Increased arterial velocity pulse index is an independent factor related to skeletal muscle mass reduction and tissue damage in patients with cardiovascular disease

2020 ◽  
Vol 43 (6) ◽  
pp. 534-542
Author(s):  
Haruhito Harada ◽  
Hisao Ikeda ◽  
Yasuhiro Nishiyama ◽  
Hiroshi Niiyama ◽  
Atsushi Katoh ◽  
...  
2019 ◽  
Vol 74 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Stefanos Tyrovolas ◽  
Demosthenes Panagiotakos ◽  
Ekavi Georgousopoulou ◽  
Christina Chrysohoou ◽  
Dimitrios Tousoulis ◽  
...  

BackgroundSkeletal muscle mass (SMM) is inversely associated with cardiometabolic health and the ageing process. The aim of the present work was to evaluate the relation between SMM and 10 year cardiovascular disease (CVD) incidence, among CVD-free adults 45+ years old.MethodsATTICA is a prospective, population-based study that recruited 3042 adults without pre-existing CVD from the Greek general population (Caucasians; age ≥18 years; 1514 men). The 10 year study follow-up (2011–2012) captured the fatal/non-fatal CVD incidence in 2020 participants (50% men). The working sample consisted of 1019 participants, 45+ years old (men: n=534; women: n=485). A skeletal muscle mass index (SMI) was created to reflect SMM, using appendicular skeletal muscle mass (ASM) standardised by body mass index (BMI). ASM and SMI were calculated with specific indirect population formulas.ResultsThe 10 year CVD incidence increased significantly across the baseline SMI tertiles (p<0.001). Baseline SMM showed a significant inverse association with the 10 year CVD incidence (HR 0.06, 95% CI 0.005 to 0.78), even after adjusting for various confounders. Additionally, participants in the highest SMM tertile had 81% (95% CI 0.04 to 0.85) lower risk for a CVD event as compared with those in the lowest SMM tertile.ConclusionsThe presented findings support the importance of SMM evaluation in the prediction of long-term CVD risk among adults 45+ years old without pre-existing CVD. Preservation of SMM may contribute to CVD health.


2021 ◽  
Vol 10 (9) ◽  
Author(s):  
Rebecca Knowles ◽  
Jennifer Carter ◽  
Susan A. Jebb ◽  
Derrick Bennett ◽  
Sarah Lewington ◽  
...  

Background There is debate whether body mass index is a good predictor of health outcomes because different tissues, namely skeletal muscle mass (SMM) and fat mass (FM), may be differentially associated with risk. We investigated the association of appendicular SMM (aSMM) and FM with fatal and nonfatal cardiovascular disease (CVD) and all‐cause mortality. We compared their prognostic value to that of body mass index. Methods and Results We studied 356 590 UK Biobank participants aged 40 to 69 years with bioimpedance analysis data for whole‐body FM and predicted limb muscle mass (to calculate aSMM). Associations between aSMM and FM with CVD and all‐cause mortality were examined using multivariable Cox proportional hazards models. Over 3 749 501 person‐years of follow‐up, there were 27 784 CVD events and 15 844 all‐cause deaths. In men, aSMM was positively associated with CVD incidence (hazard ratio [HR] per 1 SD 1.07; 95% CI, 1.06–1.09) and there was a curvilinear association in women. There were stronger positive associations between FM and CVD with HRs per SD of 1.20 (95% CI, 1.19–1.22) and 1.25 (95% CI, 1.23–1.27) in men and women respectively. Within FM tertiles, the associations between aSMM and CVD risk largely persisted. There were J‐shaped associations between aSMM and FM with all‐cause mortality in both sexes. Body mass index was modestly better at discriminating CVD risk. Conclusions FM showed a strong positive association with CVD risk. The relationship of aSMM with CVD risk differed between sexes, and potential mechanisms need further investigation. Body fat and SMM bioimpedance measurements were not superior to body mass index in predicting population‐level CVD incidence or all‐cause mortality.


Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3293
Author(s):  
Christina Chrysohoou ◽  
Matina Kouvari ◽  
George Lazaros ◽  
John Varlas ◽  
Kyriakos Dimitriadis ◽  
...  

The sex-specific effect of skeletal muscle mass (SMM) index (SMI) on 4-year first fatal/non-fatal cardiovascular disease (CVD) event in free-of-disease individuals was examined. In 2009, n = 1411 inhabitants (mean age = 64(12)) from Ikaria were selected. Follow-up was performed in 2013. SMI was created to reflect SMM through appendicular skeletal muscle mass (indirectly calculated through formulas) divided by body mass index (BMI). Fifteen and six tenths percent of participants exhibited CVD (19.8% in men/12% in women, p = 0.002). Significant U-shape trends were observed in participants >65 years old and women irrespective to age confirmed through multi-adjusted Cox regression analysis; in age >65 years, Hazard Ratio (HR)(2nd vs. 1st SMI tertile) = 0.80, 95% Confidence Interval (95%CI) (0.45, 0.96) and in women HR(2nd vs. 1st SMI tertile) = 0.71, 95% CI (0.33, 0.95), while, as for the 3rd SMI tertile, no significant trends were observed. Mediation analysis revealed that mediators of the aforementioned associations in men were the arterial distensibility and total testosterone, while, in women, inflammation, insulin resistance, and arterial distensibility. High SMM accompanied by obesity may not guarantee lower CVD risk. Specific cardiometabolic factors seem to explain this need for balance between lean and fat mass.


2021 ◽  
Vol 33 (2) ◽  
pp. 94-99
Author(s):  
Nana Takao ◽  
Junji Iwasaka ◽  
Satoshi Kurose ◽  
Takumi Miyauchi ◽  
Astuko Tamanoi ◽  
...  

Author(s):  
Bradley S Gordon ◽  
Michael L Rossetti ◽  
Robert A Casero, Jr.

Maintaining a critical amount of skeletal muscle mass is linked to reduced morbidity and mortality. In males, testicular androgens regulate muscle mass with a loss of androgens being critical as it is associated with muscle atrophy. Atrophy of the limb muscles is particularly important, but the pathways by which androgens regulate limb muscle mass remain equivocal. We used microarray analysis to identify changes to genes involved with polyamine metabolism in the tibialis anterior (TA) muscle of castrated mice. Of the polyamines, the concentration of spermidine (SPD) was significantly reduced in the TA of castrated mice. To assess whether SPD was an independent factor by which androgens regulate limb muscle mass, we treated castrated mice with SPD for 8 weeks and compared them to sham operated mice. Though this treatment paradigm effectively restored SPD concentrations in the TA muscles of castrated mice, mass of the limb muscles (i.e. TA, gastrocnemius, plantaris, and soleus) were not increased to the levels observed in sham animals. Consistent with those findings, muscle force production was also not increased by SPD treatment. Overall, these data demonstrate for the first time that SPD is not an independent factor by which androgens regulate limb skeletal muscle mass. NOVELTY BULLETS -Polyamines regulate growth in various cells/tissues -Spermidine concentrations are reduced in the limb skeletal muscle following androgen depletion -Restoring Spermidine concentrations in the limb skeletal muscle does not increase limb muscle mass or force production


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Kouvari ◽  
C Chrysohoou ◽  
P Dilaveris ◽  
G Georgiopoulos ◽  
N Magkas ◽  
...  

Abstract Background/Introduction Predictive and prognostic ability of muscle mass in CVD settings is increasingly discussed. Purpose The sex-specific effect of skeletal muscle mass index (SMI) on 10-year recurrent fatal/non fatal cardiovascular disease (CVD) event of acute coronary syndrome (ACS) patients was evaluated. Methods In 2006–2009, n=1,000 consecutive patients (n=222 females), hospitalized at a cardiology clinic with ACS diagnosis and with symptoms and left ventricular function indicative of heart failure were selected. SMI was created to reflect skeletal muscle mass through appendicular skeletal muscle mass (indirectly calculated through population formulas) divided by body mass index (BMI). Results In 10-year follow-up (2016), 55% of ACS patients exhibited recurrent fatal/non fatal CVD events (53% in females vs. 62% in males, p=0.04). Patients in 2nd SMI tertile (mostly overweight) had 10% lower risk for CVD recurrence (female:male rate ratio=0.87) over their counterparts at 1st (mostly normalweight) and 3rd tertile (mostly obese). Multivariate analysis revealed that ACS patients in 2nd SMI tertile presented 46% and 85% lower CVD event risk over their counterparts in 1st tertile (Hazard Ratio (HR)=0.54, 95% Confidence Interval (95% CI) 0.30, 0.96, p=0.002) and 3rd tertile (HR=1.85, 95% CI 1.05, 2.94, p=0.03). Sex-related sensitivity analyses revealed that even if U-shape association was retained in both males and females in crude and age- adjusted models, further adjustment for clinical, lifestyle and sociodemographic factors resulted in a significant trend only in females (HR=1.85, 95% CI 1.05, 2.94, p=0.03). Mean (95% confidence interval) survival (free-of-CVD) time (years) in females patients at 1st, 2nd and 3rd tertile was 7.4 (6.5, 8.2), 8.2 (7.1, 9.2) and 6.7 (5.5, 7.9), respectively. Inflammatory markers i.e. C-reactive protein (CRP) and white blood cells (WBC) had strong confounding effect on the association between SMI and 10-year recurrent CVD event rate in females. A significant inverse linear association between the examined factors was observed only in females (ρ(CRP)=-0.490, p<0.001 & ρ(WBC)=-0.380, p=0.05). Unadjusted analysis revealed that females of 2nd tertile had significantly lower mean values of inflammatory markers compared with their 1st tertile counterparts (all ps<0.05). Additionally, females of 3rd tertile presented slightly higher inflammation levels compared with females of 2nd tertile yet this difference was not significant. In males no significant trend was observed. Conclusion AU-shape association between SMI and 10-year CVD event especially in females was highlighted. This work reveals sex-specific remarks for “obesity-lean paradox” in secondary prevention, implying that high muscle mass accompanied by obesity and excess adiposity may not guarantee better prognosis. Acknowledgement/Funding None


Sign in / Sign up

Export Citation Format

Share Document