Arousals Are Frequent and Associated With Exacerbated Blood Pressure Response in Patients With Primary Hypertension

Carregando...
Imagem de Miniatura
Citações na Scopus
13
Tipo de produção
article
Data de publicação
2013
Título da Revista
ISSN da Revista
Título do Volume
Editora
OXFORD UNIV PRESS
Citação
AMERICAN JOURNAL OF HYPERTENSION, v.26, n.5, p.617-623, 2013
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
BACKGROUND Spontaneous arousals are relatively common during sleep, and induce hemodynamic responses. We sought to investigate the frequency and magnitude of blood pressure (BP) increases triggered by spontaneous arousals in patients with primary hypertension. METHODS We conducted a study in which we divided 18 nonobese, sedentary adults without sleep-disordered breathing into two groups, consisting of: (i) hypertensive (HT, n = 8) patients; and (ii) normotensive (NT, n = 10) controls. The groups were matched for age and body mass index. All subjects underwent full polysomnography with simultaneous monitoring of heart rate (HR) and beat-by-beat BR Each subject's BP and HR were analyzed immediately before BP peaks triggered by spontaneous arousals during stage 2 of nonrapid eye movement sleep. RESULTS The total sleep time, sleep efficiency, and sleep structure in the two study groups were similar. In contrast, the number of arousals was significantly higher in the HT than in the NT group, at 25 +/- 5 vs. 12 +/- 3 events/h, respectively (P < 0.05). The HR of the HT and NT groups was similar before arousal (65 +/- 3 bpm vs. 67 +/- 3 bpm, respectively, P < 0.01) and increased significantly and similarly in the two groups upon arousal (to 79 +/- 6 bpm vs. 74 +/- 4 bpm, respectively, P < 0.01). Systolic and diastolic BPs were significantly higher throughout sleep in the HT than in the NT group. During spontaneous arousals, BP increased in both groups (P < 0.05). However, the magnitude of the increase in systolic BP was significantly greater in the HT than in the NT group (22 +/- 3 mm Hg vs. 15 +/- 3 mm Hg, P < 0.05). CONCLUSIONS Patients with hypertension who do not have sleep-disordered breathing have an increased cardiovascular burden during sleep, which may be due to the greater number of arousals and exacerbated systolic BP response that they experience during sleep. These novel findings may have cardiovascular implications in patients with hypertension.
Palavras-chave
spontaneous arousal, sleep, hypertension, blood pressure
Referências
  1. Badr MS, 1997, SLEEP, V20, P707
  2. Bangash MF, 2008, SLEEP, V31, P321
  3. Carley DW, 1997, CHEST, V112, P1567
  4. Chobanian AV, 2003, HYPERTENSION, V42, P1206, DOI 10.1161/01.HYP.0000107251.49515.c2
  5. DAVIES RJO, 1993, J APPL PHYSIOL, V74, P1123
  6. Dempsey JA, 2010, PHYSIOL REV, V90, P47, DOI 10.1152/physrev.00043.2008
  7. Drager LF, 2010, AM J CARDIOL, V105, P1135, DOI 10.1016/j.amjcard.2009.12.017
  8. Drager LF, 2009, J HYPERTENS, V27, P1655, DOI 10.1097/HJH.0b013e32832c6982
  9. Drager LF, 2005, AM J RESP CRIT CARE, V172, P613, DOI 10.1164/rccm.200503-340OC
  10. Friedman O, 2010, AM J HYPERTENS, V23, P174, DOI 10.1038/ajh.2009.220
  11. Grassi G, 1998, HYPERTENSION, V31, P68
  12. Grassi G, 2003, HYPERTENSION, V41, P558, DOI 10.1161/01.HYP.0000058003.27729.5A
  13. Halasz P, 2004, J SLEEP RES, V13, P1, DOI 10.1111/j.1365-2869.2004.00388.x
  14. Huang YL, 2011, BLOOD PRESS MONIT, V16, P117, DOI 10.1097/MBP.0b013e328346a8b4
  15. Iber C, 2007, AASM MANUAL SCORING, P37
  16. IMHOLZ BPM, 1993, HYPERTENSION, V21, P65
  17. JOHNS MW, 1991, SLEEP, V14, P540
  18. Jordan AS, 2003, AM J RESP CRIT CARE, V168, P1512, DOI 10.1164/rccm.200302-150OC
  19. Kikuya M, 2005, HYPERTENSION, V45, P240, DOI 10.1161/01.HYP.0000152079.04553.2c
  20. Kuo TBJ, 2012, AM J HYPERTENS, V25, P1110, DOI 10.1038/ajh.2012.93
  21. Kuo TBJ, 2004, SLEEP, V27, P406
  22. Lofaso F, 1996, CHEST, V109, P896, DOI 10.1378/chest.109.4.896
  23. Mitchell HA, 2010, BIOCHEM PHARMACOL, V79, P801, DOI 10.1016/j.bcp.2009.10.004
  24. Morgan BJ, 1996, J APPL PHYSIOL, V80, P1627
  25. Morrell MJ, 2000, AM J RESP CRIT CARE, V162, P2091
  26. Murali NS, 2003, FRONT BIOSCI, V8, pS636, DOI 10.2741/1105
  27. Nerbass FB, 2011, J HYPERTENS, V29, P1236, DOI 10.1097/HJH.0b013e3283462e8b
  28. Netzer NC, 1999, ANN INTERN MED, V131, P485
  29. O'Driscoll DM, 2004, J APPL PHYSIOL, V96, P865, DOI 10.1152/japplphysiol.00749.2003
  30. Ordway G. A., 2007, BRAIN NOREPINEPHRINE, P157, DOI 10.1017/CBO9780511544156.007
  31. Pickering TG, 2001, CURR OPIN NEPHROL HY, V10, P611, DOI 10.1097/00041552-200109000-00010
  32. Rechtstaffen A, 1968, MANUAL STANDARDIZED
  33. Saper CB, 2005, NATURE, V437, P1257, DOI 10.1038/nature04284
  34. SOMERS VK, 1993, NEW ENGL J MED, V328, P303, DOI 10.1056/NEJM199302043280502
  35. Suzuki M, 1996, SLEEP, V19, P382
  36. Trinder J, 2003, SLEEP, V26, P543
  37. Ueno LM, 2009, SLEEP, V32, P637
  38. Xie AL, 1999, J PHYSIOL-LONDON, V515, P621, DOI 10.1111/j.1469-7793.1999.621ac.x
  39. Yilmaz MB, 2007, BLOOD PRESSURE, V16, P101, DOI 10.1080/08037050701343225