Background: Whereas the efficacy and safety of intravascular lithotripsy (IVL) have been confirmed in de novo calcified coronary lesions, little is known about its utility in treating stent underexpansion. This study aimed to investigate the impact of IVL in treating stent underexpansion. Methods and Results: Consecutive patients with stent underexpansion treated with IVL entered the multicenter IVL-Dragon Registry. The procedural success (primary efficacy endpoint) was defined as a relative stent expansion >80%. Thirty days device-oriented composite endpoint (DOCE) (defined as a composite of cardiac death, target lesion revascularization, or target vessel myocardial infarction) was the secondary endpoint. A total of 62 patients were enrolled. The primary efficacy endpoint was achieved in 72.6% of patients. Both stent underexpansion 58.5% (47.5–69.7) vs. 11.4% (5.8–20.7), p < 0.001, and the stenotic area 82.6% (72.4–90.8) vs. 21.5% (11.1–37.2), p < 0.001, measured by quantitative coronary angiography improved significantly after IVL. Intravascular imaging confirmed increased stent expansion following IVL from 37.5% (16.0–66.0) to 86.0% (69.2–90.7), p < 0.001, by optical coherence tomography and from 57.0% (31.5–77.2) to 89.0% (85.0–92.0), p = 0.002, by intravascular ultrasound. Secondary endpoint occurred in one (1.6%) patient caused by cardiac death. There was no target lesion revascularization or target vessel myocardial infarction during the 30-day follow-up. Conclusions: In this real-life, largest-to-date analysis of IVL use to manage underexpanded stent, IVL proved to be an effective and safe method for facilitating stent expansion and increasing luminal gain.

Results show that KYNA concentrations in all diagnostic groups were lower before ECT (not statistically significant for the SAD group) and that there were no significant changes in those concentrations (compared with the baseline) during ECT.

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Patients with diabetes mellitus (DM) type 1 and 2 are at a higher risk of cognitive decline and dementia; however, the underlying pathology is poorly understood. Kynurenic acid (KYNA), endogenous kynurenine metabolite, displays pleiotropic effects, including a blockade of glutamatergic and cholinergic receptors. Apart from well-known glial origin, kynurenic acid is robustly synthesized in the endothelium and its serum levels correlate with homocysteine, a risk factor for cognitive decline. Studies in an experimental DM model suggest that a selective, hippocampal increase of the kynurenic acid level may be an important factor contributing to diabetes-related cognitive impairment. The aim of this study was to assess the effects of chronic, four-week administration of losartan, angiotensin receptor blocker (ARB), on the brain KYNA in diabetic rats. Chromatographic and rt-PCR techniques were used to measure the level of KYNA and the expression of genes encoding kynurenine aminotransferases, KYNA biosynthetic enzymes, in the hippocampi of rats with streptozotocin-induced DM, treated with losartan. The effect of losartan on KYNA synthesis de novo was also evaluated in vitro, in brain cortical slices. The hippocampal increase of KYNA content occurred in diabetic rats treated and nontreated with insulin. Losartan did not affect KYNA levels when administered per se to naïve or diabetic animals but normalized KYNA content in diabetic rats receiving concomitantly insulin. The expression of CCBL1 (kat 1), AADAT (kat 2), and KAT3 (kat 3) genes did not differ between analyzed groups. Low concentrations of losartan did not affect KYNA production in vitro. The neuroprotective effect of ARBs in diabetic individuals may be, at least partially, linked to modulation of KYNA metabolism. The ability of ARB to modulate synthesis of KYNA in diabetic brain does not seem to result from changed expression of genes encoding KATs. We propose possible involvement of angiotensin AT4 receptors in the observed action of losartan.

The aim of the present study was to compare the concentrations of KYNA, 3-OH-KYN and the cytokines TNF-α and IL-6 in patients with depression vs. healthy controls as well as in patients with depression treated pharmacologically vs. those treated using ECT. We also evaluated the relationship between the concentrations of KYNA, 3-OH-KYN and the cytokines TNF-α and IL-6 and clinical improvement measured on the MADRS scale in patients treated pharmacologically and those treated with ECT.Subjects and methods: The study group comprised 29 patients aged 28 to 60 years with a diagnosis of a major depressive episode. Eleven of the patients received pharmacological treatment and 18 were treated with ECT.Patients were assayed for serum levels of KYNA and the cytokines IL-6 and TNF-α. Clinical improvement was measured on the MADRS depression rating scale and the clinical global impression (CGI) scale.Results: Significant differences were found in KYNA levels between depressive patients and healthy controls. Pharmacological treatment significantly contributed to the increase in KYNA levels and ECT – to the increase in TNF-α levels in depressive patients.Conclusions: Depressive patients have significantly lower concentrations of KYNA than healthy individualsDepressive patients who have undergone pharmacological treatment have significantly higher KYNA concentrations than before treatment.Depressive patients who have undergone ECT treatment have significantly lower TNF-α concentrations than before treatment.High pre-treatment levels of IL-6 are associated with a lower MADRS improvement index in pharmacologically treated patients with depression.