It has been recently suggested that perivascular tissue (PVT) releases hypothetic adipocyte- or adventitia-derived relaxing factor. The aim of the study was to assess anticontractile properties of perivascular tissue of human internal thoracic artery (ITA) and to check if this activity is nitric oxide (NO)- or prostacyclin-dependent. We also analyzed the influence of pleural adipose tissue on ITA reactivity. Human ITA rings were studied in vitro. First, skeletonized and pedicled ITA reactivity to serotonin and angiotensin II was compared. In subsequent experiments fragments of ITA were skeletonized and divided into two preparations. One was incubated alone, the other together with PVT or pleural adipose tissue floating freely in the bath. First, concentration-response curves to either serotonin or angiotensin II were constructed. Tissue was then transferred from one bath to the other and concentration-response curves were reconstructed. The same protocol was applied with the inhibition of NO synthase with L-NMMA (10(-4)M) and cyclooxygenase with indomethacin (10(-5)M). Skeletonization augmented contractile response to serotonin (E(max) 16.6+/-1.85 mN vs 43.8+/-3.87 mN; pedicled vs skeletonized ITA, respectively; p<0.001) and angiotensin II (E(max) 10.9+/-1.07 mN vs 26.6+/-1.45 mN, respectively; p<0.001). PVT presence in the bath caused decrease of E(max) from 40.8+/-5.01 to 20.1+/-2.69 mN for serotonin; p<0.001 and from 31.4+/-3.75 to 13.0+/-1.60 mN for angiotensin II, p<0.001 (PVT(-) vs PVT(+), respectively). PVT did not change ITA sensitivity (EC(50)) to serotonin or angiotensin II. Pleural adipose tissue did not change the contractile response of ITA to serotonin (E(max) 37.2+/-4.95 mN vs 36.3+/-4.83 mN, pleural fat+and pleural fat-, respectively; p=0.9). NO and prostacyclin inhibition failed to abolish anticontractile properties of perivascular tissue. PVT with cyclooxygenase and NO synthase inhibition decreased E(max) of serotonin from 46.6+/-3.03 to 28.2+/-4.02 mN, p<0.001 and E(max) of angiotensin II from 27.2+/-2.00 to 16.4+/-2.10 mN, p<0.001. Perivascular tissue of ITA releases potent, soluble, nitric oxide and prostacyclin-independent anticontractile factor. The pleural adipose tissue does not influence ITA reactivity to vasoconstrictors. Preservation of perivascular tissue may protect against vasospasm of ITA graft in clinical settings.

Background—: Re-endothelialization is delayed after drug-eluting stent (DES) implantation. In this setting, neointima is more prone to become lipid laden and develop neoatherosclerosis (NA), potentially increasing plaque vulnerability. Methods and Results—: Optical coherence tomography and near-infrared spectroscopy with intravascular ultrasound were used to characterize NA in 65 (51 DES and 14 bare-metal stents) consecutive symptomatic patients with in-stent restenosis. Median duration poststent implantation was 33 months. Optical coherence tomography–verified NA was observed in 40 stents with in-stent restenosis (62%), was more prevalent in DES than bare-metal stents (68% versus 36%; P =0.02), and demonstrated significantly higher prevalence of thin-cap neoatheroma (47% versus 7%; P =0.01) in DES. Near-infrared spectroscopy assessment demonstrated that the total lipid core burden index (34 [interquartile range, 12–92] versus 9 [interquartile range, 0–32]; P <0.001) and the density of lipid core burden index (lipid core burden index/4 mm, 144 [interquartile range, 60–285] versus 26 [interquartile range, 0–86]; P 70% in-stent restenosis. By logistic regression, prior DES was the only independent predictor of both NA (odds ratio, 7.0; 95% confidence interval, 1.7–27; P =0.006) and periprocedural myocardial infarction (odds ratio, 1.8; 95% confidence interval, 1.1–2.4; P =0.05). Conclusions—: In-stent thin-cap neoatheroma is more prevalent, is distributed more diffusely across the stented segment, and is associated with increased periprocedural myocardial infarction in DES compared with bare-metal stents. These findings support NA as a mechanism for late DES failure.

In recent years, the importance of the gut microbiome in human health and disease has increased. Growing evidence suggests that gut dysbiosis might be a crucial risk factor for coronary artery disease (CAD). Therefore, we conducted a systematic review and meta-analysis to determine whether or not CAD is associated with specific changes in the gut microbiome. The V3–V4 regions of the 16S rDNA from fecal samples were analyzed to compare the gut microbiome composition between CAD patients and controls. Our search yielded 1181 articles, of which 21 met inclusion criteria for systematic review and 7 for meta-analysis. The alpha-diversity, including observed OTUs, Shannon and Simpson indices, was significantly decreased in CAD, indicating the reduced richness of the gut microbiome. The most consistent results in a systematic review and meta-analysis pointed out the reduced abundance of Bacteroidetes and Lachnospiraceae in CAD patients. Moreover, Enterobacteriaceae, Lactobacillus, and Streptococcus taxa demonstrated an increased trend in CAD patients. The alterations in the gut microbiota composition are associated with qualitative and quantitative changes in bacterial metabolites, many of which have pro-atherogenic effects on endothelial cells, increasing the risk of developing and progressing CAD.

The Official Journal of EuroPCR and the European Association of Percutaneous Cardiovascular Interventions (EAPCI)

Optical coherence tomography (OCT) has opened new horizons for intravascular coronary imaging. It utilizes near-infrared light to provide a microscopic insight into the pathology of coronary arteries in vivo . Optical coherence tomography is also capable of identifying the chemical composition...