高血圧患者と閉塞性睡眠時無呼吸症候群の検討
閉塞性睡眠時無呼吸症候群: obstructive sleep apnea syndrome (OSAS)と高血圧については, いくつかの疫学研究で報告され, その重要性が認識されている. 高血圧とOSASとの関連を調べるため, Body Mass Index (BMI)25以上または顕著ないびき, 昼間の眠気症状のある高血圧患者連続25例に簡易型終夜ポリソムノグラフイを装着. 無呼吸低呼吸指数(AHI)と年齢, BMI, 降圧剤数, 外来血圧, 睡眠中最低酸素飽和度, 平均酸素飽和度, Creatinine, 尿酸, CRP, 脂質, をmild SAS群(AHI: 5-19.9/h), m...
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| Published in | 医療 Vol. 62; no. 5; pp. 270 - 274 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | Japanese |
| Published |
一般社団法人 国立医療学会
2008
国立医療学会 |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0021-1699 1884-8729 |
| DOI | 10.11261/iryo1946.62.270 |
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| Abstract | 閉塞性睡眠時無呼吸症候群: obstructive sleep apnea syndrome (OSAS)と高血圧については, いくつかの疫学研究で報告され, その重要性が認識されている. 高血圧とOSASとの関連を調べるため, Body Mass Index (BMI)25以上または顕著ないびき, 昼間の眠気症状のある高血圧患者連続25例に簡易型終夜ポリソムノグラフイを装着. 無呼吸低呼吸指数(AHI)と年齢, BMI, 降圧剤数, 外来血圧, 睡眠中最低酸素飽和度, 平均酸素飽和度, Creatinine, 尿酸, CRP, 脂質, をmild SAS群(AHI: 5-19.9/h), moderate SAS群(AHI: 20-39.9/h), severe SAS群(AHI: ≥40/h)別に検討した. AHI>30/hrの患者には経鼻的持続陽圧呼吸: nasal continuous positive airway pressure (nCPAP)を施行し前後の血圧を検討した. 25例全例にOSAS(AHI>5/h)を認め男女比は15対10, 平均SaO2, 収縮期血圧では有意にOSASの重症度に応じて平均SpO2の低下, 収縮期血圧の高値が認められた. AHIと降圧剤数では相関係数0.46, 有意(P<0.05)な正相関が認められ, 睡眠時無呼吸症をともなう高血圧症例ではAHIが高いほど降圧に多剤を必要とし, 降圧に難渋する傾向が認められた。AHI>30/hの高血圧患者(n=13)にnCPAPを導入し開始前と導入4週後の外来収縮期血圧は139.4±18.3vs120.9±7.7mmHg, と有意(P<0.01)に収縮期血圧の改善を認めた. nCPAP導入により降圧効果が認められ, 睡眠時無呼吸症を合併する薬剤抵抗性高血圧症例ではnCPAPは降圧剤を補助する有力な治療手段と考えられた. |
|---|---|
| AbstractList | 「要旨」閉塞性睡眠時無呼吸症候群：obstructive sleep apnea syndrome(OSAS)と高血圧については, いくつかの疫学研究で報告され, その重要性が認識されている. 高血圧とOSASとの関連を調べるため, Body Mass Index(BMI)25以上または顕著ないびき, 昼間の眠気症状のある高血圧患者連続25例に簡易型終夜ポリソムノグラフィを装着. 無呼吸低呼吸指数(AHI)と年齢, BMI, 降圧剤数, 外来血圧, 睡眠中最低酸素飽和度, 平均酸素飽和度, Creatinine, 尿酸, CRP, 脂質, をmild SAS群(AHI：5-19.9/h), moderate SAS群(AHI：20-39.9/h), severe SAS群(AHI：≧40/h)別に検討した. AHI＞30/hrの患者には経鼻的持続陽圧呼吸：nasal continuous positive airway pressure(nCPAP)を施行し前後の血圧を検討した. 25例全例にOSAS(AHI＞5/h)を認め男女比は15対10, 平均SaO2, 収縮期血圧では有意にOSASの重症度に応じて平均SpO2の低下, 収縮期血圧の高値が認められた. AHIと降圧剤数では相関係数0.46, 有意(P＜0.05)な正相関が認められ, 睡眠時無呼吸症をともなう高血圧症例ではAHIが高いほど降圧に多剤を必要とし, 降圧に難渋する傾向が認められた. AHI＞30/hの高血圧患者(n=13)にnCPAPを導入し開始前と導入4週後の外来収縮期血圧は139.4±18.3vs120.9±7.7mmHg, と有意(P＜0.01)に収縮期血圧の改善を認めた. nCPAP導入により降圧効果が認められ, 睡眠時無呼吸症を合併する薬剤抵抗性高血圧症例ではnCPAPは降圧剤を補助する有力な治療手段と考えられた. 閉塞性睡眠時無呼吸症候群: obstructive sleep apnea syndrome (OSAS)と高血圧については, いくつかの疫学研究で報告され, その重要性が認識されている. 高血圧とOSASとの関連を調べるため, Body Mass Index (BMI)25以上または顕著ないびき, 昼間の眠気症状のある高血圧患者連続25例に簡易型終夜ポリソムノグラフイを装着. 無呼吸低呼吸指数(AHI)と年齢, BMI, 降圧剤数, 外来血圧, 睡眠中最低酸素飽和度, 平均酸素飽和度, Creatinine, 尿酸, CRP, 脂質, をmild SAS群(AHI: 5-19.9/h), moderate SAS群(AHI: 20-39.9/h), severe SAS群(AHI: ≥40/h)別に検討した. AHI>30/hrの患者には経鼻的持続陽圧呼吸: nasal continuous positive airway pressure (nCPAP)を施行し前後の血圧を検討した. 25例全例にOSAS(AHI>5/h)を認め男女比は15対10, 平均SaO2, 収縮期血圧では有意にOSASの重症度に応じて平均SpO2の低下, 収縮期血圧の高値が認められた. AHIと降圧剤数では相関係数0.46, 有意(P<0.05)な正相関が認められ, 睡眠時無呼吸症をともなう高血圧症例ではAHIが高いほど降圧に多剤を必要とし, 降圧に難渋する傾向が認められた。AHI>30/hの高血圧患者(n=13)にnCPAPを導入し開始前と導入4週後の外来収縮期血圧は139.4±18.3vs120.9±7.7mmHg, と有意(P<0.01)に収縮期血圧の改善を認めた. nCPAP導入により降圧効果が認められ, 睡眠時無呼吸症を合併する薬剤抵抗性高血圧症例ではnCPAPは降圧剤を補助する有力な治療手段と考えられた. |
| Author | 竹本, 俊二 池田, 昌絵 友田, 純 梶川, 隆 |
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| References | 12) Minemura H, Akashiba T, Yamamoto H et al. Acute effects of nasal continuous positive airway pressure on 24-hour blood pressure and catecholamines in patients with obstructive sleep apnea. Intern Med 1998; 37: 1009-13. 5) Narkiewicz K, Montano N, Cogliati C et al. Altered cardiovascular variability in obstructive sleep apnea. Circulation 1998; 98: 1071-7. 9) Ip MS, Tse HF, Lam B et al. Endothelial function in obstructive sleep apnea and response to treatment. Am J Respir Crit Care Med 2004; 169: 348-53. 16) Campos RE, Perez RJ, Grilo RA et al. Long-term Effect of Continuous Positive Airway Pressure on BP in Patients With Hypertension and Sleep Apnea. Chest 2007; 132: 1847-52. 1) Peppard PE, Young T, Palta M et al. Retorospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000; 342: 1378-84. 7) Ip MS, Lam B, Ng MM et al. Obstructive sleep apnea is independently associated with insulin resistance. Am J Respir Crit Care Med 2002; 165: 670-6. 11) 石川譲治, 苅尾七臣. 睡眠時無呼吸症候群と高血圧. 血圧 2005; 12: 1168-72. 15) Campos RF, Grilo RA, Perez RJ et al. Effect of continuous positive airway pressure on ambulatory BP in patients with sleep apnea and hypertension: a placebo-controlled trial. Chest 2006; 129: 1459-67. 18) Doherty LS, Kiely JL, Swan V et al. Long-term effects of nasal continuous positive airway pressure therapy on cardiovascular outcomes in sleep apnea syndrome. Chest 2005; 127: 2076-84. 8) Kanagy NL, Walker BR, Nelin LD et al. Role of endothelin in intermittent hypoxia-induced hypertension. Hypertension 2001; 2: 511-5. 17) Modan M, Almog S, Fuchs Z et al. Obesity, glucose intolerance, hyperinsulinemia and response to antihypertensive drugs. Hypertension 1991; 17: 565-73. 6) Moller DS, Lind P, Strung B et al. Abnormal vasoactive hormones and 24-hour blood pressure in obstructive sleep apnea. Am J Hypertens 2003; 16: 274-80. 3) Logan AG, Perlikowski SM, Mente A et al. High prevalence of unrecognized sleepapnea in drugresistant hypertension. J Hypertens 2001; 19: 2271-7. 4) Somers VK, Dyken ME, Claary MP et al. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest 1995; 96: 1897-904. 2) Nieto FJ, Young TB, Lind BK et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA 2000; 283: 1829-36. 13) Akashiba T, Kurashina K, Minemura H et al. Daytime hypertension and the effects of short-term nasal continuous positive airway pressure treatment in obstructive sleep apnea syndrome. Intern Med 1995; 34: 528-32. 14) Becker HF, Jerrentrup A, Ploch T et al. Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation 2003; 107: 68-73. 10) Shamsuzzaman AS, Winnicki M, Wolk R et al. Elevated C-reactive protein in patients with obstructive sleep apnea. Circulation 2002; 105: 2462-4. |
| References_xml | – reference: 9) Ip MS, Tse HF, Lam B et al. Endothelial function in obstructive sleep apnea and response to treatment. Am J Respir Crit Care Med 2004; 169: 348-53. – reference: 4) Somers VK, Dyken ME, Claary MP et al. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest 1995; 96: 1897-904. – reference: 14) Becker HF, Jerrentrup A, Ploch T et al. Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation 2003; 107: 68-73. – reference: 12) Minemura H, Akashiba T, Yamamoto H et al. Acute effects of nasal continuous positive airway pressure on 24-hour blood pressure and catecholamines in patients with obstructive sleep apnea. Intern Med 1998; 37: 1009-13. – reference: 2) Nieto FJ, Young TB, Lind BK et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA 2000; 283: 1829-36. – reference: 13) Akashiba T, Kurashina K, Minemura H et al. Daytime hypertension and the effects of short-term nasal continuous positive airway pressure treatment in obstructive sleep apnea syndrome. Intern Med 1995; 34: 528-32. – reference: 18) Doherty LS, Kiely JL, Swan V et al. Long-term effects of nasal continuous positive airway pressure therapy on cardiovascular outcomes in sleep apnea syndrome. Chest 2005; 127: 2076-84. – reference: 3) Logan AG, Perlikowski SM, Mente A et al. High prevalence of unrecognized sleepapnea in drugresistant hypertension. J Hypertens 2001; 19: 2271-7. – reference: 16) Campos RE, Perez RJ, Grilo RA et al. Long-term Effect of Continuous Positive Airway Pressure on BP in Patients With Hypertension and Sleep Apnea. Chest 2007; 132: 1847-52. – reference: 5) Narkiewicz K, Montano N, Cogliati C et al. Altered cardiovascular variability in obstructive sleep apnea. Circulation 1998; 98: 1071-7. – reference: 1) Peppard PE, Young T, Palta M et al. Retorospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000; 342: 1378-84. – reference: 10) Shamsuzzaman AS, Winnicki M, Wolk R et al. Elevated C-reactive protein in patients with obstructive sleep apnea. Circulation 2002; 105: 2462-4. – reference: 15) Campos RF, Grilo RA, Perez RJ et al. Effect of continuous positive airway pressure on ambulatory BP in patients with sleep apnea and hypertension: a placebo-controlled trial. Chest 2006; 129: 1459-67. – reference: 8) Kanagy NL, Walker BR, Nelin LD et al. Role of endothelin in intermittent hypoxia-induced hypertension. Hypertension 2001; 2: 511-5. – reference: 11) 石川譲治, 苅尾七臣. 睡眠時無呼吸症候群と高血圧. 血圧 2005; 12: 1168-72. – reference: 6) Moller DS, Lind P, Strung B et al. Abnormal vasoactive hormones and 24-hour blood pressure in obstructive sleep apnea. Am J Hypertens 2003; 16: 274-80. – reference: 7) Ip MS, Lam B, Ng MM et al. Obstructive sleep apnea is independently associated with insulin resistance. Am J Respir Crit Care Med 2002; 165: 670-6. – reference: 17) Modan M, Almog S, Fuchs Z et al. Obesity, glucose intolerance, hyperinsulinemia and response to antihypertensive drugs. Hypertension 1991; 17: 565-73. |
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| Snippet | 閉塞性睡眠時無呼吸症候群: obstructive sleep apnea syndrome (OSAS)と高血圧については, いくつかの疫学研究で報告され, その重要性が認識されている. 高血圧とOSASとの... 「要旨」閉塞性睡眠時無呼吸症候群：obstructive sleep apnea syndrome(OSAS)と高血圧については, いくつかの疫学研究で報告され, その重要性が認識されている. 高血... |
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| Title | 高血圧患者と閉塞性睡眠時無呼吸症候群の検討 |
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