Outcomes of the novolimus-eluting bioresorbable vascular scaffold in real world clinical practice.

BACKGROUND: Most of the current data regarding the use of bioresorbable scaffolds (BRS) come from everolimus-eluting stent platforms. Adverse events with the everolimus-eluting BRSs which are the most comprehensively characterized BRS, hampered the clinical use of other BRS. There is paucity of published data regarding long term use of novolimus-eluting BRS. METHODS: This study sought to evaluate the performance of novolimus-eluting BRS device at midterm follow-up in real world clinical practice. One hundred and forty-four patients (mean age 57.5±9.7 years, 78.5% male) treated with 206 scaffolds between October 2015 and December 2017 were enrolled. A device-oriented composite endpoint (DOCE) comprising cardiac death, target vessel myocardial infarction (TV-MI), clinically driven target lesion revascularization (TLR) and rate of scaffold thrombosis were investigated. RESULTS: During a mean follow-up of 33±9 months, DOCE occurred in 9 patients (6.3%) of which cardiac death occurred in 2 patients (1.4%), and clinically driven TLR in 7 patients (4.9%), TV-MI in one patient. Target vessel revascularization (TVR) was observed in nine patients. None of the patients experienced scaffold thrombosis. CONCLUSIONS: The use of novolimus-eluting BRS in this real-world population achieved good clinical outcomes.

Evaluation of acute infection-induced endothelial dysfunction and its potential mediators.

OBJECTIVES: Inflammation plays an important role in the pathophysiology of atherosclerosis. Some studies suggest a link between chronic infections, an inflammatory state, and endothelial dysfunction. However, data related to acute infections are scant. We have investigated: (i) the effect of acute infection on endothelial function; (ii) the role of potential mediators of endothelial dysfunction. METHODS: Forty patients 40 years old with acute infection (mean age 53.9 +/- 8.8 years), without coronary artery disease or its equivalents were enrolled. Endothelial function and blood levels of high sensitive C-reactive protein, interleukin-6, tumour necrosis factor-a, high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), apolipoprotein-A1 (Apo-A1) and apolipoprotein-B100 (Apo-B100) were assessed in the acute infection phase and 1 month after recovery. Endothelial function was evaluated by brachial artery flow-mediated vasodilation (FMD). RESULTS: The intraclass correlation coefficients for intra- and interobserver agreement for FMD measurements were 0.98 (95% CI: 0.95-0.99) and 0.93 (95% CI: 0.83-0.97), respectively. FMD improved significantly 1 month after recovery (P < 0.001). Compared to the levels at 1 month, inflammatory markers, LDL cholesterol, LDL/HDL ratio, Apo-B100 and Apo-B100/Apo-A1 ratio were significantly higher. However, HDL and apo-A1 were significantly lower in the phase of acute infection. Change in FMD from baseline to 1 month after recovery correlated significantly only with the change in Apo-A1 (r = 0.35, P = 0.027). CONCLUSIONS: Acute infection causes transient endothelial dysfunction. It increases inflammatory markers and generates an atherogenic lipid profile. Among the parameters evaluated, only the change in Apo-A1 level was associated with acute infection-induced endothelial dysfunction.