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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. Graphical abstract: [Figure not available: see fulltext.] © 2022, Springer Japan KK, part of Springer Nature.

Lipoprotein(a) (Lp(a)) is a low-density lipoprotein (LDL) cholesterol-like particle bound to apolipoprotein(a). Increased Lp(a) levels are an independent, heritable causal risk factor for atherosclerotic cardiovascular disease (ASCVD) as they are largely determined by variations in the Lp(a) gene (LPA) locus encoding apo(a). Lp(a) is the preferential lipoprotein carrier for oxidized phospholipids (OxPL), and its role adversely affects vascular inflammation, atherosclerotic lesions, endothelial function and thrombogenicity, which pathophysiologically leads to cardiovascular (CV) events. Despite this crucial role of Lp(a), its measurement lacks a globally unified method, and, between different laboratories, results need standardization. Standard antilipidemic therapies, such as statins, fibrates and ezetimibe, have a mediocre effect on Lp(a) levels, although it is not yet clear whether such treatments can affect CV events and prognosis. This narrative review aims to summarize knowledge regarding the mechanisms mediating the effect of Lp(a) on inflammation, atherosclerosis and thrombosis and discuss current diagnostic and therapeutic potentials. © 2023 by the authors.

Background: Several studies have linked high Lipoprotein (a) (Lp(a)) concentrations to cardiovascular events, including the formation of Abdominal Aortic Aneurysms (AAA). We review and meta-analyze existing evidence on the association of Lp(a) levels with AAA. Methods: Studies evaluating the link of Lp(a) with AAA, up to December 27th 2021, were identified by a systematic search of PubMed, SCOPUS, and Web of Science databases. The results were qualitatively and quantita-tively synthesized according to PRISMA guidelines. Results are presented as standardized mean differences (S-MD) with 95% confidence intervals (CI). Results: A total of 5,078 subjects (1,637 patients with AAA vs. 3,441 controls) from 11 studies were included in the meta-analysis, with a mean age of 69.9 years and a male sex prevalence of 85.8%. Based on the qualita-tive synthesis, high Lp(a) concentrations are linked to abdominal aortic wall degradation and extracellular ma-trix disarrangement. Moreover, despite the considerable variability among races, high Lp(a) levels are related to increased AAA risk, independently of race differences. Accordingly, patients with AAA displayed significantly higher Lp(a) levels compared to controls (SMD: 0.86, 95% CI: 0.55-1.17, p < 0.001). The outcome was not af-fected in a sensitivity analysis excluding three outlying studies (SMD: 0.40, 95% CI: 0.22-0.58, p < 0.001). Conclusion: This meta-analysis indicates the association between high Lp(a) levels and the presence of AAA, although existing literature presents high heterogeneity. Further studies are needed to standardize Lp(a) mea-surements and to conclude whether Lp(a) can be used as a sensitive biomarker of early presymptomatic AAA diagnosis. © 2022 Bentham Science Publishers.

Coronary artery disease, autonomic neuropathy, and diabetic cardiomyopathy are the most common cardiovascular complications of diabetes. However, emerging evidence demonstrates that diabetes also affects the heart’s electrical conduction system, culminating in lethal arrhythmias and sudden cardiac death. Diabetes and rhythm disturbances have a complex relationship, and arrhythmias cannot only be attributed to ischemia and autonomic neuropathy. Hypoglycemia, hyperglycemia, and glucose fluctuations can potentially induce arrhythmias by activating various pathways. Structural remodeling can accelerate and exacerbate disease development. Mitochondrial dysfunction can also alter the structure and metabolism of cardiomyocytes and contribute to disease progression through oxidative stress and inflammation. © 2022 Bentham Science Publishers.

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 leukocyte 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 migration 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 review article, we focus on the immense role of interleukin-1 in atherosclerosis progression, inflammation cascade and in the clinical application of target anti-inflammatory treatments. © 2022 Bentham Science Publishers.

Background: Transcatheter closure of patent foramen ovale (PFO) is a highly effective therapy for patients with left circulation thromboembolism, not attributable to other conditions. Objectives: This retrospective cohort study investigates the impact of baseline foramen ovale anatomy on the severity of the postclosure shunt. Methods: Patients with PFO, who underwent percutaneous closure, were followed up for at least 5 years post-implantation. Patients were classified into two groups based on the presence of high-risk features of the baseline PFO anatomy. At the follow-up follow-up, residual right-to-left shunt was assessed for the high and non-high-risk anatomy groups, via transcranial Doppler at rest and after performing the Valsalva maneuver, with the in-jection of agitated saline. Results: 38 patients were examined after a mean follow-up period of 9 ± 3 years after implantation. After retrospective evaluation of the baseline transthoracic and transesophageal echo studies, 14 patients with high-risk PFO anatomy were identified. The degree of the residual right-to-left shunt, as assessed by the number of mi-crobubbles was higher in the high-risk PFO anatomy group compared to the non-high-risk group, both at rest [1.50 (IQR: 0.00-3.25) vs. 0.00 (IQR: 0.00-0.00), p < 0.001] and post-Valsalva maneuver [7.50 (IQR: 1.50-10.25) vs. 0.00 (IQR: 0.00-3.75), p = 0.003]. Furthermore, in the high-risk group, more microbubbles were de-tected at rest (p = 0.008) and post-Valsalva (p = 0.002) in subjects without antiplatelet treatment compared to subjects on prolonged antiplatelet therapy. Conclusion: Baseline PFO anatomy affects the severity of the residual right-to-left shunt. Prolonged antiplate-let therapy may benefit patients with high-risk anatomical features. © 2022 Bentham Science Publishers.

Little is known about the role of serum and tissue mediators in the progression of ascending aortic aneurysms and dissections. We examined how the tissue expression of microRNAs and matrix metalloproteinases (MMPs), as well as the serum levels of osteoprotegerin, adiponectin, and high sensitivity C-reactive protein (hsCRP) are associated with these entities. We enrolled 21 patients with ascending aortic aneurysm, 11 with acute Stanford type A aortic dissection and 18 controls. The serum levels of osteoprotegerin, adiponectin, and hsCRP, as well as the tissue expression of MMPs 2 and 9 and tissue microRNAs 29 and 195 were compared among groups. There was no difference regarding serum osteoprotegerin, adiponectin, and tissue MMP2 and MMP9 levels. hsCRP was higher in the dissection group (P =.03). Tissue expression of microRNA 29 was 2.11-fold higher in the dissection (P =.001) and 2.99-fold higher in the aneurysm group (P <.001), compared with the control group. Tissue expression of microRNA 195 was 2.72-fold higher in the dissection (P <.001) and 2.00-fold lower in the aneurysm group (P =.08), compared with to the control group. These findings support the contribution of microRNAs in the progression of aneurysm formation and dissection, suggesting a role as potential biomarkers and future therapeutic targets. © The Author(s) 2022.