Exercise intensity is associated with progression of coronary artery calcification in middle-aged and older athletes: findings from the MARC-2 study

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
V Aengevaeren ◽  
A Mosterd ◽  
TL Braber ◽  
S Sharma ◽  
HM Nathoe ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Dutch Heart Foundation Background  Recent studies have reported increased coronary artery calcification (CAC) in middle-aged male athletes, which is related to the amount and intensity of lifelong exercise. However, previous studies are limited by their cross-sectional study design.  Purpose  We prospectively assessed progression of CAC and its association to exercise volume and intensity in middle-aged and older athletes. Methods  318 asymptomatic middle-aged and older men were recruited in the Measuring Athlete’s Risk of Cardiovascular events (MARC) study between 2012-2014 and invited for follow-up (MARC-2) between 2019-2020. During both study visits, computed tomography imaging was performed to assess CAC. Exercise characteristics during follow-up were used to calculate exercise volumes (Metabolic equivalent of task [MET]-hours/week), whereas intensities were classified as moderate (3-6 MET), vigorous (6-9 MET) and very vigorous (>9 MET). For linear regression analyses, CAC scores were transformed (Ln delta CAC score + 1) and analyses were adjusted for baseline confounders, CAC at baseline and time between CT scans. Exercise intensities were assessed as proportion of MET-hrs/week and separately included, while adjusting for exercise volume. Results  We included 289 men (54.9 ± 6.4 years) for MARC-2, with a follow-up of 6.3 ± 0.5 years. Participants exercised for 41 [25-57] MET-hrs/week, of which the median percentage was 0% [interquartile range 0-19] at moderate, 44% [0-84] at vigorous and 34% [0-80] at very vigorous intensity. At baseline, CAC was present in 151 (52%) men, and increased to 205 (71%) men at follow-up. CAC scores increased from 1 [0-32] to 31 [0-132]. Delta CAC score (26 [0-104]) was not associated with overall exercise volume. However, delta CAC score was negatively associated with vigorous intensity exercise and positively associated with very vigorous intensity exercise (Table). Conclusion  Progression of CAC was not associated with overall exercise volume during 6-year follow-up. However, the degree of vigorous intensity exercise was associated with attenuated CAC progression, whereas very vigorous intensity exercise was associated with accelerated CAC progression. Linear regression analyses Progression of CAC (Ln Delta CAC score +1) B (95% CI) P-Value Exercise volume (MET-hours/week) .001 (-.005 - .008) .70 Exercise Intensity Moderate intensity (%) -.002 (-.009 - .005) .65 Vigorous intensity (%) -.005 (-.009 - .000) .03 Very vigorous intensity (%) .005 (.001 - .009) .02

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
V Aengevaeren ◽  
A Mosterd ◽  
T.L Braber ◽  
H.M Nathoe ◽  
T.M.H Eijsvogels ◽  
...  

Abstract Background Emerging evidence indicates increased coronary atherosclerosis in amateur athletes. However, previous studies were limited by its cross-sectional design and limited sample size, preventing the exploration of sport specific associations with coronary atherosclerosis. Purpose We aimed to compare the incidence and progression of coronary artery calcification (CAC) between runners, cyclists and other types of athletes using a prospective cohort study with repetitive measurements. Methods Asymptomatic middle-aged men, who previously underwent a sports medical evaluation without abnormalities, were recruited in the Measuring Athlete's Risk of Cardiovascular events (MARC) study (n=318) and were asked to participate in this follow-up study. CT imaging was performed to assess CAC scores. Data was collected between 2012–2014 (i.e. baseline) and 2019–2020 (i.e. follow-up). We categorized participants as runners, cyclists or “other” sports (e.g. water polo, tennis, hockey, etc.) based on their dominant sport performance at baseline. Results We included 260 men in this interim analysis, with an average follow-up time of 6.3±0.5 years. Age (61.4±6.4 years), systolic blood pressure (143±20 mmHg), BMI (25.2±2.8 kg/m2), LDL-cholesterol (3.2±0.9 mmol/L), smoking (0.3 [0–8] pack years) and family history of coronary heart disease (28%) did not differ between runners (n=64), cyclists (n=75) and other athletes (n=121, all p>0.05). CAC was present in 137 (53%) men at baseline, which increased to 181 (70%) at follow-up. CAC scores increased from 1 [0–33] to 33 [0–129]. Cyclists had a lower CAC prevalence and CAC scores compared to individuals performing other sports at follow-up (Figure 1). Of those without CAC at baseline (n=123, 47%), cyclists less often developed CAC during follow-up compared with runners (adjusted OR=0.36 [0.17–0.79], p=0.01). In the entire cohort, CAC progression (ln delta CAC+1) was less prominent in cyclists than runners (adjusted B=−0.75 [−1.39 to −0.11], p=0.02), whereas progression of CAC in participants performing other sports did not differ from the runners. In participants with CAC at baseline, cyclists also had less CAC progression than runners (B=−0.49 [−0.95 to −0.02], p=0.04). Conclusion Cyclists have a lower incidence and less progression of CAC during 6 years of follow-up compared with runners and individuals performing other sports. Figure 1. Sport specific CAC prevalence and scores Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Hartstichting


2006 ◽  
Vol 184 (1) ◽  
pp. 86-93 ◽  
Author(s):  
F. Boudík ◽  
J. Reissigová ◽  
K. Hrach ◽  
M. Tomečková ◽  
J. Bultas ◽  
...  

2011 ◽  
Vol 19 (6) ◽  
pp. 1496-1502 ◽  
Author(s):  
Mette Hjortdal Sørensen ◽  
Oke Gerke ◽  
Jess Lambrechtsen ◽  
Niels Peter Rønnow Sand ◽  
Rikke Mols ◽  
...  

Neurology ◽  
2019 ◽  
Vol 92 (16) ◽  
pp. e1878-e1889 ◽  
Author(s):  
Claire M. Erickson ◽  
Stephanie A. Schultz ◽  
Jennifer M. Oh ◽  
Burcu F. Darst ◽  
Yue Ma ◽  
...  

ObjectiveTo examine whether the KLOTHO gene variant KL-VS attenuates APOE4-associated β-amyloid (Aβ) accumulation in a late-middle-aged cohort enriched with Alzheimer disease (AD) risk factors.MethodsThree hundred nine late-middle-aged adults from the Wisconsin Registry for Alzheimer's Prevention and the Wisconsin Alzheimer's Disease Research Center were genotyped to determine KL-VS and APOE4 status and underwent CSF sampling (n = 238) and/or 11C-Pittsburgh compound B (PiB)-PET imaging (n = 183). Covariate-adjusted regression analyses were used to investigate whether APOE4 exerted expected effects on Aβ burden. Follow-up regression analyses stratified by KL-VS genotype (i.e., noncarrier vs heterozygous; there were no homozygous individuals) evaluated whether the influence of APOE4 on Aβ was different among KL-VS heterozygotes compared to noncarriers.ResultsAPOE4 carriers exhibited greater Aβ burden than APOE4-negative participants. This effect was stronger in CSF (t = −5.12, p < 0.001) compared with PiB-PET (t = 3.93, p < 0.001). In the stratified analyses, this APOE4 effect on Aβ load was recapitulated among KL-VS noncarriers (CSF: t = −5.09, p < 0.001; PiB-PET: t = 3.77, p < 0 .001). In contrast, among KL-VS heterozygotes, APOE4-positive individuals did not exhibit higher Aβ burden than APOE4-negative individuals (CSF: t = −1.03, p = 0.308; PiB-PET: t = 0.92, p = 0.363). These differential APOE4 effects remained after KL-VS heterozygotes and noncarriers were matched on age and sex.ConclusionIn a cohort of at-risk late-middle-aged adults, KL-VS heterozygosity was associated with an abatement of APOE4-associated Aβ aggregation, suggesting KL-VS heterozygosity confers protections against APOE4-linked pathways to disease onset in AD.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yingying Wang ◽  
Dandan He ◽  
Chaowei Fu ◽  
Xiaolian Dong ◽  
Feng Jiang ◽  
...  

BackgroundThe onset of puberty is influenced by thyroid function, and thyroid hormones (THs) fluctuate substantially during the period of pubertal development. However, it needs to be further clarified how THs change at specific puberty stages and how it influences pubertal development in girls. So far, longitudinal data from China are scarce.MethodsA cohort study was conducted among girls during puberty in iodine-sufficient regions of East China between 2017 to 2019. Serum thyroid stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4) were determined for each participant. Thyroid homeostasis structure parameters (THSPs), including the ratio of FT4 to FT3 (FT4/FT3), Jostel’s TSH index (TSHI), and thyroid feedback quantile-based index (TFQI), were calculated. Puberty category scores (PCS), calculated based on the Puberty Development Scale (PDS), was used to assess the stage of puberty. Girls were grouped into three categories according to PCS changes (△PCS) and six categories according puberty stage (BPFP: pre-pubertal at both baseline and follow-up; BPFL: pre-pubertal at baseline and late-pubertal at follow-up, respectively; BPFT: pre-pubertal at baseline and post-pubertal at follow-up, respectively; BLFL: late-pubertal at both baseline and follow-up; BLFT: late-pubertal at baseline and post-pubertal at follow-up, respectively; BTFT: post-pubertal at both baseline and follow-up). Multiple linear regression analyses were used to evaluate the associations of THs changes with pubertal progress.ResultsThe levels of serum TSH and FT3 decreased while serum FT4 increased during the study period (P&lt;0.001). In multiple linear regression analyses, after adjustment for covariables, FT3 decreased by an additional 0.24 pmol/L (95% CI: -0.47 to -0.01) in the higher △PCS group than the lower △PCS group. Compared with the BLFL group, the BPFT group showed an additional decline in FT3 (β= -0.39 pmol/L, 95%CI: -0.73 to -0.04), the BTFT group showed a lower decline in TSH (β=0.50 mU/L, 95% CI: 0.21 to 0.80) and a lower decline in TSHI (β=0.24, 95%CI: 0.06 to 0.41), respectively. There was no association of △FT4 or △TFQI with △PCS or the puberty pattern.ConclusionsSerum TSH and FT3 decreased while serum FT4 increased among girls during puberty. Both the initial stage and the velocity of pubertal development were related to thyroid hormone fluctuations.


2013 ◽  
Vol 41 (7) ◽  
pp. 737-743 ◽  
Author(s):  
Rikke Elmose Mols ◽  
Niels Peter Sand ◽  
Jesper Møller Jensen ◽  
Kristian Thomsen ◽  
Axel C. P. Diederichsen ◽  
...  

Circulation ◽  
2011 ◽  
Vol 124 (25) ◽  
pp. 2855-2864 ◽  
Author(s):  
Christopher J. O'Donnell ◽  
Maryam Kavousi ◽  
Albert V. Smith ◽  
Sharon L.R. Kardia ◽  
Mary F. Feitosa ◽  
...  

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Lifang Hou ◽  
Yinan Zheng ◽  
Norrina B. Allen ◽  
Drew Nannini ◽  
Zhou Zhang ◽  
...  

Background: Trajectory of AHA’s cardiovascular health (CVH) through young adulthood are associated with subclinical CVD. The human epigenome is modifiable by lifestyle and environmental factors and may be an important mechanism of CVH outcomes. We sought to determine associations of epigenetic markers with CVH trajectories and with coronary artery calcification (CAC) through young adulthood. Methods: Among CARDIA ppts, we performed methylome analysis at follow up year (Y) 15 and Y20 using Illumina Methylation EPIC array (~850K CpG loci). We compared methylome between those with optimal CVH at baseline and remained stable (optimal-stable, n=645) and individuals with baseline optimal but declining CVH during follow up (n=100) to identify methylomic biomarkers of CVH trajectories. Differentially methylated CpGs were further examined in association with incident CAC risk at Y25 (n=745), and for their potential mediating role in CVH-associated CAC risk. Results: In 1,087 CARDIA ppts (mean age=25 at baseline), we identified 25 hypermethylated CpGs (18 at Y15, 13 at Y20, including 6 seen at both Y15 and Y20) significantly associated with optimal-stable CVH trajectories. The 6 common CpGs were stable (mean ICC = 0.66) whereas the remaining 19 CpGs were dynamic (mean ICC = 0.39) over a 5-year interval. Hypermethylation of 6 stable CpGs was associated with a decreased risk of having future CAC incidence ( Table 1 ). Hypermethylation of 10 (out of 19) dynamic CpGs at Y20 was associated with a decreased risk for incident CAC while the associations was less pronounced at Y15. Mediation analyses showed that hypermethylation of these 16 CpGs at Y15 and Y20 contributed 15% and 23% reduction in the CVH-associated relative risks (RRs) of CAC incidence at Y25. Conclusion: We observed distinct methylomic patterns in young adulthood with stable optimal CVH trajectories relative to those with declining CVH. CVH associated methylomic marks may predict CAC incidence and potentially mediate the associations of CVH trajectories with incident CAC risk.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Laura F Defina ◽  
Nina B Radford ◽  
David Leonard ◽  
Stephen W Farrell ◽  
Andjelka Pavlovic ◽  
...  

Introduction: Recent studies have suggested that extreme levels of physical activity (endurance athletes) are associated with subclinical atherosclerosis as well as increased mortality. The safety of continuing high levels of physical activity is uncertain once coronary artery calcification (CAC) is discovered. Hypothesis: We hypothesized that men performing &ge3000 MET·minutes/week of physical activity would have greater all-cause and cardiovascular (CV) mortality compared to those with &lt1500 or 1500-&lt3000 MET·minutes/week of physical activity and that mortality risk would be greater in those with CAC&ge100 compared to &lt100 Agatston units. Methods: The cohort studied included 16,109 men without prevalent CV disease who reported physical activity levels and underwent EBT or MDCT scan. Physical activity was categorized into &ge3000 (n=1,266), 1500-3000 (n=3,027), and &lt1500 (n=11,816) MET·minutes/week. CAC scanning included EBT scans (1997-2007) or MDCT scans (2007-2013), and CAC score was categorized into &ge100 (n=3,547) and &lt100 (n=12,562) Agatston units. We fit separate proportional hazards regression models to follow-up times for all-cause and CV mortality. The models included all combinations of CAC and physical activity categories and were adjusted for baseline age, smoking, BMI, cholesterol, HDLc, and systolic blood pressure. Results: The average age of participants at baseline was 51.3±8.3 years. Men with the highest activity level had a lower BMI and higher HDLc. After an average follow-up of 8.9 years, there were 329 all-cause and 60 CV deaths, including 174 all-cause and 38 CV deaths in those with CAC&ge100. The sample had 80% power to detect all-cause mortality hazard ratios &ge 1.9 and 1.8 for physical activity &ge3000 versus &lt1500 in those with CAC&lt100 and &ge100, respectively. The corresponding minimum detectable CV mortality hazard ratios were 3.5 and 2.8. Comparing physical activity &ge3000 to &lt1500 in those with CAC&ge100, the hazard ratios (95% CI) were 0.9 (0.5, 1.5) for all-cause mortality and 0.9 (0.3, 3.1) for CV mortality. Hazard ratios were similar when comparing physical activity &ge3000 to 1500-&lt3000 in those with CAC &ge100. Finally, when comparing physical activity categories, there was no evidence that hazard ratios varied by CAC category, p&gt0.7. Conclusions: This sample offers no evidence that levels of activity &ge3000 MET·minutes/week are associated with increased all-cause or CV mortality compared to those with &lt1500 or 1500- &lt3000 MET·minutes/week, regardless of CAC level.


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