Medial arterial calcification (MAC) often occurs in ageing arteries, promoted by diabetes mellitus and chronic kidney disease. Advanced MAC represents a frequent cause of chronic limb-threatening ischaemia and limb amputation. Through a 1D haemodynamics simulation, we study how the mechanical properties of calcified arterial tissue and hydraulic resistance in the peripheral circulation jointly impact haemodynamics as MAC develops. We find that (i) there is a greater drop in systolic pressure across calcified arteries compared to healthy arteries, but this drop can be offset by greater peripheral resistance, provided left ventricular function is intact, (ii) both calcification and enhanced peripheral resistance lead to reduced flow rates, reduced peripheral perfusion and peripheral tissue hypoxaemia, and (iii) pressurized calcified arteries present lumen areas that are smaller than healthy arteries, even though they are larger when unpressurized. We also explore the effects of positive remodelling and elevated blood pressure. We find that a global luminal enlargement reduces the systolic and mean pressure drop across a calcified artery while increasing the mean outflow rate, thereby making a calcified artery behave more like a healthy one, hydrodynamically. Increasing the global pressure in a calcified artery further enhances the drop in systolic and mean pressure while increasing the mean outflow rate. Our simulations suggest that the increased impedance in calcified arteries results from smaller in vivo lumen areas. This can reduce the outflow rate, but the effect is complicated by arteriole closures, vessel geometry and global pressure. These findings confirm previously reported observations of flow reduction in calcified arteries. KEY POINTS: Medial arterial calcification (MAC) often occurs in ageing arteries, promoted by diabetes mellitus and chronic kidney disease. Patients with advanced calcification may develop limb-threatening ischaemia due to malperfusion. Through theoretical modelling and simulation, we find that calcified arteries experience a reduced flow rate because they present smaller lumen areas compared to healthy arteries. Systolic pressure decreases across calcified arteries, whereas in healthy arteries it usually increases. These findings have broad implications for localized detection of MAC.

Medial arterial calcification (MAC) characterizes human arterial ageing, potentially remaining clinically silent for decades. However, in susceptible individuals and patients with diabetes mellitus and chronic kidney disease, it becomes a critical risk factor for cardiovascular morbidity and mortality, and it is a significant risk factor for chronic limb-threatening ischaemia and limb amputation. A key biological feature of MAC pathogenesis is the phenotype switching of vascular smooth muscle cells, ultimately responsible for the deposition of hydroxyapatite crystals and the progressive medial layer destruction associated with intimal thickening. The signalling pathways targeting the vascular smooth muscle cells in ageing and disease are partly shared. Due to the MAC-related arterial wall stiffening and intimal thickening, MAC fundamentally alters central and peripheral haemodynamics. Yet, a comprehensive understanding of MAC’s impact on haemodynamics is lacking. Ankle-brachial index, ultrasound, and X-ray radiography can detect only advanced MAC in the clinical setting. Due to the slow progression, MAC provides many early detection, prevention, and timely intervention targets. However, no effective pharmacological treatment is currently available to alter its course, and revascularizations remain the only treatment option in symptomatic patients. To prevent, reverse, or delay MAC, further research is needed to reveal the complete picture of molecular pathogenesis and haemodynamic impact of MAC vasculopathy.

Social media (SoMe) has witnessed remarkable growth and emerged as a dominant method of communication worldwide. Platforms such as Facebook, X (formerly Twitter), LinkedIn, Instagram, TikTok, and YouTube have become important tools of the digital native generation. In the field of medicine, particularly, cardiology, attitudes towards SoMe have shifted, and professionals increasingly utilize it to share scientific findings, network with experts, and enhance teaching and learning. Notably, SoMe is being leveraged for teaching purposes, including the sharing of challenging and intriguing cases. However, sharing patient data, including photos or images, online carries significant implications and risks, potentially compromising individual privacy both online and offline. Privacy and data protection are fundamental rights within European Union treaties, and the General Data Protection Regulation (GDPR) serves as the cornerstone of data protection legislation. The GDPR outlines crucial requirements, such as obtaining 'consent' and implementing 'anonymization', that must be met before sharing sensitive and patient-identifiable information. Additionally, it is vital to consider the patient's perspective and prioritize ethical and social considerations when addressing challenges associated with sharing patient information on SoMe platforms. Given the absence of a peer-review process and clear guidelines, we present an initial approach, a code of conduct, and recommendations for the ethical use of SoMe. In conclusion, this comprehensive review underscores the importance of a balanced approach that ensures patient privacy and upholds ethical standards while harnessing the immense potential of SoMe to advance cardiology practice and facilitate knowledge dissemination. Graphical Abstract

BACKGROUND:Medial sclerosis (MeS) is a chronic systemic vascular disease that mainly affects the arteries of the lower limb. Its prevalence in the general population is approximately 2.5% (range: 1.6% to 10.0%). It is more common in men than in women.METHODS:This review is based on pertinent publications retrieved by a selective search in PubMed.RESULTS:MeS is the final common pathway of a wide variety of diseases; its pathogenesis is not fully understood. It often remains clinically silent for decades and is usually diagnosed as an incidental finding or in a late stage. MeS with or without atherosclerosis is the most common histologic finding after limb amputation. MeS of the below-the-knee arteries is a major risk factor for chronic critical leg ischemia (OR:13.25, 95% confidence interval: [1.69; 104.16]) and amputation (RR 2.27, [1.89; 2.74]). Patients with peripheral arterial occlusive disease and marked calcification have a much higher risk of amputation (OR 2.88, [1.18; 12.72]) and a higher mortality (OR 5.16, [1.13; 21.61]). MeS is a risk factor for the failure of endovascular treatment of the pedal arteries (OR 4.0, [1.1; 16.6]). The more marked the calcification, the higher the risk of major amputation (HR 10.6 [1.4; 80.7] to HR 15.5 [2.0; 119]). Patients with vascular calcifications have been found to have lower patency rates and higher treatment failure rates two years after open surgical revascularization of the below-the-knee arteries. No pharmacotherapy for MeS is available to date.CONCLUSION:MeS is an important risk factor for chronic critical lower limb ischemia, amputation, morbidity, and complications, particularly after endovascular and surgical procedures.

Undoubtedly, you have had this experience before, spending a lot of time looking for information and eventually getting lost in the internet's maze.In the old good days, journals concerning cardiovascular medicine were few and far between, suggesting covering the entire field.The papers were meticulously researched, well written, and thoroughly peer reviewed.In addition, textbooks covered most of the basic knowledge.The information was credible and trustworthy.Seemingly, there was only the all-comprising perspective of cardiology; the 'bottleneck' principle of the publishable material and 'gatekeeper' concept of editorspeer reviewers went unchallenged.Terms such as 'epistemic injustice' and 'cognitive colonization ' were not yet on the agenda.The internet, powered by digital and intelligent machine technologies, and reformists' mindsets has questioned and changed the perspective, practice, and the rest of medical publishing, so much for the good old days.In the 1960s, Doctor Warren Weaver defined communication as a 'means by which one mechanism affects another mechanism' with messages 'loaded with meaning' or 'pure non-sense'. 1 This spectrum matches all that we have now at our fingertips.Yet, which is which?Scimago Journal & Country Rank, indicator of the merits of scientific journals, lists 356 journals on cardiovascular medicine and cardiology, 2 and Directory Open Access Journals counts 174 open-access journals addressing cardiovascular medicine, with 129 dedicated to cardiology. 3 On top of the multiple web-based outlets such as e-platforms, newsletters, virtual conferences, databases, e-learning courses, e-networks, e-clubs, apps, and others, there are still the old bastions of presumed integrity and reliability.Given this number of educational resources, efficient and information maze navigation skills have become an essential working tool.What is there to be done and how?Keeping in mind two simple questions may be helpful to simplify the task: the purpose of the search and quality, reliability, and trustworthiness.Cardiologists looking up data on the internet may target learning about the essentials of a subject or domain, brushing up on the basic knowledge on a subject, staying up to date in general cardiology or in one of the

Background The preference for using transradial access (TRA) over transfemoral access (TFA) in patients requiring coronary intervention is based on evidence suggesting that TRA is associated with less bleeding and vascular complications, shorter hospital stays, improved quality of life, and a potential beneficial effect on mortality. We have limited study data comparing both access routes in a patient population with atrial fibrillation undergoing PCI, who have a particular increased risk of bleeding, while AF itself is associated with an increased risk of thromboembolism. Methods Using data from the RIVA-PCI registry, which includes atrial fibrillation patients undergoing PCI, we analyzed a high-bleeding-risk cohort. These patients were predominantly on oral anticoagulation (OAC) for atrial fibrillation and the PCI was performed via radial or femoral access. Endpoints examined were in-hospital bleeding (BARC 2-5), cerebral events (TIA, hemorrhagic or ischemic stroke) and coronary events (stent thrombosis and myocardial infarction). Results Out of 1636 patients, 854 (52.2%) underwent transfemoral access (TFA), while 782 (47.8%) received the procedure via transradial access (TRA), including nine patients with brachial artery puncture. Mean age was 75.5 years. Groups were similar in terms of age, sex distribution, atrial fibrillation type, cardiovascular history, risk factors, and comorbidities, except for a higher incidence of previous bypass surgeries, heart failure, hyperlipidemia, and chronic kidney disease (CKD) with GFR<60 ml/min in the TFA group. Clinically relevant differences in antithrombotic therapy and combinations at the time of PCI were absent. However, upon discharge, transradial PCI patients had a higher rate of triple therapy, while dual therapy was preferred after transfemoral procedures. Radial access was more frequently chosen for non-ST-segment elevation myocardial infarction (NSTEMI) and unstable angina pectoris (UAP) cases (NSTEMI 26.6% vs. 17.0%, p<0.05; UAP 21.5% vs. 14.5%, p<0.05), while femoral access was more common for elective PCI (60.3% vs. 44.1%, p<0.05). No differences were observed for ST-segment elevation myocardial infarction (STEMI). Both groups had similar rates of cerebral events (TFA 0.2% vs. TRA 0.3%, p=0.93), but TFA group had a higher incidence of bleeding (BARC 2-5) (4.2% vs. 1.5%, p<0.05), mainly driven by BARC 3 bleeding (1.5% vs. 0.4%, p<0.05). No significant differences were found for stent thrombosis and myocardial infarction (TFA 0.2% vs. TRA 0.3%, p=0.93; TFA 0.4% vs. TRA 0.1%, p=0.36). Conclusions In high-bleeding-risk (HBR) patients with atrial fibrillation (AF) undergoing PCI for acute or chronic coronary syndrome, utilizing radial access (TRA) resulted in a significant decrease of in-hospital bleeding, while not increasing the risk of embolic or ischemic events compared to femoral access.

Little is known about the efficacy and safety of rivaroxaban in patients with atrial fibrillation (AF) who underwent percutaneous coronary intervention (PCI) in clinical practice. We therefore conducted a prospective observational study to determine the rate of ischemic, embolic, and bleeding events in patients with AF and PCI treated with rivaroxaban in a real-world experience. The RIVA-PCI ("rivaroxaban in patients with AF who underwent PCI") (clinicaltrials.gov NCT03315650) is a prospective, noninterventional, multicenter study with a follow-up until 14 months, including patients with AF who underwent PCI discharged with rivaroxaban. Between January 2018 and March 2020, 700 patients with PCI treated with rivaroxaban (elective in 50.1%, non-ST-elevation acute coronary syndrome 43.0%, ST-elevation myocardial infarction in 6.9%) were enrolled at 51 German hospitals. After PCI, a dual antithrombotic therapy consisting of rivaroxaban and a P2Y12 inhibitor was administered in 70.7% and triple antithrombotic therapy in 27.9%, respectively. Follow-up information could be obtained in 695 patients (99.3%). Rivaroxaban has been stopped prematurely in 21.6% of patients. Clinical events under rivaroxaban during the 14-month follow-up compared with those observed in the PIONEER-AF PCI trial included cardiovascular death (2.0% % vs 2.0%), myocardial infarction (0.9% vs 3.0%), stent thrombosis (0.2% vs 0.8%), stroke (1.3% vs 1.3%), International Society on Thrombosis and Haemostasis major (4.2% vs 3.9%), and International Society on Thrombosis and Haemostasis nonmajor clinically relevant bleeding (15.3% vs 12.9%). Therefore, in this real-world experience, rivaroxaban in patients with AF who underwent PCI is associated with ischemic and bleeding event rates comparable with those observed in the randomized PIONEER-AF PCI trial.

Background Little is known about current patterns of antithrombotic therapy in patients with atrial fibrillation (AF) undergoing percutaneous coronary intervention (PCI) in clinical practice in Germany. Methods The RIVA-PCI is a prospective, non-interventional, multicenter study with follow-up until hospital discharge including consecutive patients with AF undergoing PCI. Results Between January 2018 and March 2020, 1636 patients (elective in 52.6%, non-ST elevation acute coronary syndrome [NSTE-ACS] in 39.3%, ST-elevation myocardial infarction in 8.2%) from 51 German hospitals were enrolled in the study. After PCI a dual antithrombotic therapy (DAT) consisting of OAC and a P2Y12 inhibitor was given to 66.0%, triple antithrombotic therapy (TAT) to 26.0%, dual antiplatelet therapy to 5.5%, and a mono-therapy to 2.5% of the patients. Non-vitamin K antagonist oral anticoagulants (NOACs) were given to 82.4% and vitamin K antagonists to 11.5% of the patients. In-hospital events included death in 12 cases (0.7%), myocardial infarction, stent thrombosis, and ischemic stroke in four (0.2%) patients each, while 2.8% of patients had bleeding complications. The recommended durations for DAT or TAT at discharge were 1 month (1.5%), 3 months (2.1%), 6 months (43.1%), and 12 months (45.6%), with a 6-month course of DAT (47.7%) most often recommended after elective PCI and a 12-month course of DAT (40.1%) after ACS. Conclusion The preferred therapy after PCI in patients with AF is DAT with a NOAC and clopidogrel. In-hospital ischemic and bleeding events were rare. The recommended durations for combination therapy vary considerably.

Performing endovascular medical interventions safely and efficiently requires a diverse set of skills that need to be practised in dedicated training sessions. Here, we used multimodal magnetic resonance (MR) imaging to determine the structural and functional plasticity and core skills associated with skill acquisition. A training group learned to perform a simulator-based endovascular procedure, while a control group performed a simpli-fied version of the task; multimodal MR images were acquired before and after training. Using a well-controlled interaction design, we found strong multimodal evidence for the role of the intraparietal sulcus (IPS) in endovas-cular skill acquisition that is in line with previous work implicating the structure in visuospatial transformations including simple visuo-motor and mental rotation tasks. Our results provide a unique window into the multi-modal nature of rapid structural and functional plasticity of the human brain while learning a multifaceted and complex clinical skill. Further, our results provide a detailed description of the plasticity process associated with endovascular skill acquisition and highlight specific facets of skills that could enhance current medical pedagogy and be useful to explicitly target during clinical resident training.

Do you say arteriosclerosis or do you call atherosclerosis?1,2 Classically three lesions have been described under arteriosclerosis:1 atherosclerosis,2 Mönckeberg’s medial sclerosis, and arteriolosclerosis.3Arteriosclerosis is a Greek term meaning ‘hardening of the arteries.’ On the other hand, the term atherosclerosis is etymologically based on the Greek terms athero (gruel or paste) and suffix -oma (growth or tumour) together indicating the formation of ‘atheroma’. In scientific literature arteriosclerosis and atherosclerosis have been accepted as synonyms each emphasizing different aspect of the disease. Medial sclerosis4 denotes calcification of the internal elastic layer and of the media of the artery wall. Recognition of the importance of lipoprotein metabolism and inflammation in atherogenesis represents one of the most significant accomplishments in recent history of cardiovascular diseases.5 Given the overriding importance of atherosclerosis and its thrombotic complications dominating coronary and non-coronary artery disease terminology the use of arteriosclerosis as a synonym is indeed inappropriate. Furthermore, it is important to separate arteriolosclerosis from atherosclerosis as the former does not involve cholesterol metabolism, denoting instead a thickening of the small artery wall characterized by one or more layers of intimal fibromuscular tissue with or without hyaline deposition frequently associated with hypertension and diabetes. So, terminology does matter!

This ESC Council on Stroke/EAPCI/EBNI position paper summarizes recommendations for training of cardiologists in endovascular treatment of acute ischaemic stroke. Interventional cardiologists adequately trained to perform endovascular stroke interventions could complement stroke teams to provide the 24/7 on call duty and thus to increase timely access of stroke patients to endovascular treatment. The training requirements for interventional cardiologists to perform endovascular therapy are described in details and should be based on two main principles: (i) patient safety cannot be compromised, (ii) proper training of interventional cardiologists should be under supervision of and guaranteed by a qualified neurointerventionist and within the setting of a stroke team. Interdisciplinary cooperation based on common standards and professional consensus is the key to the quality improvement in stroke treatment.

Medial arterial calcification (MAC) is a chronic systemic vascular disorder distinct from atherosclerosis that is frequently but not always associated with diabetes mellitus, chronic kidney disease, and aging. MAC is also a part of more complex phenotypes in numerous less common diseases. The hallmarks of MAC include disseminated and progressive precipitation of calcium phosphate within the medial layer, a prolonged and clinically silent course, and compromise of hemodynamics associated with chronic limb-threatening ischemia. MAC increases the risk of complications during vascular interventions and mitigates their outcomes. With the exception of rare monogenetic defects affecting adenosine triphosphate metabolism, MAC pathogenesis remains unknown, and causal therapy is not available. Implementation of genetics and omics-based approaches in research recognizing the critical importance of calcium phosphate thermodynamics holds promise to unravel MAC molecular pathogenesis and to provide guidance for therapy. The current state of knowledge concerning MAC is reviewed, and future perspectives are outlined.

Due to the increasing complexity of diseases in the aging population and rapid progress in catheter-based technology, the demands on operators' skills in conducting endovascular interventions (EI) has increased dramatically, putting more emphasis on training. However, it is not well understood which factors influence learning and performance. In the present study, we examined the ability of EI naïve medical students to acquire basic catheter skills and the role of pre-existing cognitive ability and manual dexterity in predicting performance. Nineteen medical students practised an internal carotid artery angiography during a three-day training on an endovascular simulator. Prior to the training they completed a battery of tests. Skill acquisition was assessed using quantitative and clinical performance measures; the outcome measures from the test battery were used to predict the learning rate. The quantitative metrics indicated that participants' performance improved significantly across the training, but the clinical evaluation revealed that participants did not significantly improve on the more complex part of the procedure. Mental rotation ability (MRA) predicted quantitative, but not clinical performance. We suggest that MRA tests in combination with simulator sessions could be used to assess the trainee's early competence level and tailor the training to individual needs.

Medial arterial calcification (MAC) is a chronic systemic vascular disorder distinct from atherosclerosis that is frequently but not always associated with diabetes mellitus, chronic kidney disease, and aging. MAC is also a part of more complex phenotypes in numerous less common diseases. The hallmarks of MAC include disseminated and progressive precipitation of calcium phosphate within the medial layer, a prolonged and clinically silent course, and compromise of hemodynamics associated with chronic limb-threatening ischemia. MAC increases the risk of complications during vascular interventions and mitigates their outcomes. With the exception of rare monogenetic defects affecting adenosine triphosphate metabolism, MAC pathogenesis remains unknown, and causal therapy is not available. Implementation of genetics and omics-based approaches in research recognizing the critical importance of calcium phosphate thermodynamics holds promise to unravel MAC molecular pathogenesis and to provide guidance for therapy. The current state of knowledge concerning MAC is reviewed, and future perspectives are outlined.