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Articles by R. A Kronmal
Total Records ( 4 ) for R. A Kronmal
  R. B Schnabel , T Aspelund , G Li , L. M Sullivan , A Suchy Dicey , T. B Harris , M. J Pencina , R. B D'Agostino , D Levy , W. B Kannel , T. J Wang , R. A Kronmal , P. A Wolf , G. L Burke , L. J Launer , R. S Vasan , B. M Psaty , E. J Benjamin , V Gudnason and S. R. Heckbert
 

Background  We sought to validate a recently published risk algorithm for incident atrial fibrillation (AF) in independent cohorts and other racial groups.

Methods  We evaluated the performance of a Framingham Heart Study (FHS)-derived risk algorithm modified for 5-year incidence of AF in the FHS (n = 4764 participants) and 2 geographically and racially diverse cohorts in the age range 45 to 95 years: AGES (the Age, Gene/Environment Susceptibility-Reykjavik Study) (n = 4238) and CHS (the Cardiovascular Health Study) (n = 5410, of whom 874 [16.2%] were African Americans). The risk algorithm included age, sex, body mass index, systolic blood pressure, electrocardiographic PR interval, hypertension treatment, and heart failure.

Results  We found 1359 incident AF events in 100 074 person-years of follow-up. Unadjusted 5-year event rates differed by cohort (AGES, 12.8 cases/1000 person-years; CHS whites, 22.7 cases/1000 person-years; and FHS, 4.5 cases/1000 person-years) and by race (CHS African Americans, 18.4 cases/1000 person-years). The strongest risk factors in all samples were age and heart failure. The relative risks for incident AF associated with risk factors were comparable across cohorts and race groups. After recalibration for baseline incidence and risk factor distribution, the Framingham algorithm, reported in C statistic, performed reasonably well in all samples: AGES, 0.67 (95% confidence interval [CI], 0.64-0.71); CHS whites, 0.68 (95% CI, 0.66-0.70); and CHS African Americans, 0.66 (95% CI, 0.61-0.71). Risk factors combined in the algorithm explained between 47.0% (AGES) and 63.6% (FHS) of the population-attributable risk.

Conclusions  Risk of incident AF in community-dwelling whites and African Americans can be assessed reliably by routinely available and potentially modifiable clinical variables. Seven risk factors accounted for up to 64% of risk.

  S Cheng , V. R.S Fernandes , D. A Bluemke , R. L McClelland , R. A Kronmal and J. A.C. Lima
 

Background— Age-related alterations of left ventricular (LV) structure and function that may predispose to cardiovascular events are not well understood.

Methods and Results— We used cardiac MRI to examine age-related differences in LV structure and function in 5004 participants without overt cardiovascular disease when enrolled in the Multi-Ethnic Study of Atherosclerosis; 1099 participants received additional strain analyses by MRI tagging. We also assessed the relation of age-associated remodeling with cardiovascular outcomes using Cox proportional hazard models adjusting for cardiovascular risk factors. Although LV mass decreased with age (–0.3 g per year), the mass-to-volume ratio markedly increased (+5 mg/mL per year, P<0.0001), driven by a substantial reduction in end-diastolic volume (–0.8 mL per year, P<0.0001). Age was also associated with a significant fall in stroke volume (–0.4 mL per year, P<0.0001), along with strain patterns reflecting systolic (P<0.0001) as well as diastolic (P<0.01) myocardial dysfunction—despite a modestly enhanced ejection fraction (+0.1% per year, P<0.0001). Increased mass-to-volume ratio conferred a significant risk for total cardiovascular events; this trend was strongest among younger (<65 years; hazard ratio, 3.69 [CI, 1.34 to 10.10]) versus older (≥65 years; hazard ratio, 1.68 [CI 0.77 to 3.68]) individuals with the highest compared to lowest mass-to-volume ratio quintile (Pinteraction=0.013).

Conclusions— Age is associated with a phenotype of LV remodeling marked by increased mass-to-volume ratio and accompanied by systolic as well as diastolic myocardial dysfunction that is not reflected by preserved ejection fraction. This pattern of ventricular remodeling confers significant cardiovascular risk, particularly when present earlier in life.

  K Nasir , R. L McClelland , R. S Blumenthal , D. C Goff , U Hoffmann , B. M Psaty , P Greenland , R. A Kronmal and M. J. Budoff
 

Background— Whether measuring and reporting of coronary artery calcium scores (CACS) might lead to changes in cardiovascular risk management is not established. In this observational study, we examined whether high baseline CACS were associated with the initiation as well continuation of new lipid-lowering medication (LLM), blood pressure–lowering medication (BPLM), and regular aspirin (ASA) use in a multi-ethnic population-based cohort.

Methods and Results— The Multi-Ethnic Study of Atherosclerosis (MESA) is a prospective cohort study of 6814 participants free of clinical cardiovascular disease at entry who underwent CAC testing at baseline examination (examination 1). Information on LLM, BPLM, and regular ASA usage was also obtained at baseline and at exams 2 and 3 (average of 1.6 and 3.2 years after baseline, respectively). In this study, we examined (1) initiation of these medications at examination 2 among participants not taking these medications at baseline; and (2) continuation of medication use to examination 3 among participants already on medication at baseline. Among MESA participants, initiation of LLM, BPLM, and ASA was greater in those with higher CACS. After taking into account age, sex, race, MESA site, LDL cholesterol, diabetes mellitus, body mass index, smoking status, hypertension, systolic blood pressure, and socioeconomic status (income, education, and health insurance), the risk ratios for medication initiation comparing those with CACS >400 versus CACS=0 were 1.53 (95% confidence interval [CI], 1.08, 2.15) for LLM, 1.55 (95% CI, 1.10 to 2.17) for BPLM, and 1.32 (95% CI, 1.03 to 1.69) for ASA initiation, respectively. The risk ratios for medication continuation among those with CAC >400 versus CACS=0 were 1.10 (95% CI, 1.01 to 1.20) for LLM, 1.05 (95% CI, 1.02 to 1.08) for BPLM, and 1.14 (95% CI, 1.04 to 1.25) for ASA initiation, respectively.

Conclusions— CACS >400 was associated with a higher likelihood of initiation and continuation of LLM, BPLM, and ASA. The association was weaker for continuation than for initiation of these preventive therapies.

 
 
 
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