, Spain. 4. Estructura de Xerencia Integrada Pontevedra e O Salnés, Servicio Galego de Saúde (SERGAS), Pontevedra, Spain. 5. Estructura de Gestión Integrada de Lugo, Cervo y Monforte de Lemos, Servicio Galego de Saúde (SERGAS), Lugo, Spain. 6. Estructura de Gestión Integrada de Santiago de Compostela, Servicio Galego de Saúde (SERGAS), Santiago de Compostela, Spain.
Abstract
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.
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.
Authors: Brian P Delisle; Alfred L George; Jeanne M Nerbonne; Joseph T Bass; Crystal M Ripplinger; Mukesh K Jain; Tracey O Hermanstyne; Martin E Young; Prince J Kannankeril; Jeanne F Duffy; Joshua I Goldhaber; Martica H Hall; Virend K Somers; Michael H Smolensky; Christine E Garnett; Ron C Anafi; Frank A J L Scheer; Kalyanam Shivkumar; Steven A Shea; Ravi C Balijepalli Journal: Circ Arrhythm Electrophysiol Date: 2021-11-01
Authors: Elissa K Hoopes; Freda Patterson; Felicia R Berube; Michele N D'Agata; Benjamin Brewer; Susan K Malone; William B Farquhar; Melissa A Witman Journal: J Hypertens Date: 2021-12-01 Impact factor: 4.844
Authors: Elissa K Hoopes; Melissa A Witman; Michele N D'Agata; Felicia R Berube; Benjamin Brewer; Susan K Malone; Michael A Grandner; Freda Patterson Journal: Chronobiol Int Date: 2021-01-13 Impact factor: 2.877
Authors: Mattias Brunström; Sverre E Kjeldsen; Reinhold Kreutz; Knut Gjesdal; Krzysztof Narkiewicz; Michel Burnier; Suzanne Oparil; Giuseppe Mancia Journal: Hypertension Date: 2021-07-07 Impact factor: 10.190