MOESM1 of Impact of metabolic syndrome on the progression of coronary calcium and of coronary artery disease assessed by repeated cardiac computed tomography scans

Additional file 1: Table S1. Comparison of baseline clinical and biochemical characteristics by genders. Figure S1. Progression of coronary artery disease from baseline cardiac computed tomography scans to 3–4 years follow-up scans. 1) Increase of coronary artery calcium deposition (A and B), 2) progression of coronary artery stenosis (C and D), 3) development of noncalcified plaque (E and F) 3–4 years

Additional file 1: Table S1. of Post-transcriptional regulation of SHANK3 expression by microRNAs related to multiple neuropsychiatric disorders

The putative miRNA families targeting the SHANK3 3′UTR predicted by TargetScan (release 6.2). The number of binding sites for each miRNA family, and the binding type (8mer, 7mer-m8, or 7mer-1A) are described. Table S2. Altered expression profiles of miR-7, miR-34a, and miR-504 in multiple neuropsychiatric disorders. Table S3. Summary of statistical analyses for the experiments. Figure S1. The secondary structures of SHANK3 (a) and SHANK2 (b) 3′UTRs predicted by RNAfold ( http://rna.tbi.univie.ac.at/cgi-bin/RNAfold.cgi ) according to the minimum free energy. The color code represents base-pair probabilities. Figure S2. The expression of Shank3 construct with 3′UTR, but not that without 3′UTR, was significantly decreased by miR-7 and miR-504 in mouse cultured neurons. Statistical analyses are in Additional file 1: Table S3. Figure S3. The ten major Shank3 isoforms (Wang et al. Molecular Autism 2014, 5:30) (a), and the nucleotide sequence of the last exon (exon 22) of Shank3 gene (b). The Shank3 isoforms containing SAM domain at the C-terminus are labeled with red color. (DOCX 3382 kb

Influence of the definition of “metabolically healthy obesity” on the progression of coronary artery calcification

<div><p>Objectives</p><p>Debates whether metabolically healthy obesity (MHO) increases the cardiovascular risk might be due to the metabolic instability of MHO or the absence of a perfect definition of MHO. Therefore, we aimed to investigate the influence of the MHO phenotype on the coronary artery calcium score (CACS) progression according to definition of MHO.</p><p>Methods</p><p>We analyzed a retrospective cohort with a CACS of 0 at baseline and available serial CACS measurements taken ≥ 12 months apart (n = 1,218). Obesity was defined as BMI ≥ 25 kg/m², and MHO was defined as obesity accompanied by ≤ 1 (MHO class I) or 0 (MHO class II) components of metabolic syndrome (MetS).</p><p>Results</p><p>During a median follow-up of 45 months, 32.2% of MHO class I and 10.2% of MHO class II subjects developed MetS. Compared to non-obese/metabolically healthy subjects (reference group), hazard ratios (HR) for development of MetS were 2.174 (95% confidence interval [CI]: 1.513–3.124) and 1.166 (95% CI: 0.434–3.129) for MHO class I and II subjects, respectively. The MHO class I subjects showed a significantly increased risk of CACS progression as compared to the reference group (HR: 1.653; 95% CI: 1.144–2.390), whereas MHO class II subjects did not (HR: 1.195; 95% CI: 0.514–2.778). Among subjects with MHO class I, no significant CACS progression was observed in the subjects who maintained metabolic health during follow-up (HR: 1.448; 95% CI: 0.921–2.278).</p><p>Conclusions</p><p>The risks of metabolic deterioration and CACS progression were significant in subjects with MHO class I, but not in those with MHO class II.</p></div

Datasheet1_The effect of non-optimal lipids on the progression of coronary artery calcification in statin-naïve young adults: results from KOICA registry.docx

BackgroundDespite the importance of attaining optimal lipid levels from a young age to secure long-term cardiovascular health, the detailed impact of non-optimal lipid levels in young adults on coronary artery calcification (CAC) is not fully explored. We sought to investigate the risk of CAC progression as per lipid profiles and to demonstrate lipid optimality in young adults.MethodsFrom the KOrea Initiative on Coronary Artery calcification (KOICA) registry that was established in six large volume healthcare centers in Korea, 2,940 statin-naïve participants aged 20–45 years who underwent serial coronary calcium scans for routine health check-ups between 2002 and 2017 were included. The study outcome was CAC progression, which was assessed by the square root method. The risk of CAC progression was analyzed according to the lipid optimality and each lipid parameter.ResultsIn this retrospective cohort (mean age, 41.3 years; men 82.4%), 477 participants (16.2%) had an optimal lipid profile, defined as triglycerides 60 mg/dl. During follow-up (median, 39.7 months), CAC progression was observed in 434 participants (14.8%), and more frequent in the non-optimal lipid group (16.5% vs. 5.7%; p ConclusionNon-optimal lipid levels were significantly associated with the risk of CAC progression in young adults, even at low-risk. Screening and intervention for non-optimal lipid levels, particularly triglycerides, from an early age might be of clinical value.</p

Kaplan-Meier survival curves for adverse cardiac events from combined cardiac CT and SPECT information.

<p>Event-free survival curves stratified by (A) coronary artery calcium score (CACS) of 400 and presence or absence of perfusion defect (PD), (B) diameter stenosis (DS) of 50% and presence or absence of PD, (C) presence of plaque in 3 or more segments of the coronary tree and presence or absence of PD, and (D) presence of non-calcified plaque (NCP) or mixed plaque (MP) in 2 or more segments of the coronary tree and presence or absence of PD.</p

CONSORT diagram of the study population selection.

<p>CCTA, coronary computed tomographic angiography; SPECT, single-photon emission computed tomography; CAD, coronary artery disease.</p

Improved prediction of adverse cardiac events with integration of cardiac computed tomography (CT) and single-photon emission computed tomography (SPECT).

<p>Comparison of the annual event rate according to (A) increasing coronary artery calcium score (CACS), (B) worsening diameter stenosis (DS), (C) presence of non-calcified plaque (NCP), (D) mixed plaque (MP), and (E) calcified plaque (CP) between patients with and without perfusion defect (PD) on SPECT.</p

Incremental prognostic value of cardiac CT findings for adverse cardiac event.

<p>Incremental prognostic value of cardiac CT findings for adverse cardiac event.</p

The occurrence of adverse cardiac event according to cardiac CT and myocardial SPECT.

<p>The occurrence of adverse cardiac event according to cardiac CT and myocardial SPECT.</p

Univariate and multivariate analysis of factors associated with adverse cardiac event.

<p>Univariate and multivariate analysis of factors associated with adverse cardiac event.</p