Lower target blood pressures are safe and effective for the prevention of recurrent stroke : the PROGRESS trial
Identifieur interne : 009E18 ( Main/Exploration ); précédent : 009E17; suivant : 009E19Lower target blood pressures are safe and effective for the prevention of recurrent stroke : the PROGRESS trial
Auteurs : Hisatomi Arima [Australie] ; John Chalmers [Australie] ; Mark Woodward [Australie] ; Craig Anderson [Australie] ; Anthony Rodgers [Nouvelle-Zélande] ; Stephen Davis [Australie] ; Stephen Macmahon [Australie] ; Bruce Neal [Australie]Source :
- Journal of hypertension [ 0263-6352 ] ; 2006.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Objective To explore the likely optimum blood pressure (BP) level for patients with a history of cerebrovascular disease. Methods The Perindopril Protection Against Recurrent Stroke Study (PROGRESS) was a randomized, placebo-controlled trial that established the beneficial effects of BP lowering in 6105 patients with cerebrovascular disease. The present study comprises two series of post hoc analyses. The first was designed to investigate the effects of randomized treatment on recurrent stroke by baseline BP levels, and the second was a corresponding observational analysis investigating the association between achieved follow-up BP levels and recurrent stroke risk. Results Analyses of the randomized treatment comparisons showed that BP lowering with combination therapy produced similar risk reductions in each of four subgroups defined by baseline BP of less than 120, 120-139, 140-159, and 160 mmHg or greater (P homogeneity = 0.5). The effects of single-drug therapy were also comparable across these subgroups (P homogeneity = 0.2), but consistently greater benefits were observed with combination compared to single-drug therapy. The analyses of achieved follow-up BP showed that the lowest risk of recurrence was among the one-quarter of participants with the lowest follow-up BP levels (median 112/72 mmHg), and that risks rose progressively with higher follow-up BP levels. Minor side-effects were progressively more common at lower BP levels (P homogeneity = 0.04), but there was no excess of serious complications (all P homogeneity > 0.2). Conclusion These analyses provide no evidence of a J-curve relationship between BP level and stroke risk among patients with cerebrovascular disease, and identify no patient group among whom more intensive BP lowering would not be expected to produce greater risk reductions.
Affiliations:
- Australie, Nouvelle-Zélande
- Nouvelle-Galles du Sud, Victoria (État)
- Melbourne, Sydney
- Université de Melbourne, Université de Sydney
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and effective for the prevention of recurrent stroke : the PROGRESS trial</title><author><name sortKey="Arima, Hisatomi" sort="Arima, Hisatomi" uniqKey="Arima H" first="Hisatomi" last="Arima">Hisatomi Arima</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>The George Institute for International Health, University of Sydney</s1><s2>Sydney</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Australie</country><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region><settlement type="city">Sydney</settlement></placeName><orgName type="university">Université de Sydney</orgName></affiliation></author><author><name sortKey="Chalmers, John" sort="Chalmers, John" uniqKey="Chalmers J" first="John" last="Chalmers">John Chalmers</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>The George Institute for International Health, University of Sydney</s1><s2>Sydney</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Australie</country><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region><settlement type="city">Sydney</settlement></placeName><orgName type="university">Université de Sydney</orgName></affiliation></author><author><name sortKey="Woodward, Mark" sort="Woodward, Mark" uniqKey="Woodward M" first="Mark" last="Woodward">Mark Woodward</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>The George Institute for International Health, University of Sydney</s1><s2>Sydney</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Australie</country><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region><settlement type="city">Sydney</settlement></placeName><orgName type="university">Université de Sydney</orgName></affiliation></author><author><name sortKey="Anderson, Craig" sort="Anderson, Craig" uniqKey="Anderson C" first="Craig" last="Anderson">Craig Anderson</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>The George Institute for International Health, University of Sydney</s1><s2>Sydney</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Australie</country><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region><settlement type="city">Sydney</settlement></placeName><orgName type="university">Université de Sydney</orgName></affiliation></author><author><name sortKey="Rodgers, Anthony" sort="Rodgers, Anthony" uniqKey="Rodgers A" first="Anthony" last="Rodgers">Anthony Rodgers</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Clinical Trials Research Unit, University of Auckland</s1><s2>Auckland</s2><s3>NZL</s3><sZ>5 aut.</sZ></inist:fA14><country>Nouvelle-Zélande</country><wicri:noRegion>Auckland</wicri:noRegion></affiliation></author><author><name sortKey="Davis, Stephen" sort="Davis, Stephen" uniqKey="Davis S" first="Stephen" last="Davis">Stephen Davis</name><affiliation wicri:level="4"><inist:fA14 i1="03"><s1>Department of Neurology, Royal Melbourne Hospital, University of Melbourne</s1><s2>Melbourne</s2><s3>AUS</s3><sZ>6 aut.</sZ></inist:fA14><country>Australie</country><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region><settlement type="city">Melbourne</settlement></placeName><orgName type="university">Université de Melbourne</orgName></affiliation></author><author><name sortKey="Macmahon, Stephen" sort="Macmahon, Stephen" uniqKey="Macmahon S" first="Stephen" last="Macmahon">Stephen Macmahon</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>The George Institute for International Health, University of Sydney</s1><s2>Sydney</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Australie</country><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region><settlement type="city">Sydney</settlement></placeName><orgName type="university">Université de Sydney</orgName></affiliation></author><author><name sortKey="Neal, Bruce" sort="Neal, Bruce" uniqKey="Neal B" first="Bruce" last="Neal">Bruce Neal</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>The George Institute for International Health, University of Sydney</s1><s2>Sydney</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Australie</country><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region><settlement type="city">Sydney</settlement></placeName><orgName type="university">Université de Sydney</orgName></affiliation></author></analytic><series><title level="j" type="main">Journal of hypertension</title><title level="j" type="abbreviated">J. hypertens.</title><idno type="ISSN">0263-6352</idno><imprint><date when="2006">2006</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of hypertension</title><title level="j" type="abbreviated">J. hypertens.</title><idno type="ISSN">0263-6352</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antihypertensive agent</term><term>Arterial pressure</term><term>Blood pressure</term><term>Cardiovascular disease</term><term>Diuretic</term><term>Hypertension</term><term>Indapamide</term><term>Perindopril</term><term>Prevention</term><term>Stroke</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Appareil circulatoire pathologie</term><term>Accident cérébrovasculaire</term><term>Hypertension artérielle</term><term>Pression artérielle</term><term>Pression sanguine</term><term>Prévention</term><term>Indapamide</term><term>Périndopril</term><term>Antihypertenseur</term><term>Diurétique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective To explore the likely optimum blood pressure (BP) level for patients with a history of cerebrovascular disease. Methods The Perindopril Protection Against Recurrent Stroke Study (PROGRESS) was a randomized, placebo-controlled trial that established the beneficial effects of BP lowering in 6105 patients with cerebrovascular disease. The present study comprises two series of post hoc analyses. The first was designed to investigate the effects of randomized treatment on recurrent stroke by baseline BP levels, and the second was a corresponding observational analysis investigating the association between achieved follow-up BP levels and recurrent stroke risk. Results Analyses of the randomized treatment comparisons showed that BP lowering with combination therapy produced similar risk reductions in each of four subgroups defined by baseline BP of less than 120, 120-139, 140-159, and 160 mmHg or greater (P homogeneity = 0.5). The effects of single-drug therapy were also comparable across these subgroups (P homogeneity = 0.2), but consistently greater benefits were observed with combination compared to single-drug therapy. The analyses of achieved follow-up BP showed that the lowest risk of recurrence was among the one-quarter of participants with the lowest follow-up BP levels (median 112/72 mmHg), and that risks rose progressively with higher follow-up BP levels. Minor side-effects were progressively more common at lower BP levels (P homogeneity = 0.04), but there was no excess of serious complications (all P homogeneity > 0.2). Conclusion These analyses provide no evidence of a J-curve relationship between BP level and stroke risk among patients with cerebrovascular disease, and identify no patient group among whom more intensive BP lowering would not be expected to produce greater risk reductions.</div></front></TEI><affiliations><list><country><li>Australie</li><li>Nouvelle-Zélande</li></country><region><li>Nouvelle-Galles du Sud</li><li>Victoria (État)</li></region><settlement><li>Melbourne</li><li>Sydney</li></settlement><orgName><li>Université de Melbourne</li><li>Université de Sydney</li></orgName></list><tree><country name="Australie"><region name="Nouvelle-Galles du Sud"><name sortKey="Arima, Hisatomi" sort="Arima, Hisatomi" uniqKey="Arima H" first="Hisatomi" last="Arima">Hisatomi Arima</name></region><name sortKey="Anderson, Craig" sort="Anderson, Craig" uniqKey="Anderson C" first="Craig" last="Anderson">Craig Anderson</name><name sortKey="Chalmers, John" sort="Chalmers, John" uniqKey="Chalmers J" first="John" last="Chalmers">John Chalmers</name><name sortKey="Davis, Stephen" sort="Davis, Stephen" uniqKey="Davis S" first="Stephen" last="Davis">Stephen Davis</name><name sortKey="Macmahon, Stephen" sort="Macmahon, Stephen" uniqKey="Macmahon S" first="Stephen" last="Macmahon">Stephen Macmahon</name><name sortKey="Neal, Bruce" sort="Neal, Bruce" uniqKey="Neal B" first="Bruce" last="Neal">Bruce Neal</name><name sortKey="Woodward, Mark" sort="Woodward, Mark" uniqKey="Woodward M" first="Mark" last="Woodward">Mark Woodward</name></country><country name="Nouvelle-Zélande"><noRegion><name sortKey="Rodgers, Anthony" sort="Rodgers, Anthony" uniqKey="Rodgers A" first="Anthony" last="Rodgers">Anthony Rodgers</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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