Abstract 15328: Higher Non-exercise Estimated Cardiorespiratory Fitness in Midlife is Associated With Lower Risk of Incident Heart Failure: The Framingham Heart Study

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Joowon Lee ◽  
Tara Shrout ◽  
Ramachandran S Vasan ◽  
Vanessa Xanthakis

Introduction: Non-exercise estimated cardiorespiratory fitness (eCRF) algorithms have shown similar accuracy to CRF estimated from submaximal and maximal exercise tests in healthy adults. Using easily accessible health indicators, eCRF measurement does not involve in-person exercise testing, trained personnel, or specialized equipment for measuring CRF. Thus, eCRF may be a cost-effective alternative for heart disease risk stratification. The relation between eCRF and Heart failure (HF) remains unclear. Hypothesis: We hypothesized that higher midlife eCRF is associated with a lower risk of incident HF in later life. Methods: We evaluated 2,226 Framingham Offspring cohort participants attending examination cycles 2 and 7 (mean age of 42- 61years; 53% women). We used a validated longitudinal non-exercise algorithm for eCRF including age, sex, body mass index, waist circumference, resting heart rate, physical activity, and smoking status. Midlife eCRF was defined as a sex-specific standardized average of eCRF (z-score of the average eCRF with mean=0 and a standard deviation [SD]=1) between cycles 2 and 7. The sex-specific midlife eCRF were then categorized into three groups based on tertiles and was also analyzed as a continuous variable (per 1 SD increment). We used multivariable Cox proportional hazards regression models for pooled sexes to relate the midlife eCRF to incident HF after examination cycle 7. Results: Overall, 189 participants developed HF during a median of 17 years of follow-up. Participants in either moderate or high eCRF group experienced a 52% lower risk of HF compared to those in the low eCRF group, after adjustment for potential confounders. Additionally, each SD increment in midlife eCRF was associated with a 40% lower risk of HF in later life. The associations remained significant after excluding participants on antihypertensive treatment (Table). Conclusions: Lower eCRF during midlife may be a marker of higher HF risk in later life.

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Joowon Lee ◽  
Ramachandran S Vasan ◽  
Vanessa Xanthakis

Introduction: Studies have demonstrated that higher cardiorespiratory fitness (CRF) is associated with a lower risk of cardiovascular disease (CVD) and mortality. However, exercise CRF test is not routinely performed in clinical settings because it requires specialized equipment and trained personnel. Therefore, non-exercise estimated CRF (eCRF) using easily accessible health indicators in clinical practice may be a time- and cost-effective alternative for evaluating fitness. Hypothesis: We hypothesized that higher eCRF in midlife will be associated with a lower risk of CVD and all-cause mortality in later life. Methods: We evaluated 2,501 Framingham Offspring cohort participants (mean age 65 yrs., 52% women). We used a longitudinal non-exercise algorithm that includes age, sex, body mass index, waist circumference, resting heart rate, physical activity, and smoking status. We then used SAS PROC TRAJ to identify sex-specific latent patterns of eCRF (low, moderate, and high eCRF categories) between exam 2 and 8 (1979-2008). Multivariable Cox proportional hazards regression models were used to relate the long-term trajectories of eCRF to incident CVD and all-cause mortality on follow-up. Results: We identified three distinct trajectories of eCRF (Low [n=268, 10.7%] vs. moderate [n=1,273, 50.9%] vs. high [n=960, 38.4%]). Overall, 265 participants developed CVD and 429 died during 10 years of median follow-up. Participants in the “high eCRF” group were at lower risk of CVD and all-cause mortality compared to those in the “low eCRF” group, after adjustment for potential confounders ( Table ). Conclusions: Our findings suggest that lower eCRF during midlife may be a marker of risk of CVD and mortality in older adulthood.


Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Casey M Rebholz ◽  
Elizabeth Selvin ◽  
Menglu Liang ◽  
Christie M Ballantyne ◽  
Ron C Hoogeveen ◽  
...  

Introduction: Galectin-3 is a 35 kDa β-galactoside-binding lectin which has been proposed as a novel biomarker of heart failure primarily due to its involvement in myocardial fibrosis. Elevated levels of galectin-3 may be associated with fibrosis of other organs, such as the kidney, and increase the risk of developing kidney disease. Methods: Using Cox proportional hazards regression, we prospectively analyzed Atherosclerosis Risk in Communities (ARIC) study participants with measurements of plasma galectin-3 levels at baseline (visit 4, 1996-98) and without prevalent kidney disease or heart failure (N=9,647). Incident chronic kidney disease was defined as estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m 2 accompanied by 25% eGFR decline, chronic kidney disease-related hospitalization or death, or end-stage renal disease between baseline and December 31, 2013. Results: 2,105 participants (22%) developed incident chronic kidney disease over a median follow-up of 16 years. The mean (standard deviation) plasma level of galectin-3 was 14.7 (4.4) ng/mL. At baseline, galectin-3 was cross-sectionally associated with eGFR (r = -0.31) and urine albumin-to-creatinine ratio (UACR) (r = 0.19). After adjusting for demographics and kidney disease risk factors, there was a significant, graded, and positive association between galectin-3 and incident chronic kidney disease (quartile 4 vs. 1 HR: 1.84, 95% CI: 1.62, 2.09, p for trend <0.001). The association between galectin-3 and incident chronic kidney disease was attenuated but remained significant after accounting for eGFR and UACR (quartile 4 vs. 1 HR: 1.58, 95% CI: 1.39, 1.80, p for trend <0.001). The association was similar by diabetes status (p for interaction = 0.33) and stronger among those with hypertension (p for interaction = 0.004). Conclusion: In this community-based population, higher plasma galectin-3 levels were associated with elevated risk of developing incident chronic kidney disease, particularly among those with hypertension.


Author(s):  
Peng Li ◽  
Arlen Gaba ◽  
Patricia M. Wong ◽  
Longchang Cui ◽  
Lei Yu ◽  
...  

Background Disrupted nighttime sleep has been associated with heart failure (HF). However, the relationship between daytime napping, an important aspect of sleep behavior commonly seen in older adults, and HF remains unclear. We sought to investigate the association of objectively assessed daytime napping and risk of incident HF during follow‐up. Methods and Results We studied 1140 older adults (age, 80.7±7.4 [SD] years; female sex, 867 [76.1%]) in the Rush Memory and Aging Project who had no HF at baseline and were followed annually for up to 14 years. Motor activity (ie, actigraphy) was recorded for ≈10 days at baseline. We assessed daytime napping episodes between 9 am and 7 pm objectively from actigraphy using a previously published algorithm for sleep detection. Cox proportional hazards models examined associations of daily napping duration and frequency with incident HF. Eighty‐six participants developed incident HF, and the mean onset time was 5.7 years (SD, 3.4; range, 1–14). Participants who napped longer than 44.4 minutes (ie, the median daily napping duration) showed a 1.73‐fold higher risk of developing incident HF than participants who napped <44.4 minutes. Consistently, participants who napped >1.7 times/day (ie, the median daily napping frequency) showed a 2.20‐fold increase compared with participants who napped <1.7 times/day. These associations persisted after adjustment for covariates, including nighttime sleep, comorbidities, and cardiovascular disease/risk factors. Conclusions Longer and more frequent objective napping predicted elevated future risk of developing incident HF. Future studies are needed to establish underlying mechanisms.


Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Joowon Lee ◽  
Tara Shrout ◽  
Emelia J Benjamin ◽  
Vasan S Ramachandran ◽  
Vanessa Xanthakis

Introduction: Atrial fibrillation (AF) is the most common arrhythmia and a leading cause of stroke. Blood pressure (BP) responses to submaximal exercise are associated with incident cardiovascular disease and mortality. The association of BP responses to submaximal exercise with incident AF in the community is unknown. Hypothesis: We hypothesized that higher BP during and slower BP recovery after submaximal exercise are associated with a higher risk of incident AF. Methods: We evaluated Framingham Offspring Study participants who attended examination cycle 7, were free of AF, and underwent submaximal treadmill exercise testing. Systolic BP (SBP) and diastolic BP (DBP) were obtained pre-exercise (standing), during exercise (second stage, 2.5 mph at 12% grade), and 3-minutes post-exercise (supine). ΔBP during exercise was defined as exercise BP minus pre-exercise BP. ΔBP during recovery was defined as peak exercise BP minus 3-minutes post-exercise BP. We related exercise BP variables to risk of AF using Cox proportional hazards regression, adjusting for age, sex, height, weight, resting heart rate, resting SBP, resting DBP, use of antihypertensive medication, current smoking status, and diabetes. Results: We studied 2,002 participants (mean age 58 years; 53% women). During a median follow-up of 15 years, 236 participants (39% women) developed AF. We observed a positive association of exercise DBP and ΔDBP during exercise with risk of AF (Hazards Ratio [HR] per standard deviation [SD] increase 1.28, 95% CI 1.12-1.47 and HR 1.22, 95% CI 1.07-1.39, respectively). There was also a positive association between 3 minutes post-exercise SBP and AF risk (HR per SD-increase 1.31, 95% CI 1.07-1.60) and an inverse relation between ΔSBP during recovery and AF risk (HR per SD-increase 0.79, 95% CI 0.66-0.94, Table ) Conclusions: BP responses to submaximal exercise during midlife may serve as a marker for AF risk in later life.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jeremiah P Depta ◽  
Kyle Smoot ◽  
Kelly Cho ◽  
Galina Sokolovskaya ◽  
David R Gagnon ◽  
...  

Background: Cigarette smoking potentiates the antiplatelet effect of clopidogrel. Guidelines recommend clopidogrel for 12 months after percutaneous coronary intervention (PCI) with bare-metal (BMS) or drug-eluting (DES) stents. Whether smoking affects the risk of ischemic events related to clopidogrel use beyond 12 months after PCI is unknown Methods: We identified all PCIs performed in the Veterans Affairs (VA) health system from 2002-2006 and linked the information with the VA pharmacy database. VA and non-VA clinical outcomes were identified by ICD-9 codes from the VA National Patient Care and CMS/Medicare databases. All patients who were event-free at 12 months were followed for death, myocardial infarction (MI), or target vessel revascularization (TVR) up to 4 years following PCI. Prolonged (i.e., > 12 months) vs. clopidogrel use for < 12 months was assessed for each outcome within each stent type using propensity score adjusted inverse probability of weighting (IPW) Cox-proportional hazards analyses. Results: From 2002-2006, 28,507 patients included in the study underwent PCI and were event free at 12 months. Of these, 42% were smokers (n = 11,989) at the index PCI, 51% received a DES (n = 14, 594) and 45% were treated with prolonged clopidogrel use (n = 12,968). Following a 12-month landmark period, 2,194 deaths, 2,288 death or MIs, and 2,010 TVRs occurred. In smokers, prolonged clopidogrel use was associated with a lower risk of death and death or MI with both stent types (interaction p ≤ 0.10). In non-smokers, prolonged clopidogrel use was associated with a lower risk of death (interaction p = 0.04) and death or MI (interaction p = 0.03) in patients receiving DES only (Table). Conclusions: Prolonging clopidogrel more than 12 months after PCI may lower the risk of death or MI in smokers irrespective of stent type and in non-smokers receiving DES only. This study suggests that the duration of clopidogrel use after PCI may be tailored to smoking status and stent-type.


Author(s):  
Daniel B Ibsen ◽  
Emily B Levitan ◽  
Agneta Åkesson ◽  
Bruna Gigante ◽  
Alicja Wolk

Abstract Aims Trials demonstrate that following the DASH diet lowers blood pressure, which may prevent development of heart failure (HF). We investigated the association between long-term adherence to the DASH diet and food substitutions within the DASH diet on the risk of HF. Methods Men and women aged 45-83 years without previous HF, ischemic heart disease or cancer at baseline in 1998 from the Cohort of Swedish Men (n = 41,118) and the Swedish Mammography Cohort (n = 35,004) were studied. The DASH diet emphasizes intake of fruit, vegetables, whole grains, nuts and legumes and low-fat dairy and deemphasizes red and processed meat, sugar-sweetened beverages and sodium. DASH diet scores were calculated based on diet assessed by food frequency questionnaires in late 1997 and 2009. Incidence of HF was ascertained using the Swedish Patient Register. Multivariable Cox proportional hazards models were used to estimate hazard ratios (HR) with 95% confidence intervals (CI). Results During the median 22 years of follow-up (1998-2019) 12,164 participants developed HF. Those with the greatest adherence to the DASH diet had a lower risk of HF compared to those with the lowest adherence (HR 0.85, 95% CI 0.80, 0.91 for baseline diet and HR 0.83, 95% CI 0.78, 0.89 for long-term diet, comparing quintiles). Replacing 1 serving/day of red and processed meat with emphasized DASH diet foods was associated with an 8-12% lower risk of HF. Conclusion Long-term adherence to the DASH diet and relevant food substitutions within the DASH diet were associated with a lower risk of HF.


2019 ◽  
Vol 14 (11) ◽  
pp. 1562-1571 ◽  
Author(s):  
Joshua D. Bundy ◽  
Xuan Cai ◽  
Rupal C. Mehta ◽  
Julia J. Scialla ◽  
Ian H. de Boer ◽  
...  

Background and objectivesPatients with CKD are at high risk for cardiovascular disease, ESKD, and mortality. Vascular calcification is one pathway through which cardiovascular disease risks are increased. We hypothesized that a novel measure of serum calcification propensity is associated with cardiovascular disease events, ESKD, and all-cause mortality among patients with CKD stages 2–4.Design, setting, participants, & measurementsAmong 3404 participants from the prospective, longitudinal Chronic Renal Insufficiency Cohort Study, we quantified calcification propensity as the transformation time (T50) from primary to secondary calciprotein particles, with lower T50 corresponding to higher calcification propensity. We used multivariable-adjusted Cox proportional hazards regression models to assess the associations of T50 with risks of adjudicated atherosclerotic cardiovascular disease events (myocardial infarction, stroke, and peripheral artery disease), adjudicated heart failure, ESKD, and mortality.ResultsThe mean T50 was 313 (SD 79) minutes. Over an average 7.1 (SD 3.1) years of follow-up, we observed 571 atherosclerotic cardiovascular disease events, 633 heart failure events, 887 ESKD events, and 924 deaths. With adjustment for traditional cardiovascular disease risk factors, lower T50 was significantly associated with higher risk of atherosclerotic cardiovascular disease (hazard ratio [HR] per SD lower T50, 1.14; 95% confidence interval [95% CI], 1.05 to 1.25), ESKD within 3 years from baseline (HR per SD lower T50, 1.68; 95% CI, 1.52 to 1.86), and all-cause mortality (HR per SD lower T50, 1.16; 95% CI, 1.09 to 1.24), but not heart failure (HR per SD lower T50, 1.06; 95% CI, 0.97 to 1.15). After adjustment for eGFR and 24-hour urinary protein, T50 was not associated with risks of atherosclerotic cardiovascular disease, ESKD, and mortality.ConclusionsAmong patients with CKD stages 2–4, higher serum calcification propensity is associated with atherosclerotic cardiovascular disease events, ESKD, and all-cause mortality, but this association was not independent of kidney function.PodcastThis article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2019_10_28_CJN04710419.mp3


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
N Bondonno ◽  
K Murray ◽  
C P Bondonno ◽  
J R Lewis ◽  
K D Croft ◽  
...  

Abstract Background Our understanding of how diet affects future risk of atrial fibrillation (AF) is limited. Evidence suggests that higher habitual intakes of flavonoids, bio-active compounds found in plant-based foods and beverages, lower cardiovascular disease risk, attenuate inflammation, and may have anti-arrhythmic properties. Purpose To investigate the association between flavonoid intake and clinically apparent AF in a large cohort of Danish men and women. Methods Baseline data from 55 634 participants without AF of the Danish Diet, Cancer and Health Study, recruited from 1993 to 1997, were cross-linked with Danish nationwide registries. Flavonoid intake was calculated from validated food frequency questionnaires using the Phenol-Explorer database. Associations between flavonoid intake and AF hospitalisation were examined using restricted cubic splines based on Cox proportional hazards models with adjustments for age, sex, BMI, smoking status, physical activity, alcohol intake, income, and hyperthyroidism. Results After a median [IQR] follow-up of 21 [18–22] years, 6 301 participants were hospitalised with AF. Non-linear associations were observed for total flavonoid intake and for all flavonoid sub-classes. For total flavonoid intake, after adjusting for potential lifestyle confounders and compared to participants in quintile 1 (median intake: 173 mg/day), those in quintile 3 (median intake: 320 mg/day) and quintile 4 (median intake: 494 mg/day) had a significantly lower risk of AF, with hazard ratios (95% CI) of 0.93 (0.87, 0.99) and 0.92 (0.86, 0.98), respectively. Compared to median intake in the lowest quintile, a total flavonoid intake of 1000 mg/day was associated with a lower risk of AF in smokers [0.86 (0.77, 0.96)] but not in non-smokers [0.96 (0.88, 1.05)], a lower risk of AF in high alcohol consumers [>20 g/d: 0.84 (0.75, 0.94)] but not in low-to-moderate alcohol consumers [<20 g/d: 0.97 (0.89, 1.06], a trending lower risk of AF in diabetics [0.76 (0.51, 1.14)] but not in non-diabetics [0.95 (0.89, 1.02)], and a trending lower risk of AF in those with ischaemic heart disease [0.84 (0.65, 1.09)] but not in those without [0.96 (0.89, 1.03), Figure 1]. Figure 1 Conclusion We observed an inverse association between total flavonoid intake and AF, most notably in sub-populations with known lifestyle and disease risk factors for AF. This finding warrants investigation in randomised controlled trials. If confirmed, ensuring the adequate consumption of flavonoid-rich foods, particularly in individuals “at risk”, may be an important strategy to mitigate AF risk. Acknowledgement/Funding The Danish Diet, Cancer, and Health Study was funded by the Danish Cancer Society.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
L.A Shpagina ◽  
O.S Kotova ◽  
I.S Shpagin ◽  
G.V Kuznetsova ◽  
N.V Kamneva ◽  
...  

Abstract Background Heart failure decompensation requiring hospitalization is an important event, associated with mortality and investigating its predictors is topical problem. Chronic obstructive pulmonary disease (COPD) is a common comorbidity for heart failure. Both conditions share common molecular mechanisms such as systemic inflammation. COPD is heterogeneous and subpopulations with different inflammation patterns may interact with heart failure in different manner. Airway inflammation in occupational COPD may differs from COPD in tobacco smokers. Additionally cardiotoxicity of industrial chemicals influence heart failure features. Despite this biological plausibility, heart failure and occupational COPD comorbidity is not studied enough. Purpose To reveal predictors of hospitalizations for heart failure decompensation in patients with heart failure and occupational COPD comorbidity. Methods Occupational COPD patients (n=115) were investigated in a prospective cohort observational study. Comparison group – 115 tobacco smokers with COPD. Control group – 115 healthy persons. Controls were selected by propensity score matching, covariates were COPD duration, age and gender. Then COPD groups were stratified according to heart failure. Working conditions, echocardiography, spirometry, pulsoxymetry, 6-mitute walking test were done. Molecular markers of tissue damage – chemokine ligand 18 (CCL 18), lactate dehydrogenase, cardiac troponin T, N-terminal pro-B-type natriuretic peptide (NT pro-BNP), protein S100 beta, von Willebrand factor were measured in serum by ELISA. Follow up after initial assessment was 12 month. Predictors were determined by Cox proportional hazards regression with ROC analysis. Results Heart failure rate in occupational COPD patients were higher – 54.8% versus 36.5% in tobacco smokers with COPD, p&lt;0.05. Heart failure with preserved ejection fraction was predominant – 40.9%. Prevalence of biventricular heart failure was 38.3%, isolated right heart failure – 13%, left heart failure – 2.6%. Cumulative hospitalization rate in occupational COPD with heart failure group was higher than in comparison group, 17.5% and 9.5% respectively, p=0.01. In Cox proportional hazards regression model predictors of hospitalizations for heart failure decompensation during 12 months in this group were length of service (HR 1.22, 95% CI: 1.03–2.5), aromatic hydrocarbons concentration at workplaces air (HR 1.4, 95% CI: 1.15–1.96), serum protein S100 beta (HR 1.10, 95% CI: 1.02–1.87), SaO2 (HR 1.2, 95% CI: 1.06–2.13). Area under the ROC curve was 0.82. Conclusion Length of service, aromatic hydrocarbons concentration at workplaces air, serum protein S100 beta, SaO2 are considered to be independent risk factors of heart failure decompensation required hospitalization in patients with heart failure and occupational COPD comorbidity. Funding Acknowledgement Type of funding source: None


Author(s):  
Laurie Grieshober ◽  
Stefan Graw ◽  
Matt J. Barnett ◽  
Gary E. Goodman ◽  
Chu Chen ◽  
...  

Abstract Purpose The neutrophil-to-lymphocyte ratio (NLR) is a marker of systemic inflammation that has been reported to be associated with survival after chronic disease diagnoses, including lung cancer. We hypothesized that the inflammatory profile reflected by pre-diagnosis NLR, rather than the well-studied pre-treatment NLR at diagnosis, may be associated with increased mortality after lung cancer is diagnosed in high-risk heavy smokers. Methods We examined associations between pre-diagnosis methylation-derived NLR (mdNLR) and lung cancer-specific and all-cause mortality in 279 non-small lung cancer (NSCLC) and 81 small cell lung cancer (SCLC) cases from the β-Carotene and Retinol Efficacy Trial (CARET). Cox proportional hazards models were adjusted for age, sex, smoking status, pack years, and time between blood draw and diagnosis, and stratified by stage of disease. Models were run separately by histotype. Results Among SCLC cases, those with pre-diagnosis mdNLR in the highest quartile had 2.5-fold increased mortality compared to those in the lowest quartile. For each unit increase in pre-diagnosis mdNLR, we observed 22–23% increased mortality (SCLC-specific hazard ratio [HR] = 1.23, 95% confidence interval [CI]: 1.02, 1.48; all-cause HR = 1.22, 95% CI 1.01, 1.46). SCLC associations were strongest for current smokers at blood draw (Interaction Ps = 0.03). Increasing mdNLR was not associated with mortality among NSCLC overall, nor within adenocarcinoma (N = 148) or squamous cell carcinoma (N = 115) case groups. Conclusion Our findings suggest that increased mdNLR, representing a systemic inflammatory profile on average 4.5 years before a SCLC diagnosis, may be associated with mortality in heavy smokers who go on to develop SCLC but not NSCLC.


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