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Articles by M. J Pencina
Total Records ( 8 ) for M. J Pencina
  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.

  M. J Pencina , R. B D'Agostino , M. G Larson , J. M Massaro and R. S. Vasan
 

Background— Present cardiovascular disease (CVD) risk prediction algorithms were developed for a ≤10-year follow up period. Clustering of risk factors at younger ages and increasing life expectancy suggest the need for longer-term risk prediction tools.

Methods and Results— We prospectively followed 4506 participants (2333 women) of the Framingham Offspring cohort aged 20 to 59 years and free of CVD and cancer at baseline examination in 1971–1974 for the development of "hard" CVD events (coronary death, myocardial infarction, stroke). We used a modified Cox model that allows adjustment for competing risk of noncardiovascular death to construct a prediction algorithm for 30-year risk of hard CVD. Cross-validated survival C statistic and calibration 2 were used to assess model performance. The 30-year hard CVD event rates adjusted for the competing risk of death were 7.6% for women and 18.3% for men. Standard risk factors (male sex, systolic blood pressure, antihypertensive treatment, total and high-density lipoprotein cholesterol, smoking, and diabetes mellitus), measured at baseline, were significantly related to the incidence of hard CVD and remained significant when updated regularly on follow-up. Body mass index was associated positively with 30-year risk of hard CVD only in models that did not update risk factors. Model performance was excellent as indicated by cross-validated discrimination C=0.803 and calibration 2=4.25 (P=0.894). In contrast, 30-year risk predictions based on different applications of 10-year functions proved inadequate.

Conclusions— Standard risk factors remain strong predictors of hard CVD over extended follow-up. Thirty-year risk prediction functions offer additional risk burden information that complements that of 10-year functions.

  W Lieb , V Xanthakis , L. M Sullivan , J Aragam , M. J Pencina , M. G Larson , E. J Benjamin and R. S. Vasan
 

Background— Information is limited on the longitudinal tracking of left ventricular (LV) mass over the adult life course and the determinants of such change.

Methods and Results— We used multilevel modeling to evaluate the correlates of LV mass prospectively over a 16-year period in 4217 Framingham study participants (mean age 45 years, 53% women) using up to 4 serial routine echocardiographic observations on each individual (11 762 observations). Age, sex, body mass index, systolic blood pressure, antihypertensive treatment, smoking, and diabetes mellitus were related to longitudinal measures of LV mass. Women and participants with diabetes mellitus experienced a steeper increase in LV mass with advancing age (compared with men and those without diabetes mellitus; P for interactions <0.0001 and 0.0003, respectively). Women also displayed greater increments in LV mass with increasing body mass index (compared with men, P=0.04 for interaction). Participants with optimal values of these risk factors experienced lesser increases in LV mass over time. Analyses evaluating short-term (4-year) changes in LV mass (2605 unique individuals providing 4494 observations) identified the same key determinants that influenced its long-term trajectory (ie, body mass index, sex, systolic blood pressure, antihypertensive treatment, and smoking).

Conclusions— Our longitudinal observations on a large community-based sample identified higher blood pressure, excess adiposity, smoking, and diabetes mellitus as fundamental determinants of LV mass tracking over the adult life course. These observations are consistent with the notion that maintenance of optimal levels of these risk factors in midlife will reduce the burden of LV hypertrophy, and possibly heart failure, in older age.

  S. R Preis , M. J Pencina , S. J Hwang , R. B D'Agostino , P. J Savage , D Levy and C. S. Fox
 

Background— Individuals with diabetes mellitus are at 2- to 3-fold increased risk for cardiovascular disease (CVD) relative to those without diabetes. Our objective was to examine CVD risk factor level changes among individuals with and without type 2 diabetes mellitus from 1970 to 2005 in the Framingham Heart Study.

Methods and Results— We included 4195 participants (3990 with no diabetes and 205 with diabetes) 50 years of age and 3495 participants (3178 with no diabetes and 317 with diabetes) 60 years of age. Contemporaneous CVD risk factor levels were measured; linear regression models were used to assess the interaction between diabetes status and calendar year on CVD risk factor levels. Among 50-year-olds without diabetes mellitus, there was an increase in body mass index of 0.39 kg/m2 per 10 years, whereas for those with diabetes, there was an increase of 2.52 kg/m2 (P value for the diabetes-by–calendar year interaction [P for interaction] <0.001). For low-density lipoprotein cholesterol, the mean decrease was –7.43 mg/dL per decade (nondiabetes) and –15.5 mg/dL for diabetes (P for interaction=0.002). For systolic blood pressure, the mean decrease was –3.35 mm Hg per decade (nondiabetes) and –3.50 mm Hg for diabetes (P for interaction=0.97). The direction of the trends for those with diabetes relative to those without diabetes was similar for 60-year-olds.

Conclusions— Compared with individuals without diabetes mellitus, individuals with diabetes experienced a greater increase in body mass index, a greater decrease in low-density lipoprotein cholesterol, and a similar magnitude of decline in systolic blood pressure. Individuals with diabetes mellitus have not experienced the necessary declines in CVD risk factors to overcome their increased risk of CVD. Further efforts are needed to aggressively control CVD risk factors among individuals with diabetes mellitus.

  R. S Vasan , M. J Pencina , S. J Robins , J. P Zachariah , G Kaur , R. B D'Agostino and J. M. Ordovas
 

Background— Plasma high-density lipoprotein cholesterol concentration is related inversely to the risk of cardiovascular disease (CVD). Inhibiting cholesteryl ester transfer protein (CETP) activity raises high-density lipoprotein cholesterol and may be cardioprotective, but an initial clinical trial with a CETP inhibitor was stopped prematurely because of increased CVD in treated patients, raising concerns about this approach. Data relating circulating CETP concentrations to CVD incidence in the community are conflicting.

Methods and Results— Plasma CETP activity was measured in 1978 Framingham Heart Study participants (mean age, 51 years; 54% women) who attended a routine examination in 1987–1990 and were free of CVD. On follow-up (mean, 15.1 years), 320 participants experienced a first CVD event (fatal or nonfatal coronary heart disease, cerebrovascular disease, peripheral vascular disease, or heart failure). In multivariable analyses adjusted for standard risk factors including high-density lipoprotein cholesterol, plasma CETP activity was related inversely to the incidence of CVD events (hazard ratio for activity, at or above the median of 0.72; 95% confidence interval, 0.57 to 0.90; P=0.004 [compared with below median]; hazard ratio per SD increment, 0.86; 95% confidence interval, 0.76 to 0.97; P=0.01). The inverse association of CETP activity with CVD incidence remained robust in time-dependent models updating standard risk factors every 4 years and was maintained in analyses of incident "hard" CVD events (myocardial infarction, stroke, or heart failure).

Conclusions— In our prospective investigation of a community-based sample, lower plasma CETP activity was associated with greater CVD risk. These observations, if confirmed, challenge the concept that CETP inhibition may lower CVD risk.

  J. M Stolker , K. F Kennedy , J. B Lindsey , S. P Marso , M. J Pencina , D. E Cutlip , L Mauri , N. S Kleiman , D. J Cohen and on behalf of the EVENT Investigators
  Background—

Prediction of restenosis after percutaneous coronary intervention (PCI) remains challenging, and existing risk assessment algorithms were developed before the widespread adoption of drug-eluting stents (DES).

Methods and Results—

We used data from the EVENT registry to develop a risk model for predicting target lesion revascularization (TLR) in 8829 unselected patients undergoing DES implantation between 2004 and 2007. Using a split-sample validation technique, predictors of TLR at 1 year were identified from two thirds of the subjects (derivation cohort) using multiple logistic regression. Integer point values were created for each predictor, and the summed risk score (range, 0 to 10) was applied to the remaining sample (validation cohort). At 1 year, TLR occurred in 4.2% of patients, and after excluding stent thrombosis and early mechanical complications, the incidence of late TLR (more likely representing restenosis-related TLR) was 3.6%. Predictors of TLR were age <60, prior PCI, unprotected left main PCI, saphenous vein graft PCI, minimum stent diameter ≤2.5 mm, and total stent length ≥40 mm. Comparison of observed versus predicted rates of TLR according to risk score demonstrated good model fit in the validation set. There was more than a 3-fold difference in TLR rates between the lowest risk category (score=0; TLR rate, 2.2%) and the highest risk category (score ≥5; TLR rate, 7.5%).

Conclusions—

The overall incidence of TLR remains low among unselected patients receiving DES in routine clinical practice. A simple risk model incorporating 6 readily available clinical and angiographic variables helps identify individuals at extremely low (<2%) and modestly increased (>7%) risk of TLR after DES implantation.

 
 
 
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