BACKGROUND: Among apparently healthy men, elevated levels of C-reactive protein (CRP), a marker for systemic inflammation, predict risk of myocardial infarction and thromboembolic stroke. Whether increased levels of CRP are also associated with the development of symptomatic peripheral arterial disease (PAD) is unknown. METHODS AND RESULTS: Using a prospective, nested, case-control design, we measured baseline levels of CRP in 144 apparently healthy men participating in the Physicians' Health Study who subsequently developed symptomatic PAD (intermittent claudication or need for revascularization) and in an equal number of control subjects matched on the basis of age and smoking habit who remained free of vascular disease during a follow-up period of 60 months. Median CRP levels at baseline were significantly higher among those who subsequently developed PAD (1.34 versus 0.99 mg/L; P=.04). Furthermore, the risks of developing PAD increased significantly with each increasing quartile of baseline CRP concentration such that relative risks of PAD from lowest (referent) to highest quartile of CRP were 1.0, 1.3, 2.0, and 2.1 (Ptrend=.02). Compared with those with no clinical evidence of disease, the subgroup of case patients who required revascularization had the highest baseline CRP levels (median= 1.75 mg/L; P= .04); relative risks from lowest to highest quartile of CRP for this end point were 1.0, 1.8, 3.8, and 4.1 (Ptrend=.02). Risk estimates were similar after additional control for body mass index, hypercholesterolemia, hypertension, diabetes, and a family history of premature atherosclerosis. CONCLUSIONS: These prospective data indicate that among apparently healthy men, baseline levels of CRP predict future risk of developing symptomatic PAD and thus provide further support for the hypothesis that chronic inflammation is important in the pathogenesis of atherothrombosis.
RCT Entities:
BACKGROUND: Among apparently healthy men, elevated levels of C-reactive protein (CRP), a marker for systemic inflammation, predict risk of myocardial infarction and thromboembolic stroke. Whether increased levels of CRP are also associated with the development of symptomatic peripheral arterial disease (PAD) is unknown. METHODS AND RESULTS: Using a prospective, nested, case-control design, we measured baseline levels of CRP in 144 apparently healthy men participating in the Physicians' Health Study who subsequently developed symptomatic PAD (intermittent claudication or need for revascularization) and in an equal number of control subjects matched on the basis of age and smoking habit who remained free of vascular disease during a follow-up period of 60 months. Median CRP levels at baseline were significantly higher among those who subsequently developed PAD (1.34 versus 0.99 mg/L; P=.04). Furthermore, the risks of developing PAD increased significantly with each increasing quartile of baseline CRP concentration such that relative risks of PAD from lowest (referent) to highest quartile of CRP were 1.0, 1.3, 2.0, and 2.1 (Ptrend=.02). Compared with those with no clinical evidence of disease, the subgroup of case patients who required revascularization had the highest baseline CRP levels (median= 1.75 mg/L; P= .04); relative risks from lowest to highest quartile of CRP for this end point were 1.0, 1.8, 3.8, and 4.1 (Ptrend=.02). Risk estimates were similar after additional control for body mass index, hypercholesterolemia, hypertension, diabetes, and a family history of premature atherosclerosis. CONCLUSIONS: These prospective data indicate that among apparently healthy men, baseline levels of CRP predict future risk of developing symptomatic PAD and thus provide further support for the hypothesis that chronic inflammation is important in the pathogenesis of atherothrombosis.
Authors: Véronique L Roger; Alan S Go; Donald M Lloyd-Jones; Emelia J Benjamin; Jarett D Berry; William B Borden; Dawn M Bravata; Shifan Dai; Earl S Ford; Caroline S Fox; Heather J Fullerton; Cathleen Gillespie; Susan M Hailpern; John A Heit; Virginia J Howard; Brett M Kissela; Steven J Kittner; Daniel T Lackland; Judith H Lichtman; Lynda D Lisabeth; Diane M Makuc; Gregory M Marcus; Ariane Marelli; David B Matchar; Claudia S Moy; Dariush Mozaffarian; Michael E Mussolino; Graham Nichol; Nina P Paynter; Elsayed Z Soliman; Paul D Sorlie; Nona Sotoodehnia; Tanya N Turan; Salim S Virani; Nathan D Wong; Daniel Woo; Melanie B Turner Journal: Circulation Date: 2011-12-15 Impact factor: 29.690
Authors: Véronique L Roger; Alan S Go; Donald M Lloyd-Jones; Robert J Adams; Jarett D Berry; Todd M Brown; Mercedes R Carnethon; Shifan Dai; Giovanni de Simone; Earl S Ford; Caroline S Fox; Heather J Fullerton; Cathleen Gillespie; Kurt J Greenlund; Susan M Hailpern; John A Heit; P Michael Ho; Virginia J Howard; Brett M Kissela; Steven J Kittner; Daniel T Lackland; Judith H Lichtman; Lynda D Lisabeth; Diane M Makuc; Gregory M Marcus; Ariane Marelli; David B Matchar; Mary M McDermott; James B Meigs; Claudia S Moy; Dariush Mozaffarian; Michael E Mussolino; Graham Nichol; Nina P Paynter; Wayne D Rosamond; Paul D Sorlie; Randall S Stafford; Tanya N Turan; Melanie B Turner; Nathan D Wong; Judith Wylie-Rosett Journal: Circulation Date: 2010-12-15 Impact factor: 29.690
Authors: Mandar S Joshi; Liyue Tong; Angela C Cook; Brandon L Schanbacher; Hong Huang; Bing Han; Leona W Ayers; John Anthony Bauer Journal: Cardiovasc Pathol Date: 2012-01-28 Impact factor: 2.185
Authors: Tariq Ahmad; Mona Fiuzat; Daniel B Mark; Ben Neely; Megan Neely; William E Kraus; Dalane W Kitzman; David J Whellan; Mark Donahue; Faiez Zannad; Ileana L Piña; Kirkwood Adams; Christopher M O'Connor; G Michael Felker Journal: Am Heart J Date: 2013-11-04 Impact factor: 4.749