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Abstract: Cardiovascular disease is the leading cause of mortality worldwide. Inflammation has long been established as a key component in the pathophysiology of coronary artery disease. The interleukin-1 family consists of 11 members that regulate the inflammatory response through both pro- and anti-inflammatory properties with the Nod-like receptor (NLR) family pyrin domain con-taining 3 inflammasome having a pivotal role in the process of converting interleukin-1 beta and in-terleukin-18, two key inflammatory mediators, into their mature forms. Interleukin-1 affects various cell types that participate in the pathogenesis of atherosclerosis as it enhances the expression of leu-kocyte adhesion molecules on the surface of endothelial cells and augments the permeability of the endothelial cell barrier, attracting monocytes and macrophages into the vessel wall and aids the mi-gration of smooth muscle cells toward atheroma. It also enhances the aggregation of low-density lipoprotein particles in endothelium and smooth muscle cells and exhibits procoagulant activity by inducing synthesis, cell-surface expression and release of tissue factor in endothelial cells, promot-ing platelet adhesion. The value of interleukin-1 as a diagnostic biomarker is currently limited, but interleukin-1 beta, interleukin-18 and interleukin-37 have shown promising data regarding their prognostic value in coronary artery disease. Importantly, target anti-inflammatory treatments have shown promising results regarding atherosclerosis progression and cardiovascular events. In this re-view article, we focus on the immense role of interleukin-1 in atherosclerosis progression, inflam-mation cascade and in the clinical application of target anti-inflammatory treatments.

Coronavirus disease-19 (COVID-19) has extended implications namely the long COVID-19 syndrome. We assessed over-time changes in left ventricular (LV) function, aortic stiffness, autonomic function, and ventricular-arterial coupling (VAC) in post-COVID-19 patients. We followed 34 post-COVID-19 subjects, up to 6 months post-hospital discharge. Subjects without COVID-19 served as control. We evaluated LV global longitudinal strain (LV-GLS), arterial stiffness [carotid-femoral pulse wave velocity (cf-PWV)], and heart rate variability -standard deviation of normal RR intervals (SDNN). VAC was estimated as the ratio of cf-PWV to LV-GLS. Post-COVID-19 individuals (1-month post-hospital discharge) presented with impaired LV-GLS [-18.4%(3.1) vs. -22.0%(2.7), P 0.001], cf-PWV [12.1 m/s (3.2) vs. 9.6 m/s (1.9), P 0.001], SDNN [111.3 ms (22.6) vs. 147.2 ms (14.0), P 0.001], and VAC [-0.68 (0.22) vs. -0.44 (0.10), P 0.001] compared to control. LV-GLS, SDNN, and VAC improved at the 6-month follow-up however they did not reach control levels. In post-COVID-19 subjects, SDNN and VAC were correlated at the 1-month (R = 0.499, P = 0.003) and 6-month (R = 0.372, P = 0.04) follow-up. Long COVID-19 syndrome was associated with impaired LV-GLS, SDNN, and VAC. Post-COVID-19 subjects presented with autonomic dysregulation associated with aortic stiffness, ventricular-arterial impairment, and LV dysfunction, even 6-months post-hospital discharge. These abnormalities may be related to the presence of long COVID-19 syndrome.

'Cover index' has been proposed to appraise the congruence between the aortic annulus and the device, with the assumption of not taking into account the actual device implantation depth. The aim of this study was to investigate whether the annulus-prosthesis mismatch, as expressed with the new proposed 'true cover index' according to actual implantation depth, can predict aortic regurgitation (AR) after transcatheter aortic valve implantation (TAVI).Patients who had undergone TAVI with the self-expandable CoreValve device, were retrospectively studied. All available prosthesis sizes were ex-vivo scanned and the precise diameter at 0.3mm intervals along each device was measured. The 'true cover index' was evaluated, as a ratio of the following: 100×([prosthesis actual diameter at implantation depth-annulus diameter]/prosthesis actual diameter at implantation depth). AR was echocardiographically evaluated at discharge and 30days and classified as prominent if moderate, or trivial if none or mild.Overall, 120 patients who had undergone TAVI, were considered eligible for the study. 'True cover index' was statistically significantly lower among patients with prominent AR in comparison with trivial AR at discharge (5.7±4.8mm vs 9±5.1, p=0.025), as well as at one month post-TAVI (5.4±5.1mm vs 9.0±5.1, p=0.023), indicating increased AR for smaller index. After adjustment for severe annulus calcification, impaired baseline LVEF and previous valvuloplasty, it remained an independent predictor of one month prominent AR (OR: 0.854, CI: 0.730-0.999; p=0.048). 'True cover index' of4.3 was shown to predict one-month prominent AR with sensitivity =75% and specificity =82.5%.'True cover index' is strongly and independently correlated with the short and mid-term AR after CoreValve implantation.

Whether non-thienopyridines may protect patients more efficiently from microembolic events during TAVI has not been investigated. We hypothesized that ticagrelor+ASA will reduce the number of microemboli towards the cerebral circulation during TAVI comparing to the combination of clopidogrel+ASA.

Transcatheter interventions for structural heart disease represent an emerging field in interventional cardiology. Undoubtedly, there is an absolute necessity for antiplatelet and/or anticoagulation treatment prior, during and post such interventions. However, currently administered regimens are mainly based in expert consensus recommendations. In the present review we aim to summarize data regarding anti platelet and/or anticoagulation treatment in the following transcatheter structural heart interventions: left atrial appendage closure, atrial septal defect closure, patent foramen oval closure, paravalvular leak closure.

Coronary rupture during cardiac catheterization and angioplasty is an uncommon but serious complication. Predisposing factors to this dreadful complication are not well defined. We present a case of coronary artery rupture during an urgent percutaneous intervention in a patient under chronic immunosuppressive therapy with corticosteroids and azathioprine, despite intravascular ultrasound (IVUS) guidance. Initially, the perforation was successfully managed with balloon inflation and finally, a covered stent was deployed at the site. The unexpected rupture, despite optimal IVUS sizing, indicates a possible role of immunosuppressive therapy in coronary artery wall vulnerability. Extra caution should be exerted in such patients while performing coronary interventions and using intracoronary devices.

Cardiovascular disease and complications are often mediated by the development and rupture of atherosclerotic plaques. Plaque composition is a major factor that determines plaque vulnerability. Intravascular ultrasound (IVUS) and spectral analysis of the radio frequency signal provide an in vivo tissue characterisation of atherosclerotic plaques, known as virtual histology (VH-IVUS). In VH-IVUS analysis, four histological tissue components are classified: fibrous, fibro/fatty, necrotic core and calcium. Existing technology determines only the area of each component within the plaque. Quantitative, objective characterisation of other plaque components' patterns within the plaque is lacking. The aim of this study was to determine new compositional and structural indices which indicate spatial distribution, heterogeneity and dispersity of each VH-IVUS-derived component within the plaque area and also with respect to the plaque-lumen border. We developed an automated computational system in Java for the analysis of both single cross-sectional segments and the whole length of the examined plaque (volumetric analysis). The following parameters were computed: the number of different solid segments and the area of the largest solid segment of each component within the plaque, the per cent of the lumen border that is surrounded by each component, the number of different solid segments and the largest area of a solid segment of each component that adjoins the lumen border. Especially components' localisation in relation to the lumen border may significantly influence plaque vulnerability and plaque-stent interaction, which should be investigated in future clinical studies.

Before proceeding with the clinical and research utility of Intravascular Imaging, it is important to examine in detail the principles that the acquisition of the IVUS signal is based on. This chapter provides an insight into the principles of the IVUS imaging, while describing the image quality factors. Additionally, the equipment for IVUS examination is described, and the acquisition and display techniques are detailed. Finally, a brief summary of the limitations of the IVUS signal is attempted.