Platelets were traditionally considered to purely have a role in the maintenance of haemostasis. Recently their role in vasomotor function, inflammation and atherosclerosis has been very well-recognized. Endothelium which was originally considered as a simple passive barrier, it is now viewed as an organ whose normal functioning is crucial for maintaining vascular health. When endothelial balance is disturbed, vascular disease initiates. Platelet interactions with endothelium have an important contribution in this process. Low-grade inflammation, endothelial dysfunction, and platelet hyper-reactivity are all independently associated with an increased risk of cardiovascular events. Older antiplatelet agents like aspirin and clopidogrel and newer more potent agents like prasugrel and ticagrelor have been proven effective in all the clinical spectrum of coronary artery disease patients. Current antiplatelet medications and especially newer generation P2Y12 inhibitor ticagrelor, offer clinical benefits not only due to their well-recognized antithrombotic effect, but also via the attenuation of platelet inflammatory action, impediment of P2Y12 activation effects in other cells and through other complex and sometimes undefined pathways. Future research is expected to better define platelet-endothelium interactions and the multiple impact of current antiplatelet therapy on them.

Interventional cardiologists in everyday practice are often confronted with calcified coronary lesions indicated for percutaneous transluminal coronary angioplasty (PTCA). PTCA of calcified lesions is associated with diverse technical challenges resulting in suboptimal coronary stenting and adverse long-term clinical outcomes. Angiography itself offers limited information regarding coronary calcification, and the adjuvant use of intracoronary imaging such as intravascular ultrasound (IVUS) and Optical Coherence Tomography (OCT) can guide the treatment of calcified coronary lesions, optimizing the different stages of the procedure. This review offers a description of why, when, and how to use intracoronary imaging for PTCA of calcified coronary lesions in order to obtain the most favorable results. We used the PubMed and Google Scholar databases to search for relevant articles. Keywords were calcified coronary lesions, intracoronary imaging, IVUS, OCT, coronary calcium modification techniques, PTCA, and artificial intelligence in intracoronary imaging. A total of 192 articles were identified. Ninety-one were excluded because of repetitive or non-important information.

Cardiorenal syndrome (CRS) reflects the intricate and bidirectional interplay between cardiac and renal dysfunction, commonly resulting in diagnostic uncertainty, therapeutic dilemmas and poor outcomes. While traditional biomarkers like serum creatinine (Cr) and natriuretic peptides remain widely used, their limitations in specificity, timing and contextual interpretation often hinder optimal management. This narrative review synthesizes the current evidence on established and emerging biomarkers in CRS, with emphasis on their clinical relevance, integration into real-world practice, and potential to inform precision therapy. Markers of glomerular filtration rate beyond creatinine—such as cystatin C—offer more accurate assessment in frail or sarcopenic patients, while tubular injury markers such as NGAL, KIM-1, and urinary L-FABP (uL-FABP) provide early signals of structural renal damage. The FDA-approved NephroCheck^® test—based on TIMP-2 and IGFBP7— enables risk stratification for imminent AKI up to 24 h before functional decline. Congestion-related markers such as CA125 and bio-adrenomedullin outperform natriuretic peptides in certain CRS phenotypes, particularly in right-sided heart failure or renally impaired patients. Fibrosis and inflammation markers (galectin-3, sST2, GDF-15) add prognostic insights, especially when combined with NT-proBNP or troponin. Rather than presenting biomarkers in isolation, this review proposes a framework that links them to specific clinical contexts—such as suspected decongestion-related renal worsening or persistent congestion despite therapy—to support actionable interpretation. A tailored, scenario-based, multi-marker strategy may enhance diagnostic precision and treatment safety in CRS. Future research should prioritize prospective biomarker-guided trials and standardized pathways for clinical integration.

Introduction: Acute cardiorenal syndrome (ACRS) is a common complication of acute heart failure (AHF), leading to worse outcomes and therapeutic challenges. This study aimed to identify clinical parameters associated with ACRS and evaluate its impact on prognosis in hospitalized AHF patients. Methods: This prospective observational study included patients hospitalized for AHF at the Venizelio Cardiology Department from February to November 2023. Demographic characteristics, comorbidities, medications, laboratory and echocardiographic parameters, hospital stay, and in-hospital mortality were recorded. Patients with incomplete data or end-stage chronic kidney disease (CKD) were excluded. Survivors were followed for six months to assess renal function changes, readmissions, initiation of renal replacement therapy (RRT), and mortality. ACRS was defined as a serum creatinine increase of ≥0.3 mg/dL or ≥1.5 times baseline. Results: Among 218 hospitalized AHF patients, 112 (51.3%) developed ACRS. These patients were older, had higher CKD prevalence, worse New York Heart Association (NYHA) functional class, lower hemoglobin, and higher N-terminal Pro-B-type Natriuretic peptide (NT-proBNP) levels. Multivariate analysis identified CKD stage (OR 2.30, 95% CI 1.64–3.23, p < 0.001) and creatinine change on admission (OR 3.53, 95% CI 2.02–6.18, p < 0.001) as independent predictors of ACRS. ACRS was associated with higher in-hospital mortality, longer hospital stays, increased vasoactive medication use, worsening renal function, and higher six-month all-cause readmission and mortality rates. Conclusions: ACRS is a frequent and severe complication in AHF. CKD stage and creatinine on admission are key predictors. Early recognition for risk stratification and individualized management are crucial to improving outcomes in this high-risk population.

Chloride, long considered a passive extracellular anion, has emerged as a key determinant in the pathophysiology and management of heart failure (HF) and cardiorenal syndrome. In contrast to sodium, which primarily reflects water balance and vasopressin activity, chloride exerts broader effects on neurohormonal activation, acid–base regulation, renal tubular function, and diuretic responsiveness. Its interaction with With-no-Lysine (WNK) kinases and chloride-sensitive transporters underscores its pivotal role in electrolyte and volume homeostasis. Hypochloremia, frequently observed in HF patients treated with loop diuretics, is independently associated with adverse outcomes, diuretic resistance, and arrhythmic risk. Conversely, hyperchloremia—often iatrogenic—may contribute to renal vasoconstriction and hyperchloremic metabolic acidosis. Experimental data also implicate chloride dysregulation in myocardial electrical disturbances and an increased risk of sudden cardiac death. Despite mounting evidence of its clinical importance, serum chloride remains underappreciated in contemporary risk assessment models and treatment algorithms. This review synthesizes emerging evidence on chloride’s role in HF, explores its diagnostic and therapeutic implications, and advocates for its integration into individualized care strategies. Future studies should aim to prospectively validate these associations, evaluate chloride-guided therapeutic interventions, and assess whether incorporating chloride into prognostic models can improve risk stratification and outcomes in patients with heart failure and cardiorenal syndrome.

Background: In the setting of ST-segment elevation myocardial infarction (STEMI), the faster and stronger antiplatelet action of ticagrelor compared to clopidogrel, as well as its pleiotropic effects, could result in a greater degree of cardioprotection and final infarct size (FIS) limitation. The aim of our study was to comparatively evaluate the effect of ticagrelor and clopidogrel on myocardial salvage index (MSI) in STEMI patients undergoing thrombolysis. Methods: Forty-two STEMI patients treated with thrombolysis were randomized to receive clopidogrel (n = 21) or ticagrelor (n = 21), along with aspirin. Myocardial area at risk (AAR) was calculated according to the BARI and the APPROACH jeopardy scores. FIS was quantified by cardiac magnetic resonance imaging (CMR) performed 5–6 months post-randomization. MSI was calculated as (AAR-FIS)/AAR × 100%. Primary endpoint of our study was MSI. Secondary endpoints were FIS and CMR-derived left ventricular ejection fraction (LVEF) at 5 –6 months post-randomization. Results: By using the BARI score for AAR calculation, mean MSI was 52.25 ± 30.5 for the clopidogrel group and 54.29 ± 31.08 for the ticagrelor group (p = 0.83), while mean MSI using the APPROACH score was calculated at 51.94 ± 30 and 53.09 ± 32.39 (p = 0.9), respectively. Median CMR-derived FIS—as a percentage of LV—was 10.7% ± 8.25 in the clopidogrel group and 12.09% ± 8.72 in the ticagrelor group (p = 0.6). Mean LVEF at 5–6 months post-randomization did not differ significantly between randomization groups. Conclusions: Our results suggest that the administration of ticagrelor in STEMI patients undergoing thrombolysis offer a similar degree of myocardial salvage, compared to clopidogrel.