Aortitis—inflammation of the aortic wall—presents at the interface of vasculitis, infection, structural aortic disease, and cardiovascular risk. It may occur in giant cell arteritis (GCA), Takayasu arteritis, immunoglobulin G4 (IgG4)-related disease, drug-induced injury, infection, or as an isolated finding after aortic surgery. Modern imaging detects aortic inflammation more frequently, but the main challenge is classification rather than detection: determining whether disease is infectious or immune-mediated, active or dominated by fixed structural damage, systemic or isolated, and whether the dominant threat is aneurysm, dissection, undertreated infection, or avoidable immunosuppression. This review considers aortitis as a high-risk vascular syndrome requiring aetiology-first classification rather than descriptive labelling. Before escalating immunosuppression, infection must be actively excluded and inflammatory activity distinguished from fixed vascular damage. Treatment should be individualised according to phenotype, age, vascular territory, comorbidity, and toxicity risk, with surveillance continuing even after symptoms and inflammatory markers improve. Optimal care depends on multidisciplinary assessment integrating rheumatology, infectious diseases, vascular surgery, radiology, and cardiology expertise. Progress will require standardised imaging definitions, registries linking inflammatory control with structural vascular outcomes, and validation of artificial intelligence (AI) tools before clinical adoption.

Cardiovascular disease remains Europe’s leading cause of death and disability despite mature evidence for prevention, acute and chronic treatment, rehabilitation, and secondary prevention. This structured critical narrative review evaluates whether the European Safe Hearts Plan can convert this evidence into coordinated, measurable, and accountable cardiovascular pathways. We appraise the plan’s ten flagship actions by evidence maturity and implementation readiness; distinguish shared system functions from disease-specific delivery for acute coronary syndromes, heart failure, and atrial fibrillation; compare selected European Society of Cardiology and American Heart Association/American College of Cardiology recommendations; and propose a core indicator set and staged Cyprus pilot. Guideline-supported interventions should be standardised and audited, whereas screening technologies, digital health, artificial intelligence, and novel phenotyping require governed implementation and prospective assessment of patient outcomes, costs, equity, and unintended consequences. Cyprus is presented as a bounded implementation setting rather than a directly generalisable European model. The plan should be judged through a limited set of clinical, implementation, and equity indicators, including premature cardiovascular mortality, risk factor control, guideline-directed therapy, rehabilitation participation, registry completeness, reach, and fidelity.

(1) Introduction: Early identification of patients at high risk of recurrent events after hospitalization for acute decompensated heart failure (ADHF) remains challenging. The Larissa Heart Failure Risk Score (LHFRS) is a simple prognostic tool based on hypertension, coronary artery disease, and red blood cell distribution width. Urinary sodium has recently emerged as an objective marker of natriuretic response and decongestion. We prospectively evaluated whether incorporation of urinary sodium improves the prognostic performance of the LHFRS. (2) Methods: This prospective single-center observational study enrolled 130 consecutive adults hospitalized with ADHF. Clinical, laboratory, electrocardiographic, and echocardiographic data were collected at admission. Spot urinary sodium and chloride were measured at admission and 2 h after intravenous loop diuretic administration according to a standardized decongestion protocol. The primary endpoint was heart failure rehospitalization within 3 months. Secondary endpoints included all-cause mortality and the composite of death or heart failure rehospitalization. Multivariable logistic regression with bootstrap internal validation (1000 resamples) was used to identify independent predictors of outcomes. (3) Results: The study population included patients across the spectrum of heart failure phenotypes (HFrEF 58%, HFmrEF 7%, HFpEF 35%). During follow-up, 48 patients (36.9%) experienced heart failure rehospitalization and 23 (17.7%) died. The LHFRS independently predicted 3-month rehospitalization (B = 0.490, p = 0.041). Admission urinary sodium and 2-h urinary sodium provided incremental prognostic information beyond the LHFRS and remained independently associated with rehospitalization after multivariable adjustment (p = 0.008 and p = 0.001, respectively). Urinary chloride demonstrated similar prognostic associations, whereas conventional renal biomarkers, including serum creatinine, urea, estimated glomerular filtration rate, serum sodium, and NT-proBNP, did not consistently retain independent prognostic significance. The LHFRS was also significantly associated with the composite endpoint of death or rehospitalization (B = 1.173, p = 0.002), while its association with mortality alone was not statistically significant (B = −5.551, p = 0.256). (4) Conclusions: Lower admission and 2-h urinary sodium concentrations were associated with 3-month HF rehospitalization after adjustment for the LHFRS. These findings are hypothesis-generating and require confirmation in larger, externally validated multicenter cohorts.

Artificial intelligence (AI) and machine learning (ML) are increasingly being evaluated as decision-support tools for forecasting postoperative complications after cardiothoracic surgery. This narrative review synthesises peer-reviewed clinical, biomedical informatics, and digital-health literature across acute kidney injury (AKI), postoperative atrial fibrillation (POAF), pulmonary complications, neurological outcomes, mortality, wound monitoring, wearable surveillance, and post-discharge monitoring. Rather than treating reported AUC values as interchangeable evidence of algorithmic superiority, this review emphasises that model performance depends on at least three interacting factors: algorithmic architecture, data richness, and validation strategy. Conventional tools such as EuroSCORE II and Society of Thoracic Surgeons (STS) models remain clinically useful because they are familiar, transparent, and externally established; however, many rely on static perioperative snapshots and are less suited to continuously updated intraoperative and postoperative data streams. Contemporary ML models, including gradient-boosting approaches, support-vector methods, convolutional neural networks, and wearable-based algorithms, may improve discrimination in selected settings, particularly when dynamic laboratory trajectories, physiological time-series, imaging data, or remote-monitoring signals are available. However, current evidence remains limited by single-centre development, heterogeneous endpoints, inconsistent calibration reporting, limited decision-curve analysis, low positive predictive values in surveillance applications, and sparse prospective implementation. Future work should prioritise multicentre external validation, calibration, clinical utility analysis, standards-based electronic medical record interoperability, and implementation pathways that preserve clinician oversight.

Few disorders have evoked more interest and controversy in cardiology over recent centuries than floppy mitral valve (FMV)/mitral valve prolapse (MVP). FMV/MVP is a complex entity with multiple genotypes and phenotypes in which the clinical manifestations may not be directly related to the severity of mitral regurgitation. Furthermore, there is a lack of a precise definition of this complex entity. This review emphasises a diagnostic approach based mostly on FMV rather than solely on MVP, which frequently may be a non-specific finding. In addition, a clinical classification of FMV/MVP is presented that separates patients with symptoms not directly related to the severity of mitral regurgitation (referred to as FMV/MVP syndrome) from those in whom symptoms are directly related to mitral regurgitation and its complications. In the future, genetic variants will likely be incorporated into the diagnostic classification and management of this complex entity as this odyssey continues.

Heart failure (HF) represents a systemic syndrome defined by the myocardium’s inability to maintain adequate cardiac output. Although foundational, traditional reductionist methodologies have encountered limitations in comprehensively elucidating the multifaceted pathophysiology of HF. This paper examines HF through the theoretical frameworks of complexity science, including quantum biology, evolutionary biology, nonequilibrium thermodynamics, chaos theory, and systems biology. Theoretical constructs, such as quantum oxidative stress, offer novel perspectives on bioenergetic decline. From an evolutionary standpoint, the heart’s optimization for oxygen delivery may lack the requisite redundancy to mitigate modern stressors. Thermodynamic and chaos theory models characterize the myocardium as a dissipative structure and define heart failure as a loss of physiological chaos. However, translating these theoretical models into clinical practice remains challenging. Although systems biology attempts to integrate these concepts, it necessitates substantial data and computational resources. Furthermore, abstract signatures—such as diminished quantum efficiency or loss of fractal dynamics—currently lack standardized clinical assays. Although reframing HF as a failure of organized complexity provides a compelling conceptual model, significant translational barriers persist. Nevertheless, by continuing to bridge the divide between abstract physics and clinical physiology, it may ultimately be possible to identify novel pathways for understanding and managing this complex condition.

Postoperative atrial fibrillation (POAF) is the most frequent post-cardiac surgical arrhythmia and is associated with haemodynamic instability, longer hospital stays, higher healthcare utilisation, stroke and adverse long-term outcomes. Conventional models of POAF focus on advancing age, pre-existing atrial substrate, increasing operative complexity, inflammatory responses related to cardiopulmonary bypass, disturbances in autonomic balance, and acute metabolic insults during the perioperative period. Although these explanations are important, they may be incomplete. Malignancy and the cancer-associated systemic environment involve biological processes potentially relevant to postoperative atrial vulnerability, such as chronic inflammation, oxidative stress, impaired vascular function, hypercoagulability, altered immune response, frailty, and treatment-related myocardial, pericardial, or conduction-system injury. This review assesses whether malignancy should be regarded as an underrecognised modifier of susceptibility rather than as a coincidental comorbidity. Most available data are extrapolated from cardio-oncology and thoracic oncology studies or general studies related to atrial fibrillation (AF) rather than studies focused on cardiac surgery. While malignancy cannot be dismissed as irrelevant to the generation of POAF, it also does not permit causal inference. Future studies should move beyond binary cancer status and incorporate cancer activity, treatment exposures, biomarker profiles, and atrial substrate measures to determine whether malignancy improves perioperative POAF risk stratification.

Postoperative atrial fibrillation (POAF) after cardiac surgery is often managed as a transient inpatient arrhythmia, yet recurrent or silent atrial fibrillation (AF) after discharge may identify persistent atrial vulnerability. This issue is particularly relevant in cancer survivors, whose thrombotic and bleeding risks vary according to cancer activity, treatment exposure, thrombocytopenia, frailty and planned procedures. For this narrative review, PubMed/MEDLINE and Scopus were searched from inception to 16 June 2026, with Google Scholar used for supplementary citation tracking. A total of 50 publications were included in the final narrative synthesis. Direct evidence at the intersection of cancer, cardiac surgery, POAF and digital monitoring remains limited. Accordingly, the proposed “Digital Cancer-POAF Survivorship Pathway” is presented as a conceptual, hypothesis-generating framework, rather than a validated clinical algorithm. Its distinctive contribution is to connect cancer-state phenotyping and treatment-specific arrhythmic risk with post-discharge rhythm surveillance, electrocardiogram (ECG) confirmation, multidisciplinary interpretation, data governance and outcomes for prospective validation. Digital monitoring may increase AF detection; however, whether it reduces stroke, bleeding, readmission, or healthcare utilisation in this population is unknown. Neither a low detected AF burden nor the absence of AF during finite monitoring has been validated as an independent basis for anticoagulation decisions.

BACKGROUND:Despite advances in durable left ventricular assist device (LVAD) technology and improved survival outcomes, significant disparities persist in its utilization across Europe, particularly in Southern regions. AIMS:To evaluate variability in LVAD implantation rates among representative European countries and estimate the unmet needs in Greece. METHODS:Market data reflecting the sales of long-term LVAD systems across various countries from 2019 to 2024 were combined with registry-based LVAD implantation records to estimate the number of eligible patients and actual LVAD implantations in selected European countries. A stepwise epidemiological modeling approach was applied to estimate LVAD-eligible patients in Greece. RESULTS:In several Southern European countries, LVAD implantation rates in 2024 were no more than 2 per million population (Greece: 0.78/million, Italy: 1.89/million, Spain: 1.79/million, Portugal: 0.88/million). In Greece, even though an estimated 349 patients were eligible for LVAD implantation in 2024, based on demographic and clinical criteria, only seven devices were implanted while 24 patients underwent heart transplantation, reflecting a treatment gap of 318 patients (approximately 91% of the eligible population). In contrast, countries in Western and Northern Europe (Austria: 4.57/million, Germany: 8.74/million, France: 2.47/million, the Netherlands: 5.71/million, Switzerland: 3.28/million, Hungary: 2.08/million, Czech Republic: 6.19/million, Sweden: 2.19/million) reported LVAD implantation rates up to 9 per million. Significant discrepancies were reported also in the number of available LVAD centers as well as LVAD implantations per million between Greece and countries with similar populations (≈10 million residents) from Europe and Asia. CONCLUSIONS:LVAD implantation rates vary among representative Southern European countries, with the lowest rates being observed in Greece. Insufficient number of implanting centers, limited reimbursement, and fragmented post-implant care contribute to this disparity.

Inflammation has a key role in coronary atherosclerotic disease (CAD), as it contributes to the development, progression, instability and rupture of the atherosclerotic plaque. The long-term treatment and continuous suppression of inflammation is a therapeutic goal for patients with increased cardiovascular risk and chronic CAD syndromes. In contrast, in acute myocardial infarction (MI), the presence of inflammation is necessary for smooth healing, tissue neovascularization, and limitation of left ventricular remodeling, rendering a "controlled amount" of inflammation desirable in this context. As a result, the use of nonselective, broad-spectrum anti-inflammatory drugs does not offer any beneficial effect and may turn out to be harmful. Nevertheless, the possibility that modification of a usual inflammatory response in MI with selective anti-inflammatory agents cannot be excluded. Conversely, an excessive, uncontrolled, and prolonged inflammatory response after an acute MI may result in extensive irreversible myocardial damage and should be timely recognized and treated, preferably with a selective anti-inflammatory agent. In the present review we highlight the key role of inflammation in chronic and acute CAD, discuss the underlying pathophysiology, and present the results of representative experimental and clinical studies evaluating the pharmaceutical modification of the inflammatory response in this context.

Artificial intelligence (AI) has recently been introduced into clinical practice with the potential to revolutionize medicine. AI will provide the physician with unlimited power, which is almost impossible to foresee at present. In addition, AI can be used for the development of pharmacologic agents and antibodies with unprecedented accuracy and speed. AI will assist the physician in defining individuals at high risk for developing a certain disease and, in turn, provide appropriate care to delay or prevent the disease. Using vast information related to a certain disease, the physician will be able to apply individualized care in contrast to the current approach based on guidelines where "one size fits all." With prevention and individualized care, the cost of health care will decrease, human suffering will diminish, and overall mortality will decline. However, in this endless evolution of medicine, the role of the physician remains constant, which is to maintain the health of a human being. In addition to diagnosis and management, the physician should apply common sense, courage, and compassion when dealing with the difficulties of human life that may escape machines. Humanistic values, among others, are basic for the caring physician. Thus, the humanistic approach to the patient and the divine vocation of the physician should never be forgotten and should be based on a solid ethical foundation. The greatest challenge for physicians and medical leadership in the 21st century will not be living with and adapting to changing technology, but determining the proper balance between clinical wisdom and evolving technology.

Hereditary transthyretin (TTR) amyloidosis (ATTRv amyloidosis) is a devastating disease characterized by broad range of clinical manifestations, including predominantly neurological, predominantly cardiac, and mixed phenotypes. This wide phenotypic variability hindered timely disease diagnosis and risk stratification in the past, especially in individuals with absent or uncharted family history. However, recent advances in noninvasive testing have led to greater awareness and earlier diagnosis. Further, medications have been discovered which proved effective in controlling the disease and improving outcomes including stabilizing TTR, silencing TTR variants, and removing TTR amyloid from affected tissues. Importantly, CRISPR gene editing, a groundbreaking technology, offers the unique potential to cure ATTRv amyloidosis, transforming lives and opening new doors in medical science. This review provides an update on ATTRv amyloidosis mechanisms, diagnosis, and management emphasizing the importance of early diagnosis as the steadfast underpinning for the capitalization of the advances in medical treatment to the benefit of the patients.

Aging is associated with aortic stiffening (AoSt), a condition characterized by diminished aortic elasticity that predisposes individuals to cognitive decline, including Alzheimer’s disease (AD). Emerging evidence implicates medin, which is derived from milk fat globule-EGF factor 8 protein (MFG-E8), as a key link between AoSt and AD. Medin aggregates into aortic medial amyloid (AMA), which is found in approximately 97% of Caucasian individuals aged 50 and above, contributing to vascular inflammation, calcification, and loss of arterial elasticity. These changes may promote hyperpulsatile cerebral blood flow and impair glymphatic clearance, resulting in increased deposition of neurotoxic proteins, such as amyloid-β (Aβ) and possibly medin, which colocalizes with vascular Aβ in the brain. Medin enhances Aβ aggregation, generating heterologous fibrils, and thereby contributes to cerebrovascular dysfunction and neuroinflammation. This interaction (cross-seeding) may deteriorate amyloid pathology in both the vasculature and the parenchyma in AD. Furthermore, medin per se causes endothelial dysfunction, increases oxidative stress, and activates glial cells, promoting the development of a pro-inflammatory environment that enhances cognitive decline. In this manuscript, we contend that medin might act as a bridge connecting the age-related increase in aortic stiffness to AD, and therefore, medin might present a novel therapeutic target within this context. This hypothesis deserves experimental and clinical validation.

Background/Objectives: Postoperative atrial fibrillation (POAF) occurs frequently after cardiac surgery and is associated with increased morbidity and mortality. The pathogenesis of POAF in this setting is complex and not completely understood. Since cancer is a well-known risk factor for AF, the aim of this study was to identify potential predictors, including cancer, of POAF after cardiac surgery. Methods: This prospective study included 400 consecutive patients in sinus rhythm who underwent elective cardiac surgery in Aretaeio Hospital (Nicosia, Cyprus) from January 2020 till January 2023. The primary outcome was the development of POAF during hospitalization, defined as any documented AF episode lasting >30 s. Predictors of the primary outcome were studied using univariable and multivariable logistic regression analysis. Results: Of the 400 patients (68 [61–73] years, 64 [16%] females) studied, 66 (16.5%) developed POAF. Among the variables examined, the only predictors of POAF were cardiopulmonary bypass time (odds ratio [OR] = 1.001, 95% confidence interval = [95% CI, 1.000–1.001], p = −0.031) and cancer (OR = 3.852, 95% CI = [1.535–9.664], p = 0.004). Cancer was present in 13 (4%) and in 10 (15%) of patients without and with POAF, respectively (p < 0.001). Conclusions: Cancer was associated with a dramatic increase in POAF risk early after elective cardiac surgery in this study. Whether patients developing POAF after cardiac surgery should be searched for cancer deserves further investigation.

Background: Postoperative atrial fibrillation (POAF) is the most frequent arrhythmic complication following cardiac surgery, affecting nearly 20–30% of patients. While conventional risk factors such as age, hypertension, and atrial enlargement are well known, emerging evidence suggests that cancer itself constitutes a significant, yet underrecognized, contributor to POAF risk. Objective: This review aims to systematically examine the association of cancer with POAF, explore underlying pathophysiological mechanisms, and discuss clinical implications for risk stratification and management in cardiac surgical patients with concurrent or historical malignancies. Methods: A comprehensive review of recent literature was conducted using PubMed and Scopus databases. Studies focusing on the epidemiology, mechanisms, and clinical management of POAF in patients with cancer were evaluated. AI-assisted tools (OpenAI’s ChatGPT) were used for formatting the graphical abstract. Results: Lung, breast, gastrointestinal, hematologic, and prostate cancers demonstrate the strongest association with POAF. The arrhythmogenic mechanisms include systemic inflammation, hypercoagulability, direct cardiotoxicity from cancer therapies, autonomic dysregulation, and paraneoplastic syndromes. Integration of oncologic variables into perioperative cardiovascular care is essential for precision risk assessment and outcome optimization. In a recent prospective cardiac surgery cohort, active or historical cancer independently conferred ~4-fold higher odds of POAF (adjusted OR: 3.85, 95% CI: 1.54–9.66), with cancer present in 15% of POAF cases versus 4% of non-POAF patients. Conclusions: Cancer represents a pivotal and multifactorial risk factor for POAF after cardiac surgery. Recognizing its role calls for a multidisciplinary approach that aligns oncologic and cardiovascular care to mitigate arrhythmic risk and improve surgical outcomes.

A dominant event determining the course of heart failure (HF) includes the disruption of the delicate sodium (Na+) and water balance leading to (Na+) and water retention and edema formation. Although incomplete decongestion adversely affects outcomes, it is unknown whether interventions directly targeting (Na+), such as strict dietary (Na+) restriction, intravenous hypertonic saline, and diuretics, reverse this effect. As a result, it is imperative to implement (Na+)-targeting interventions in selected HF patients with established congestion on top of quadruple therapy with angiotensin receptor neprilysin inhibitor, β-adrenergic receptor blocker, mineralocorticoid receptor antagonist, and sodium glucose cotransporter 2 inhibitor, which dramatically improves outcomes. The limited effectiveness of (Na+)-targeting treatments may be partly due to the fact that the current metrics of HF severity have a limited capacity of foreseeing and averting episodes of congestion and guiding (Na+)-targeting treatments, which often leads to dysnatremias, adversely affecting outcomes. Recent evidence suggests that spot urinary sodium measurements may be used as a guide to monitor (Na+)-targeting interventions both in chronic and acute HF. Further, the classical (2)-compartment model of (Na+) storage has been displaced by the (3)-compartment model emphasizing the non-osmotic accumulation of (Na+), chiefly in the skin. 23(Na+) magnetic resonance imaging (MRI) enables the accurate and reliable quantification of tissue (Na+). Another promising approach enabling tissue (Na+) monitoring is based on wearable devices employing ion-selective electrodes for electrolyte detection, including (Na+) and (Cl–). Undoubtably, further studies using 23(Na+)-MRI technology and wearable sensors are required to learn more about the clinical significance of tissue (Na+) storage and (Na+)-related mechanisms of morbidity and mortality in HF.

Heart transplantation (HTx) remains the last therapeutic resort for patients with advanced heart failure. The present work is a clinically focused review discussing current issues in heart transplantation. Several factors have been associated with the outcome of HTx, such as ABO and HLA compatibility, graft size, ischemic time, age, infections, and the cause of death, as well as imaging and laboratory tests. In 2018, UNOS changed the organ allocation policy for HTx. The aim of this change was to prioritize patients with a more severe clinical condition resulting in a reduction in mortality of people on the waiting list. Advanced heart failure and resistant angina are among the main indications of HTx, whereas active infection, peripheral vascular disease, malignancies, and increased body mass index (BMI) are important contraindications. The main complications of HTx include graft rejection, graft angiopathy, primary graft failure, infection, neoplasms, and retransplantation. Recent advances in the field of HTx include the first two porcine-to-human xenotransplantations, the inclusion of hepatitis C donors, donation after circulatory death, novel monitoring for acute cellular rejection and antibody-mediated rejection, and advances in donor heart preservation and transportation. Lastly, novel immunosuppression therapies such as daratumumab, belatacept, IL 6 directed therapy, and IgG endopeptidase have shown promising results.