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(Hypertension. 2006;47:e27.)
© 2006 American Heart Association, Inc.
Letters to the Editor |
Departments of Clinical Pharmacology and Therapeutics, Tohoku University Graduate School of Pharmaceutical Science and Medicine, Comprehensive Research and Education Center for Planning of Drug Development and Clinical Evaluation, Tohoku University 21st Century COE Program, Sendai, Japan
Department of Drug Development and Clinical Evaluation, Tohoku University Graduate School of Pharmaceutical Science and Medicine, Comprehensive Research and Education Center for Planning of Drug Development and Clinical Evaluation, Tohoku University 21st Century COE Program, Sendai, Japan
Departments of Clinical Pharmacology and Therapeutics, Tohoku University Graduate School of Pharmaceutical Science and Medicine, Comprehensive Research and Education Center for Planning of Drug Development and Clinical Evaluation, Tohoku University 21st Century COE Program, Sendai, Japan, for the Ohasama Study Group
We appreciate the comments by Tsivgoulis et al1 regarding our article.2 They pointed out the differences among our results,2 their own results,3 and the results by Kario et al.4 In the study by Kario et al,4 the subjects were older, high-risk hypertensive subjects; the risk of intracerebral hemorrhage (ICH) was not adjusted by the average ambulatory blood pressure (BP) value, which is the most important confounding factor for ICH. In their cross-sectional study, Tsivgoulis et al reported that an inverted dippertype of circadian BP variation was associated with ICH.3 Although they did adjust for baseline characteristics and ambulatory BP values, their ambulatory BP monitoring was done in a hospital setting in patients who were admitted for acute ICH. It is possible that the inverted dipper pattern in their cross-sectional study was the result of ICH.
Tsivgoulis et al also mentioned our apparent lack of adjustment for other possible confounding factors. However, even after adjustment for alcohol consumption and body mass index, the significant results did not change. With respect to the antihypertensive treatment of the study population at the time of the baseline survey, a short-acting calcium antagonist was primarily used.5 Although this drug may have affected circadian BP variation, the use of antihypertensive treatment did not significantly interact with the results (all P>0.7). Regarding the probable causes of ICH, there was only one case with ICH that had a history of heart disease and that was a possible candidate for anticoagulation therapy. None of the other subjects with ICH had a known history of secondary causes of ICH. Therefore, the effect of secondary causes would be minimal in the present study, as shown by another Japanese population study where the subjects were diagnosed by autopsy.6
The time of stroke onset in different stroke subtypes is an important consideration. In the present study, the time of stroke onset could be determined in 80 cases (63% of the total stroke cases; ICH, 21; cerebral infarction, 45; others, 14). Thirty-three percent (7 cases) of ICH occurred in the morning (6:00 AM to 11:59 AM), whereas 19% occurred in the afternoon (12:00 PM to 5:59 PM), 33% in the evening (6:00 PM to 11:59 PM), and 14% occurred at night (12:00 AM to 5:59 AM). Cerebral infarction occurred most frequently (64%) in the morning, while 13% occurred in the afternoon, 16% in the evening, and 7% at night. This distribution of the time of stroke onset was consistent with the report by Marler et al.7 Nevertheless, it was difficult to distinguish the stroke cases that actually occurred in the morning from those that had occurred during sleep but had only been noticed in the morning.7 Furthermore, because ambulatory BP values were not measured on the day that the stroke occurred, it was impossible to compare the direct associations between circadian BP patterns and the time of stroke onset. However, these factors would be related to the recorded time of stroke onset and the prognostic significance of the circadian BP patterns for a specific type of stroke, as demonstrated by the present study.
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2. Metoki H, Ohkubo T, Kikuya M, Asayama K, Obara T, Hashimoto J, Totsune K, Hoshi H, Satoh H, Imai Y. Prognostic significance for stroke of a morning pressor surge and a nocturnal blood pressure decline: the Ohasama study. Hypertension. 2006; 47: 149154.
3. Tsivgoulis G, Vemmos KN, Zakopoulos N, Spengos K, Manios E, Sofia V, Zis V, Mavrikakis M. Association of blunted nocturnal blood pressure dip with ICH. Blood Press Monit. 2005; 10: 189195.[CrossRef][Medline] [Order article via Infotrieve]
4. Kario K, Pickering TG, Matsuo T, Hoshide S, Schwartz JE, Shimada K. Stroke prognosis and abnormal nocturnal blood pressure falls in older hypertensives. Hypertension. 2001; 38: 852857.
5. Chonan K, Hashimoto J, Ohkubo T, Tsuji I, Nagai K, Kikuya M, Hozawa A, Matsubara M, Suzuki M, Fujiwara T, Araki T, Satoh H, Hisamichi S, Imai Y. Insufficient duration of action of antihypertensive drugs mediates high blood pressure in the morning in hypertensive population: the Ohasama study. Clin Exp Hypertens. 2002; 24: 261275.[CrossRef][Medline] [Order article via Infotrieve]
6. Hasuo Y, Ueda K, Kiyohara Y, Wada J, Kawano H, Kato I, Yanai T, Fujii I, Omae T, Fujishima M. Accuracy of diagnosis on death certificates for underlying causes of death in a long-term autopsy-based population study in Hisayama, Japan; with special reference to cardiovascular diseases. J Clin Epidemiol. 1989; 42: 577584.[CrossRef][Medline] [Order article via Infotrieve]
7. Marler JR, Price TR, Clark GL, Muller JE, Robertson T, Mohr JP, Hier DB, Wolf PA, Caplan LR, Foulkes MA. Morning increase in onset of ischemic stroke. Stroke. 1989; 20: 473476.
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