2005 Fiscal Year Final Research Report Summary
Effect of nocturnal hypoxia on diurnal blood pressure variation and target organ damage in Japanese hypertensive patients
| Project/Area Number |
14570688
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | JICHI MEDICAL SCHOOL |
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Principal Investigator |
KARIO Kazuomi Jichi Medical University, Division of Cardiovascular Medicine, Department of Medicine, 医学部, 教授 (60285773)
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| Co-Investigator(Kenkyū-buntansha) |
SIMADA Kazuyuki Jichi Medical University, Division of Cardiovascular Medicine, Department of Medicine, 医学部, 教授 (90145128)
MITUHASHI Takeshi Jichi Medical University, Division of Cardiovascular Medicine, Department of Medicine, 医学部, 助教授 (60275675)
MURATA Mitunobu Jichi Medical University, Division of Cardiovascular Medicine, Department of Medicine, 医学部, 助手 (10326853)
HOSHIDE Satoshi Jichi Medical University, Division of Cardiovascular Medicine, Department of Medicine, 医学部, 助手 (90326851)
ISHIKAWA Joji Jichi Medical University, Division of Cardiovascular Medicine, Department of Medicine, 医学部, 研究員 (90382879)
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| Project Period (FY) |
2002 – 2005
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| Keywords | Hypertension / Sleep apnea syndrome / Target organ damage / Sympathetic activity / Renin-angiotensin system / Insulin resistance / C-reactive protein |
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| Research Abstract |
Objective : Sleep apnea syndrome (SAS) is often associated with various neurohumoral activations and multiple risk factors. SAS patients have increased risk of sleep-onset cardiovascular events and frequently exhibits non-dipper pattern (blunted nocturnal decline of systolic blood pressure (BP) <10%), which predicts poor cardiovascular outcome. We investigated SAS-associated neurohumoral activation and risk factors in relation to nocturnal BP dipping pattern.
Methods : We conducted sleep plysomonography and ambulatory BP monitoring, and measured cardiovascular risk factors including high-sensitivity C-reactive protein (hsCRP) and tissue-type plasminogen activator inhibitor-1 (PAI-1 ; a marker of hypofibrinolytic activity), and neurohumoral factors in 121 SAS-suspected outpatients.
Results : Non-dippers with SAS had significantly higher serum hsCRP level than non-dippers without SAS (geometric mean : 1.64 vs. 0.36mg/L, P<0.001) and than dippers with SAS (0.80mg/L, P=0.036). Non-dippers wi
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th SAS had significantly higher PAI-1 (41.5±18.1ng/ml vs. 26.7±12.2ng/ml, P=0.007) and aldosterone (108.5±51.0pg/ml vs. 74.7±31.1pg/ml, P=0.009) than non-dippers without SAS, while there were no significant differences in these factors between non-dippers with SAS and dippers with SAS. Even after adjustment for confounding factors such as age, sex, and BMI, non-dippers with SAS had significantly higher serum hsCRP level than non-dippers without SAS (geometric mean 1.40 vs. 0.41mg/L, P<0.001). There were positive correlations of aldosterone level with hsCRP (r=0.180, P=0.048) and PAI-1 (r=0.168, P=0.065).
Conclusion : Non-dippers and SAS additively increased levels of hsCRP. Increased PAI-1 in relation to increased aldosterone level in non-dippers with SAS than non-dippers without SAS, indicating that SAS per se associated with impaired fibrinolysis in relation to activation of renin-angiotensin-aldosteron system. However, non-dippers without SAS is not associated with these risk factors. Less
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