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Respiratory muscle strength and the risk of incident cardiovascular events.
Tuesday,2012-11-06 12:06 America/Los_Angeles — eenright
| Title | Respiratory muscle strength and the risk of incident cardiovascular events. |
| Publication Type | Journal Article |
| Year of Publication | 2004 |
| Authors | van der Palen, J, Rea, TD, Manolio, TA, Lumley, T, Newman, AB, Tracy, RP, Enright, PL, Psaty, BM |
| Journal | Thorax |
| Volume | 59 |
| Issue | 12 |
| Pagination | 1063-7 |
| Date Published | 2004 Dec |
| ISSN | 0040-6376 |
| Keywords | Cardiovascular 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> |
| DOI | 10.1136/thx.2004.021915 |
| Alternate Journal | Thorax |
| PubMed ID | 15563706 |
| PubMed Central ID | PMC1746892 |