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Respiratory muscle strength and the risk of incident cardiovascular events.

TitleRespiratory muscle strength and the risk of incident cardiovascular events.
Publication TypeJournal Article
Year of Publication2004
Authorsvan der Palen, J, Rea, TD, Manolio, TA, Lumley, T, Newman, AB, Tracy, RP, Enright, PL, Psaty, BM
JournalThorax
Volume59
Issue12
Pagination1063-7
Date Published2004 Dec
ISSN0040-6376
KeywordsCardiovascular Diseases, Female, Follow-Up Studies, Forced Expiratory Volume, Humans, Male, Maximal Voluntary Ventilation, Prospective Studies, Respiratory Muscles, Risk Factors, Vital Capacity
Abstract<p><b>BACKGROUND: </b>Maximal inspiratory pressure (MIP) is a measure of inspiratory muscle strength. The prognostic importance of MIP for cardiovascular events among elderly community dwelling individuals is unknown. Diminished forced vital capacity (FVC) is a risk factor for cardiovascular events which remains largely unexplained.</p><p><b>METHODS: </b>MIP was measured at the baseline examination of the Cardiovascular Health Study. Participants had to be free of prevalent congestive heart failure (CHF), myocardial infarction (MI), and stroke.</p><p><b>RESULTS: </b>Subjects in the lowest quintile of MIP had a 1.5-fold increased risk of MI (HR 1.48, 95% CI 1.07 to 2.06) and cardiovascular disease (CVD) death (HR 1.54, 95% CI 1.09 to 2.15) after adjustment for non-pulmonary function covariates. There was a potential inverse relationship with stroke (HR 1.36, 95% CI 0.97 to 1.90), but there was little evidence of an association between MIP and CHF (HR 1.22, 95% CI 0.93 to 1.60). The addition of FVC to models attenuated the HR associated with MIP only modestly; similarly, addition of MIP attenuated the HR associated with FVC only modestly.</p><p><b>CONCLUSIONS: </b>A reduced MIP is an independent risk factor for MI and CVD death, and a suggestion of an increased risk for stroke. This association with MIP appeared to be mediated through mechanisms other than inflammation.</p>
DOI10.1136/thx.2004.021915
Alternate JournalThorax
PubMed ID15563706
PubMed Central IDPMC1746892