The effects of long-term vigorous endurance exercise on the coronary arteries

2019 ◽  
Vol 67 (2) ◽  

Moderate endurance training is known to improve cardiovascular risk factors, and prolongs life expectancy. On the other hand, there has been some discussion whether “too much” exercise might have a contrarious effect by accelerating coronary atherosclerosis. The goal of this review was to evaluate the current literature on the effects of long-term vigorous endurance training on the coronary vasculature. In summary, data point to an increased calcium score, and a higher burden of atherosclerotic plaque in male athletes compared to sedentary controls. However, the plaques found in athletes were more prone to be calcified. The pathogenesis and clinical relevance of this athlete coronary artery disease phenotype remains incompletely understood and represents an area of important future work.

2019 ◽  
Vol 67 (2) ◽  

Moderate endurance training is known to improve cardiovascular risk factors, and prolongs life expectancy. On the other hand, there has been some discussion whether “too much” exercise might have a contrarious effect by accelerating coronary atherosclerosis. The goal of this review was to evaluate the current literature on the effects of long-term vigorous endurance training on the coronary vasculature. In summary, data point to an increased calcium score, and a higher burden of atherosclerotic plaque in male athletes compared to sedentary controls. However, the plaques found in athletes were more prone to be calcified. The pathogenesis and clinical relevance of this athlete coronary artery disease phenotype remains incompletely understood and represents an area of important future work.


2019 ◽  
Vol 67 (2) ◽  

Moderate endurance training is known to improve cardiovascular risk factors, and prolongs life expectancy. On the other hand, there has been some discussion whether “too much” exercise might have a contrarious effect by accelerating coronary atherosclerosis. The goal of this review was to evaluate the current literature on the effects of long-term vigorous endurance training on the coronary vasculature. In summary, data point to an increased calcium score, and a higher burden of atherosclerotic plaque in male athletes compared to sedentary controls. However, the plaques found in athletes were more prone to be calcified. The pathogenesis and clinical relevance of this athlete coronary artery disease phenotype remains incompletely understood and represents an area of important future work.


2019 ◽  
Vol 67 (2) ◽  

Moderate endurance training is known to improve cardiovascular risk factors, and prolongs life expectancy. On the other hand, there has been some discussion whether “too much” exercise might have a contrarious effect by accelerating coronary atherosclerosis. The goal of this review was to evaluate the current literature on the effects of long-term vigorous endurance training on the coronary vasculature. In summary, data point to an increased calcium score, and a higher burden of atherosclerotic plaque in male athletes compared to sedentary controls. However, the plaques found in athletes were more prone to be calcified. The pathogenesis and clinical relevance of this athlete coronary artery disease phenotype remains incompletely understood and represents an area of important future work.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
G Benetos ◽  
M Goncalves ◽  
E Von Felten ◽  
G Rampidis ◽  
O Clerc ◽  
...  

Abstract Background Coronary computed tomography angiography (CCTA) provides incremental prognostic information over traditional risk factors in patients with suspected coronary artery disease. However, little is known about the long-term predictive performance of CCTA-derived coronary volumes and mid-diastolic left ventricular (LV) mass. Purpose To assess long-term prognostic value of coronary volumes and mid-diastolic LV mass as novel potential imaging predictors derived from low-dose prospectively ECG-triggered CCTA. Methods Consecutive patients with suspected or known coronary artery disease, referred for low-dose CCTA, were included. Patients with previous revascularization were excluded. The following parameters were evaluated: calcium score, segment involvement score (SIS: 1 point for each coronary segment with presence of plaque), coronary volume, mid-diastolic LV mass and coronary volume indexed to LV mass. Major adverse cardiovascular events (MACE) were defined as all-cause death, non-fatal myocardial infarction and revascularization (PCI or CABG). The association between CCTA measures and the occurrence of events was quantified using cox regression hazard and Kaplan Meier analysis. Results A total of 147 consecutive patients were included in the study. Of them, 93 (63.3%) were male and 79 (53.7%) hat one or more traditional cardiovascular risk factors. There was a weak but statistical significant inverse correlation between indexed coronary volume and both calcium score (R=-0.3, p=0.01) and SIS (R=-0.24, p=0.005). After a median follow-up of 5.8 years 30 MACE occurred in 25 patients, including 3 deaths, 26 revascularizations and 1 non-fatal myocardial infarction. In univariate cox regression hazard analysis calcium score (HR=12.69, 95% CI 2.99–53.83, p<0.001), SIS (HR=1.66, 95% CI 1.43–1.94, p<0.001), LV mass (HR=1.02, 95% CI 1.01–1.03, p=0.007) and indexed coronary volume (HR=0.89, 95% 0.82–0.96, p=0.004) were associated with outcome. In multivariate analysis, indexed coronary volume, remained an independent predictor for MACE when adjusted for traditional risk factors and SIS (HR=0.93, 95% CI 0.87–1.00, p=0.05), while LV mass did not reach statistical significance (p=0.46). By ROC curve analysis, a value of 21.85 mm3/gr was defined as optimal cutoff for indexed coronary volume. In Kaplan Meier plots, patients with low indexed coronary volume (<21.85 mm3/gr) showed higher event rates (log rank p<0.001) compared to high indexed coronary volume (≥21.85 mm3/gr). Conclusions Indexed coronary volume, derived from low-dose CCTA, independently predicts cardiovascular events. Larger studies are mandated to confirm the predictive value of this potential new biomarker.


Author(s):  
Laura D’Erasmo ◽  
Ilenia Minicocci ◽  
Alessia Di Costanzo ◽  
Giovanni Pigna ◽  
Daniela Commodari ◽  
...  

Background Familial hypercholesterolemia (FH) may arise from deleterious monogenic variants in FH‐causing genes as well as from a polygenic cause. We evaluated the relationships between monogenic FH and polygenic hypercholesterolemia in influencing the long‐term response to therapy and the risk of atherosclerosis. Methods and Results A cohort of 370 patients with clinically diagnosed FH were screened for monogenic mutations and a low‐density lipoprotein‐rising genetic risk score >0.69 to identify polygenic cause. Medical records were reviewed to estimate the response to lipid‐lowering therapies and the occurrence of major atherosclerotic cardiovascular events during a median follow‐up of 31.0 months. A subgroup of patients (n=119) also underwent coronary computed tomographic angiography for the evaluation of coronary artery calcium score and severity of coronary stenosis as compared with 135 controls. Two hundred nine (56.5%) patients with hypercholesterolemia were classified as monogenic (FH/M+), 89 (24.1%) as polygenic, and 72 (19.5%) genetically undefined (FH/M−). The response to lipid‐lowering therapy was poorest in monogenic, whereas it was comparable in patients with polygenic hypercholesterolemia and genetically undetermined. Mean coronary artery calcium score and the prevalence of coronary artery calcium >100 units were significantly higher in FH/M+ as compared with both FH/M− and controls. Finally, after adjustments for confounders, we observed a 5‐fold higher risk of incident major atherosclerotic cardiovascular events in FH/M+ (hazard ratio, 4.8; 95% CI, 1.06–21.36; P adj =0.041). Conclusions Monogenic cause of FH is associated with lower response to conventional cholesterol‐lowering therapies as well as with increased burden of coronary atherosclerosis and risk of atherosclerotic‐related events. Genetic testing for hypercholesterolemia is helpful in providing important prognostic information.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Senoner ◽  
F Barbieri ◽  
A Adukauskaite ◽  
M Sarcletti ◽  
F Plank ◽  
...  

Abstract Purpose To assess coronary artery disease (CAD) characteristics by coronary CT-angiography (CTA) in individuals with HIV-infection on long-term ART in a retrospective matched case-controlled cohort study. Methods 69 HIV positive patients who underwent 128-slice dual source coronary CTA (mean age 54.9 years, 26.1% females) with mean 17.8±9.4 years of HIV-infection and a mean duration on ART of 13±7.3 years were propensity score matched with 69 HIV negative controls. CTA was evaluated for: Stenosis severity (CAD-RADS), total plaque burden, mixed-non-calcified plaque burden (G-score), high-risk-plaque (HRP) features (Napkin-Ring-Sign, low-attenuation-plaque, spotty calcification, positive remodeling), perivascular fat attenuation index (FAI) and ectatic coronary segments. Results CAD-RADS was higher in HIV-positive participants as compared to controls (2.21±1.4 vs 1.69±1.5, p=0.031). A higher prevalence of CAD and G-score (p=0.043 and p=0.003) were found. HRP prevalence (23 (34.3%) vs 8 (12.1%); p=0.002) and the number of HRP (36 vs 10, p<0.001) were higher in HIV-positive individuals. A positive perivascular FAI >-70 HU was present in 27.8% of HRP. Ectatic coronary arteries were found in 10 (14.5%) individuals with HIV-infection vs 0% in controls (p=0.003). Conclusion(s) HIV positive individuals on long-term ART display higher CAD burden and more HRP indicating vulnerable, potentially inflamed plaques. CT- Angiography results HIV+ (N=67) HIV− (N=67) P-value CAD prevalence (any plaque), n (%) 56 (83.6) 46 (68.7) 0.043 SSS, mean ±SD 1.16±1.6 0.95±2.1 0.038 CAD RADS   0 11 22   1 11 7   2 10 21 <0.001   3 23 4   4 12 13   Total >50%, n (%) 35 (52.2) 17 (25.4) 0.001 CAD RADS, mean ±SD 2.21±1.4 1.69±1.5 0.031 SIS, mean ±SD 3.93±3.0 3.06±3.1 0.067 G-score, mean ±SD 10.04±8.5 5.76±5.9 0.003 Calcium score, mean ±SD 149.4±287.1 133.2±329.3 0.015 HRP, n (%) 23 (34.3) 8 (12.1) 0.002 HRP, n 36 10 <0.001 Non-calcifying plaque component, n (%) 44 (65.7) 34 (51.5) 0.097 Ectatic coronary segments, n (%) 10 (14.5) 0 (0) 0.003 CAD RADS: coronary artery disease reporting and data system; CCS: coronary calcium score; HRP: high-risk plaque; SIS: segment involvement score; SSS: stenosis severity score. 60 yo HIV-infected (31 yrs) male patient These features strongly support the predominant inflammatory theory of cardiovascular events in HIV-infected individuals. Acknowledgement/Funding None


2013 ◽  
Vol 36 (1) ◽  
pp. 42 ◽  
Author(s):  
Chia-Chang Hsu ◽  
Yung-Chuan Lu ◽  
Cheng-An Chiu ◽  
Teng-Hung Yu ◽  
Wei-Chin Hung ◽  
...  

Purpose: Indoxyl sulfate (IS) is linked to endothelial damage, NF-κB activation and induced development of atherosclerosis. The purpose of this study was to investigate the relationship between serum IS levels and the severity of coronary artery stenosis. In addition, the relationship among IS and various cardiovascular risk factors was also explored. Methods: Serum IS concentrations were measured using ultra performance liquid chromatography in 191 consecutive patients presenting with stable angina. The associations between serum IS levels and angiographic indexes of the number of diseased vessels, modified Gensini scores and calcium scores were determined. Results: Patients with significant coronary artery stenosis were found to have higher serum IS levels than patients with normal coronary arteries. Using multivariate analysis, serum IS levels were found to be independently associated with the presence and severity of coronary artery disease (CAD). Furthermore, statistically significant correlation was observed between the serum IS levels and age, Agatston calcium score, volume calcium score, modified Gensini score, coronary lesions, coronary disease and Framingham-10 year risk score. Conclusion:This study indicates that serum IS levels are significantly higher in the presence of CAD and correlate with the severity of the disease and coronary atherosclerosis scores, which suggest that increased serum IS may be involved in the pathogenesis of coronary atherosclerosis.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
T.P.D Silva ◽  
M.C Costa ◽  
A.F Gabriel ◽  
M Selas ◽  
F Silva ◽  
...  

Abstract Introduction The mechanisms underlying the different phenotypic presentations of atherosclerosis are still poorly understood. MicroRNAs regulate genetic expression at the post-transcriptional level and each has specific biological functions. MicroRNAs could therefore be useful for understanding the epigenetic drivers for development of isolated coronary atherosclerosis and more extensive disease (coronary and extra-coronary). We evaluated if the expression profile of circulating microRNAs was associated with coronary and multiterritorial atherosclerosis. Methods We prospectively recruited three groups of age- and sex-matched participants, with: 1) no coronary atherosclerosis (calcium score=0, no soft plaques in coronary angioCT scan), neither carotid or inferior limbs atherosclerosis (controls); 2) isolated obstructive coronary artery disease (CAD) (≥50% for the left main, ≥70% for other epicardial vessels) (isolated CAD group); 3) obstructive disease of the coronary, inferior limbs and carotid arterial beds (multi-territorial disease group). Obstructive atherosclerosis of carotid and inferior limbs arteries (≥50% stenosis by Doppler or angioCT imaging) was assessed in all participants. Acute atherosclerotic events or coronary revascularization within 12 months, heart failure, infections, malignancy and severe renal dysfunction were exclusion criteria. Six microRNAs with diverse mechanisms of action were selected (mir-21, miR-27b, miR-29a, miR-126, miR-146, miR-218) and measurements of their circulating levels were performed in a blinded fashion, using RT-PCR SYBR Green. Results Twenty four patients were included, including 8 patients in each group. Mean age was 61±9 years, and 83% were male. In patients with atherosclerosis, classical cardiovascular risk factors were globally more prevalent. The expression of miR-146 and miR-218, both of which regulate endothelial function, was significantly decreased in the isolated CAD group compared to controls (Figure; data are expressed as median [IQR]). There was a further decrease in the expression of both microRNAs in patients with multiterritorial atherosclerosis compared to patients with isolated CAD. The expression of other microRNAs did not differ. Smoking was associated with the presence of isolated CAD and multiterritorial atherosclerosis (14% vs 30% vs 56% of smokers across groups, p=0.002), and with a decreased expression of miR-218 (1.6 [0.02–83] fold vs 0.1 [0.001–0.7] fold, p=0.023). Conclusions The expression of the endothelial regulators miR-146 and miR-218 was decreased in patients with isolated CAD compared to controls, and even more hampered in patients with multiterritorial atherosclerosis. Higher degrees of endothelial dysfunction may therefore contribute to a more diffuse atherosclerotic presentation through miR-146 and miR-218. Atherogenesis related to smoking may be partially mediated by miR-218. Funding Acknowledgement Type of funding source: None


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