Objective: Hybrid coronary revascularization (HCR) is a treatment strategy for the revascularization of multivessel coronary disease that combines the advantages of both minimally invasive surgical techniques and percutaneous coronary intervention (PCI). The optimal sequence by which revascularization should be accomplished has not been determined. We investigated clinical outcomes in a series of patients planned for HCR via robotically assisted totally endoscopic coronary artery bypass (TECAB) and standard PCI based on revascularization sequence. Methods: A total of 238 patients planned for HCR between 2001 and 2011 were divided into three groups based on treatment sequence: (a) TECAB before PCI, (b) PCI before TECAB, and (c) same-session procedure. Multiple procedural and clinical end points before discharge and up to 2 years after the procedure were compared between the three groups in an intention-to-treat analysis. Demographic features were reviewed to determine baseline differences between each group. Results: Of the 238 patients, 175 (73.5%) underwent TECAB before PCI, 38 patients (16.0%) underwent PCI before TECAB, and 25 (10.5%) underwent a simultaneous revascularization procedure. At baseline, the patients undergoing TECAB before PCI were significantly older. There was a significantly higher incidence of previous myocardial infarction in the PCI-first group (P < 0.001). There was a significant difference in intensive care unit (ICU) length of stay (LOS), with shorter ICU stays in the simultaneous revascularization group (P = 0.031) and shorter hospital LOS in the PCI before TECAB group (P = 0.021). Conclusions: In conclusion, revascularization sequence did not dramatically impact clinical outcomes in our observational study. The patients undergoing PCI-first and same-session interventions had shorter hospital and ICU LOS compared with the patients undergoing surgery first. Our findings suggest that no revascularization approach is arbitrarily superior and that revascularization sequence should be individualized on the basis of patient presentation and anatomical considerations.

Pericoronary adipose tissue (PCAT) has been linked to underlying coronary artery disease (CAD) and proposed to modulate adjacent atherosclerotic plaque formation over pro-inflammatory pathways. In vitro and ex vivo studies support the bilateral communication of adipose tissue and vessel wall. We quantified PCAT and its dynamics in a low coronary risk cohort with a semi-automated software in serial coronary computed tomography angiography (CTA). We retrospectively included patients from a tertiary care hospital who underwent serial coronary CTA with a low cardiovascular risk profile. All examinations were evaluated in a standardized approach: epicardial adipose tissue (EAT) volume and attenuation was quantified in total, in the atrioventricular (RCA, LCX) or interventricular (LAD) sulcus and within a 5 mm radius for each coronary artery (PCAT). Coronary plaques were quantified using a semi-automated software and compared for progression, stability or regression. Of 120 patients (27% females), 59.2% showed atherosclerotic plaques. After 36 months mean follow-up, 22 (18.3%) showed plaque regression, 39 (32.5%) were stable and 49 (40.8%) were progressive. Total EAT volume decreased by -15.6 ± 37.2 mm³ in the regressive group, increased by 2.7 ± 30.6 mm³ in the stable group and by 24.3 ± 37.1 mm³ in the progressive group (p = 0.003). Per-vessel analysis showed a significant decrease of PCAT attenuation in patients with CAD regression (-3.8 ± 7.6HU) compared to the stable (1.2 ± 9.1HU) and progressive group (3.5 ± 8.2HU, p < 0.0001). Mean sulcus EAT attenuation did not show a significant change (p = 0.135). Epicardial adipose tissue volume is mutually changing with the progression or regression of coronary artery disease. Perivascular but not epicardial attenuation levels correlate to adjacent plaque and support a direct bilateral influence.

Background: Vitamin D supplementation may be associated with lower cardiovascular (CV) events, but the data are controversial. It remains speculative whether vitamin D supplementation has a direct effect on coronary atherosclerosis. We therefore set out to assess the influence of vitamin D supplementation on the coronary atherosclerosis profile quantified by coronary computed tomography angiography (CTA) in a retrospective case–control cohort study. Methods: 176 patients (age: 62.4 ± 10.4) referred to coronary CTA for clinical indications were included. A total of 88 patients receiving vitamin D supplementation (mean duration 65.3 ± 81 months) were 1:1 propensity score matched with 88 controls for age, gender, smoking, arterial hypertension, positive family history, dyslipidemia, and diabetes. Coronary stenosis severity (CAD-RADS^TM), mixed plaque burden (weighted for non-calcified), high-risk-plaque (HRP) features, and plaque density (HU) were quantified by CTA. Serum 25-hydroxyvitamin D (OH)-levels were measured in 138 patients and categorized into four groups (0: 60 ng/mL) and compared with CTA. Results: The prevalence of atherosclerosis by CTA was similar in both groups (75.6% versus 74.3%, p = 0.999), >50% coronary stenosis was slightly higher in controls (p = 0.046), but stenosis severity score (CAD-RADS) was not different (p = 0.106). Mixed plaque burden (weighted for non-calcified) was lower in patients receiving vitamin D supplementation (p = 0.002) and high-risk-plaque prevalence was markedly lower (3.8% versus 32%, p < 0.001). CT plaque density (HU) was higher (p < 0.001) in the vitamin D group. Patients with serum vitamin D (OH) levels >60 ng/mL had higher plaque density (p = 0.04), indicating more calcified and less vulnerable plaque. Conclusions: In this retrospective case–control cohort study, vitamin D supplementation was associated with less high-risk plaque, less non-calcified plaque burden, and a higher calcified plaque independent of CV risk factors.