scholarly journals Widespread pain is a risk factor for cardiovascular mortality: results from the Framingham Heart Study

2019 ◽  
Vol 40 (20) ◽  
pp. 1609-1617 ◽  
Author(s):  
Jonas Tesarz ◽  
Wolfgang Eich ◽  
David Baumeister ◽  
Thomas Kohlmann ◽  
Ralph D'Agostino ◽  
...  
Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Gearoid M McMahon ◽  
Sarah R Preis ◽  
Shih-Jen Hwang ◽  
Caroline S Fox

Background: Chronic Kidney Disease (CKD) is an important public health issue and is associated with an increased risk of cardiovascular disease. Risk factors for CKD are well established, but most are typically assessed at or near the time of CKD diagnosis. Our hypothesis was that risk factors for CKD are present earlier in the course of the disease. We compared the prevalence of risk factors between CKD cases and controls at time points up to 30 years prior to CKD diagnosis. Methods: Participants were drawn from the Framingham Heart Study Offspring cohort. CKD was defined as an estimated glomerular filtration rate of ≤60ml/min/1.73m2. Incident CKD cases occurring at examination cycles 6, 7, and 8 were age- and sex-matched 1:2 to controls. Risk factors including systolic blood pressure (SBP), hypertension, lipids, diabetes, smoking status, body mass index (BMI) and dipstick proteinuria were measured at the time of CKD diagnosis and 10, 20 and 30 years prior. Logistic regression models, adjusted for age, sex, and time period, were constructed to compare risk factor profiles at each time point between cases and controls Results: During follow-up, 441 new cases of CKD were identified and these were matched to 882 controls (mean age 69.2 years, 52.4% women). Up to 30 years prior to CKD diagnosis, those who ultimately developed CKD were more likely to have hypertension (OR 1.74, CI 1.21-2.49), be obese (OR 1.74, CI 1.15-2.63) and have higher triglycerides (OR 1.43, CI 1.12-1.84, p=0.005 per 1 standard deviation increase). Each 10mmHg increase in SBP was associated with an OR of 1.22 for future CKD (95% CI 1.10-1.35) Additionally, cases were more likely to have diabetes (OR 2.90, CI 1.59-5.29) and be on antihypertensive therapy (OR 1.65, CI 1.14-2.40, p=0.009) up to 20 years prior to diagnosis. Increasing HDLc was associated with a lower risk of CKD (OR 0.84, CI 0.81-0.97 per 10mg/dl). Conclusions: As many as 30 years prior to diagnosis, risk factors for CKD are identifiable. In particular, modifiable risk factors such as obesity, hypertension and dyslipidemia are present early in the course of the disease. These findings demonstrate the importance of early identification of risk factors in patients at risk of CKD through a life-course approach.


2017 ◽  
Vol 151 ◽  
pp. 57-62 ◽  
Author(s):  
Marja K Puurunen ◽  
Shih-Jen Hwang ◽  
Chris J O'Donnell ◽  
Geoffrey Tofler ◽  
Andrew D Johnson

2010 ◽  
Vol 3 (5) ◽  
pp. 559-566 ◽  
Author(s):  
George Thanassoulis ◽  
Joseph M. Massaro ◽  
Udo Hoffmann ◽  
Amir A. Mahabadi ◽  
Ramachandran S. Vasan ◽  
...  

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Norrina B Allen ◽  
Hongyan Ning ◽  
John Wilkins ◽  
Daniel Levy ◽  
Donald Lloyd-Jones

Background: Having a first CVD event increases the risk for subsequent events; however, the long-term patterns in the development and sequence of multiple CVDs, including stroke, myocardial infarction (MI) and chronic heart failure (CHF) are unknown. The aim of this study was to identify distinct long-term patterns in the order and timing of MI, stroke and CHF occurrence. Methods: We used publicly available data from the Framingham Heart Study (FHS). The occurrence of fatal/non-fatal MI, stroke and CHF were examined separately using discrete mixture modeling implemented in SAS (Proc Traj) to identify trajectory groups for the risk of each CVD event starting at age 30. We included both first and subsequent events. Clusters of disease specific trajectory groups were examined. Baseline demographics and risk factors were compared across clusters. Results: Among 5,079 participants (ppts) in FHS, we identified 8 unique patterns in the development of CVDs (see figure). The majority, 72.5%, of Framingham ppts experienced average age- related increases in the yearly risk for all three endpoints of MI, stroke and heart failure (Average Risk group) other groups experienced early or higher risks for specific CVDs including the High CHF Risk group (6% of ppts), Early CHF group (2%), High Stroke Risk group (9%), High CHF and Stroke Risk group (1%), High MI Risk group (4%), High MI and CHF Risk group (1%), Early CHF and MI Risk group (1%). Groups in which stroke and/or HF risk was elevated had higher prevalence of smoking and greater baseline BP levels; those groups at elevated risk of MI had higher total cholesterol levels and higher BMI. Conclusions: We identified distinct patterns in development and ordering of MI, stroke and CHF associated with diverse risk factor profiles. By understanding the life-course and likely sequence of CVD events related to distinct risk factor profiles, clinicians may be able to consider personalized prevention strategies with the highest likelihood of preventing first CVD events and reducing the overall burden of CVD.


2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 749-749
Author(s):  
Jason Sanders

Abstract Interstitial lung abnormalities (ILA) exist in ~10% of adults >50 and associate with increased morbidity/mortality. Their pathobiology is poorly understood; age is the strongest risk factor. In the Framingham Heart Study, we determined associations between ILA and 10 blood biomarkers previously robustly associated with aging and mortality. Odds of ILA increased directly with ln-transformed GDF15 (OR [95% CI] = 3.20 [1.74-5.91], p=0.0002), TNF-αRII (2.41 [1.34-4.34], p=0.003), IL6 (1.76 [1.39-2.22], p<0.0001), insulin (1.56 [1.11-2.20], p=0.01), and CRP (1.53 [1.27-1.84], p<0.0001). Causal analysis showed GDF15 (p=0.008), TNF-αRII (p=0.004), and IL6 (p<0.0001) mediate the age effect on ILA. In adjusted survival models, only higher ln(GDF15) and ln(TNF-αRII) were associated with mortality (HR [95% CI] = 4.3 [2.3-8.1], p<0.0001 and 2.9 [1.5-5.8], p=0.002). GDF15 results were replicated in the COPDGene Study. These results suggest aging biomarkers may help risk stratify adults with ILA, and unmeasured ILA may confound prior associations between biomarkers and mortality.


Author(s):  
Leroy L. Cooper ◽  
Jian Rong ◽  
Martin G. Larson ◽  
Emelia J. Benjamin ◽  
Naomi M. Hamburg ◽  
...  

Community-based studies have evaluated cross-sectional age relations of aortic stiffness measures, which are not often recapitulated in longitudinal studies. We examined baseline and longitudinal change in aortic stiffness in 5491 participants (mean age, 49.5±14.5 years; 54% women) who attended 2 sequential examinations (6.0±0.6 years apart) of the Framingham Heart Study. Cross-sectional relations of central hemodynamics (mean arterial pressure, central pulse pressure, carotid-femoral pulse wave velocity, and characteristic impedance) with age and risk factors were assessed at visits 1 and 2 (models 1 and 2). We used model 1 coefficients (M 1 ), visit 1 risk factor levels (R 1 ), and age at each visit (A 1 , A 2 ) to estimate values at visits 1 (M 1 R 1 A 1 ) and 2 (M 1 R 1 A 2 ). While using model 1 coefficients, we accounted for age and risk factor level (R 2 ) changes to predict values at visit 2 (M 1 R 2 A 2 ). Using model 2 coefficients (M 2 ) and visit 2 age and risk factor levels, we predicted visit 2 values (M 2 R 2 A 2 ). We calculated predicted change 3 ways: delta1=M 1 R 1 A 2 −M 1 R 1 A 1 , delta2=M 1 R 2 A 2 −M 1 R 1 A 1 , and delta3=M 2 R 2 A 2 −M 1 R 1 A 1 . Delta1 values were biased and correlated poorly with actual changes ( r =−0.02–0.14). For mean arterial pressure, delta1=1.9±0.8 mm Hg ( r =0.14), observed change=−3.3±10.3 mm Hg, and discrepancy=5.2±10.2 mm Hg ( P <0.0001). For characteristic impedance, delta1=7.2±14.7 dyne×sec/cm 5 ( r =0.07), observed change=20.5±68.2 dyne×sec/cm 5 , and discrepancy=−13.3±68.7 dyne×sec/cm 5 ( P <0.0001). Delta2 values were moderately correlated with change ( r =0.17–0.54) but remained biased whereas delta3 values were moderately correlated with change with no bias. Projected change in hemodynamic measures extrapolated from cross-sectional age relations may differ substantially from actual change, particularly for variables with nonlinear age relations.


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