Search Results (110)

Background: Thrombocytopenia (platelet count < 100 × 10⁹/L) occurs in 20–40% of critically ill patients with sepsis and is associated with adverse outcomes. Most prior studies have treated thrombocytopenia as a static risk indicator rather than a dynamic process. We investigated whether platelet recovery within 7 days provides independent prognostic information in patients with sepsis. Methods: We performed a retrospective cohort study using the MIMIC-IV database. Among 22,513 adults with sepsis admitted to intensive care units, 5401 developed thrombocytopenia within 24 h of admission and had sufficient follow-up data. The primary exposure was sustained platelet recovery to ≥100 × 10⁹/L within 7 days. The primary outcomes were 28-day and in-hospital mortality. Propensity-score matching and overlap weighting were used to adjust for demographic characteristics, comorbid conditions, illness severity, and organ-support therapies. Results: Among 5401 septic ICU patients with thrombocytopenia, 3193 (59%) achieved platelet recovery within 7 days. A total of 2056 patients (38%) recovered by day 3, and 1137 (21%) recovered between days 4 and 7. After multivariable adjustment, platelet recovery was independently associated with markedly lower mortality (adjusted risk ratio, 0.56; 95% CI, 0.53–0.67 for in-hospital death; and 0.60; 95% CI, 0.53–0.67 for 28-day death) and more than a doubling of survival time (adjusted ratio, 2.08; 95% CI, 1.65–2.63). Early and intermediate recovery conferred similar benefits. Higher baseline platelet counts, antiplatelet therapy, and heparin use were associated with recovery, whereas cirrhosis, greater illness severity, and continuous renal replacement therapy were associated with non-recovery. Conclusions: In patients with sepsis and thrombocytopenia, platelet recovery within 7 days was a strong and independent predictor of survival. Exploratory timing-stratified analyses yielded similar associations across subgroups. These findings support platelet recovery as a useful prognostic marker reflecting broader physiologic stabilization in sepsis. Full article

(1) Background: Whether anticoagulation can be resumed in atrial fibrillation (AF) combined with intracranial hemorrhage (ICH), and which anticoagulation modality is used with better efficacy and safety, is unknown. (2) Method: Randomized controlled trials (RCTs) and observational studies on relevant topics were included by searching five databases: PubMed, EMBASE, EBSCO, Cochrane Central Register of Controlled Trial and ClinicalTrials. Bayesian network meta-analysis was performed to analyze the effect of oral anticoagulant (OAC), new oral anticoagulant (NOAC), warfarin, antiplatelet, left atrial appendage occlusion (LAAO) and no therapy in patients with AF after intracranial hemorrhage. (3) Results: We included 16 studies involving 25,483 patients. Compared with no antithrombotic therapy, the risk of thromboembolism and all-cause mortality were both reduced with OAC (OR: 0.38, 95% CI: 0.21–0.67; OR: 0.45, 95% CI: 0.25–0.8) and LAAO (OR: 0.11, 95% CI: 0.01–0.76; OR: 0.11, 95% CI: 0.01–0.88), and there was no increased risk of recurrent intracranial hemorrhage. Regarding thromboembolism, OAC (OR: 0.28, 95% CI: 0.11–0.69) was superior to antiplatelet therapy, and antiplatelet therapy (OR: 12.59, 95% CI: 1.57–133.50) was associated with a higher risk of thromboembolism than LAAO. There were no significant differences in recurrent intracranial hemorrhage between the interventions. LAAO appeared to be the best option for reducing thromboembolism (SUCRA: 0.96), recurrent intracranial hemorrhage (SUCRA: 0.75) and all-cause mortality (SUCRA: 0.94). (4) Conclusions: Based on this network meta-analysis, we hypothesize that LAAO has the highest likelihood of reducing the risk of thromboembolism and recurrent intracranial hemorrhage, as well as all-cause mortality in patients with AF after intracranial hemorrhage, followed by OAC. Full article

Background/Objectives: Complex aneurysms of the posterior inferior cerebellar artery (PICA) remain challenging because of their deep location, variable morphology, and proximity to critical neurovascular structures. Although endovascular therapy is preferred, its feasibility is limited in wide-necked, fusiform, or dissecting lesions. We describe our tertiary referral hospital single-center experience with tailored microsurgical and endovascular strategies—emphasizing occipital artery–PICA (OA-PICA) bypass, transcondylar fossa craniotomy, and cerebellomedullary fissure opening—and analyze perioperative factors that influence outcome. Methods: All consecutive patients treated for PICA origin or distal-PICA aneurysms between January 2021 and April 2025 were retrospectively reviewed. Demographics, aneurysm characteristics, procedure type, antithrombotic regimen, complications, diffusion-weighted MRI findings, and 3-month modified Rankin Scale scores were collected. Results: Twelve aneurysms (mean age 61.4 ± 15.2 years; 8 women) were treated: trapping + OA-PICA bypass in 5, direct clipping in 2, flow diverter in 1, endovascular parent artery occlusion in 2, coil embolization in 1, and a hybrid bypass-plus-coil strategy in 1. Two cases were ruptured aneurysms. Perioperative aspirin was used in 2/5 bypass cases; heparin was added in one hybrid case. Asymptomatic PICA-territory infarcts occurred in the three bypasses performed without antiplatelet therapy (one with intra-anastomotic thrombus). No leaks or subcutaneous collections of cerebrospinal fluid were encountered, and no graft occlusions were observed. At 3 months, 9/12 patients achieved a good outcome (mRS 0–2); among them, only one patient with subarachnoid hemorrhage (SAH) experienced postoperative worsening of the mRS. Two cranial nerve palsies (one permanent, one transient) and one wound site hematoma (heparin-associated) resolved without sequelae. Conclusions: Meticulous operative planning allows safe treatment of complex PICA aneurysms. Perioperative aspirin appears beneficial for OA-PICA bypass, whereas perioperative heparin increases bleeding risk. Individualized selection of endovascular, microsurgical, or combined strategies yields favorable early neurological outcomes in this demanding subset of cerebrovascular disease. Full article

(1) Background: Cranial neuropathy is a commonly encountered condition with various underlying etiologies. While carotid artery dissection (CAD) is a well-recognized cause of ischemic stroke, CAD-related cranial neuropathy is rare and poorly characterized. We have conducted a comprehensive review of the published literature to better characterize its clinical course and outcomes. (2) Methods: We systematically reviewed the PubMed, CENTRAL, Ovid MEDLINE, and Embase literature for CAD-related cranial neuropathy. Data extracted included demographics, affected cranial nerves, symptoms, time course, diagnostic approach, and therapeutic interventions. (3) Results: From 635 screened studies, 97 met the inclusion criteria, yielding data on 108 patients with CAD- or dissecting pseudoaneurysm (dPSA)-related cranial neuropathy. The hypoglossal nerve (CN XII) was most commonly affected (76%), and the distal cervical internal carotid artery was the most frequently involved segment (89%). Most patients (90%) were treated with antithrombotic therapy which included either antiplatelets (47%) or anticoagulants (43%). Thirteen patients (12%) underwent endovascular intervention, nearly all with a diagnosed dPSA (mean size, 14.8 mm). Outcomes were favorable, with 94% experiencing symptom improvement. (4) Conclusions: Despite inherent limitations, our study demonstrates that CAD-related cranial neuropathy is typically a benign condition that has excellent outcomes with medical management. Endovascular treatment is rarely performed and is primarily reserved for cases involving diagnosed dPSA. Full article

Contrast-induced encephalopathy (CIE) is a rare complication after percutaneous coronary intervention (PCI) that mimics intracranial hemorrhage (ICH). Its computed tomography (CT) findings (cortical contrast enhancement, sulci effacement) overlap with cerebrovascular conditions (e.g., cerebral infarction, subarachnoid hemorrhage). Dual-energy CT (DECT) differentiates blood/calcification from iodinated contrast medium (CM) extravasation via material decomposition, contributing to the accurate diagnosis of CIE. We report a CIE case highlighting DECT’s value. A 74-year-old woman underwent PCI. 50 min post-PCI, she had moderate headache (Numeric Rating Scale 4), dizziness, non-projectile vomiting (no seizures); vital signs were stable, no focal deficits, mannitol ineffective. Non-contrast CT demonstrated a left parietal 75 Hounsfield unit (HU) high-attenuation lesion, indistinguishable from acute intracerebral hemorrhage. Conventional non-contrast CT revealed a high-attenuation lesion (75 HU) in the left parietal lobe—indistinguishable from ICH. DECT clarified the diagnosis: virtual non-contrast maps showed CM extravasation, iodine concentration maps confirmed focal CM accumulation, and effective atomic number maps improved lesion visualization. The patient’s headache resolved within 5 h; follow-up non-contrast CT at 24 h showed complete disappearance of the lesion. She resumed clopidogrel, discharged day 3 without sequelae. This case underscores DECT’s role in distinguishing CIE (transient CM, normal neuro exam) from ICH (persistent hemorrhage), guiding safe post-PCI antiplatelet therapy. Full article

Atherosclerosis as a multifactorial disease remains the first cause of death worldwide. Current oral lipid-lowering drugs (especially statins) reduce low-density lipoprotein cholesterol (LDLC) levels in the blood, but their clinical efficacy seems to be partially attributed to pleiotropic effects on different pathophysiologic factors of atherosclerosis extending beyond lipid-lowering properties such as anti-inflammatory, antithrombotic and antioxidative features. Novel drugs that interfere with proprotein convertase subtilisin/kexin type 9 (PCSK9) axis of LDL-C receptors (LDLRs) degradation, from the group of monoclonal antibodies (e.g., alirocumab, evolocumab) or small interfering RNA (siRNA), e.g., inclisiran, are effective in reducing LDLC as well. However, data depicting their antithrombotic and antiplatelet activity are scarce, whereas prothrombotic properties of PCSK9 are widely described. Thus, we performed a study to assess the effects of inclisiran on subclinical prothrombotic [fibrinogen, coagulation factor VIII (FVIII), plasminogen activator inhibitor-1 (PAI-1)] and platelet activation markers (platelet factor-4 (PF-4), soluble p-selectin (sCD62P)). Ten patients at high cardiovascular risk with concomitant heterozygous familial hypercholesterolemia (HeFH)—study group 1, and fourteen patients at very high cardiovascular risk without concomitant HeFH—study group 2, were recruited for the study. Lipid profile, subclinical prothrombotic and platelet activation markers were assessed at the beginning and after 3 months of therapy with inclisiran. During therapy, statistically significant reductions in both study groups were seen in total cholesterol levels (study group 1: from 287.6 ± 94.2 to 215.2 ± 89.1 (mg/dL), p = 0.022; study group 2: from 211.7 ± 52.7 to 147.6 ± 55.4 (mg/dL), p < 0.001) and LDL-c (study group 1: from 180.8 ± 73.3 to 114.7 ± 71.5 (mg/dL), p = 0.031; study group 2: from 129.6 ± 46.8 to 63.4 ± 43.6 (mg/dL), p < 0.001). Lipid profile changes were associated with significant decrease in the concentration of FVIII in both groups (study group 1: from 33.3 ± 22 to 22 ± 14.5 (ng/mL), p = 0.006; study group 2: from 37 ±16.9 to 29.3 ±16.4 (ng/mL), p = 0.002) and fibrinogen, but only in study group 2 (from 51.4 (33.2–72.7) to 42.6 (31.3–57.2) (µg/mL), p = 0.035). Among platelet activation markers, a significant decrease in PF-4 in study group 2 was noted (from 286 (272–295.5) to 272 (268–281.5) (ng/mL), p = 0.047). However, there were no statistically significant changes in PAI-1 and sCD62P throughout the study. In our study, inclisiran appeared to be an effective lipid-lowering drug in patients at high cardiovascular risk. Moreover, it was shown that beyond lipid-lowering properties, the drug may also partially affect thrombogenesis and platelet activation. Full article

Platelets carry out their aggregatory and procoagulant roles in two distinct phenotypes. Aggregatory platelets initiate adhesion to the injured endothelium and extend the platelet plug, where procoagulant platelets accelerate thrombin formation and fibrinogen cleaving by exposing a procoagulant-rich outer membrane that facilitates coagulation factor assembly. Conventional anti-platelet therapies inhibit the aggregatory phenotype but fall short on restraining procoagulant platelets. Although procoagulant platelets are crucial for normal hemostasis, a shift toward excess procoagulant platelets is associated with human thrombotic disorders such as ischemic stroke. Although veterinary data is limited, recent studies show that feline and canine platelets display similar procoagulant phenotypes in response to potent agonists, suggesting that procoagulant platelets may play similar roles in the pathogenesis of thromboembolic disorders in veterinary species. Species-specific differences in platelet physiology and molecular structures, however, pose significant challenges. This review aims to (1) summarize cross-species evidence on the mechanisms driving procoagulant platelet formation, their defining features, and characteristics, (2) provide perspectives on procoagulant platelets as thrombotic biomarkers and outline the technical challenges of generating and detecting them in small animal medicine, and (3) summarize potential therapeutic targets and highlight priority research areas to advance the diagnosis and management of thromboembolic diseases in veterinary medicine. Full article

Background: Dual antiplatelet therapy (DAPT) with a potent P2Y12 inhibitor is recommended for patients with acute coronary syndrome (ACS) following percutaneous coronary intervention (PCI). On-treatment platelet reactivity has been associated with ischemic endpoints and may vary between male and female patients. We, therefore, investigated sex-related differences in on-treatment platelet reactivity in ACS patients receiving ticagrelor or prasugrel. Methods: Maximal platelet aggregation by light-transmission aggregometry (LTA) and platelet surface P-selectin expression in response to arachidonic acid (AA), ADP, collagen, TRAP (a protease-activated receptor [PAR-1] agonist), and AYPGKF (a PAR-4 agonist) were assessed in 80 prasugrel- and 77 ticagrelor-treated patients 3 days after PCI. Results: In the overall study population (n = 157), women were older and had lower serum creatinine, hemoglobin, and hematocrit levels than men (all p < 0.05). Women exhibited higher ADP-inducible platelet aggregation in response to both 10 μM and 5 μM of ADP (both p < 0.05), while no sex-related differences were observed for AA-, TRAP-, collagen-, or AYPGKF-inducible platelet aggregation and agonist-inducible platelet surface P-selectin expression. In prasugrel-treated patients, women had higher ADP-inducible platelet aggregation and P-selectin expression compared with men (both p < 0.05), whereas no sex-related differences were found in ticagrelor-treated patients. In the multivariate linear regression analyses, female sex remained an independent predictor of higher platelet aggregation in response to 5 μM of ADP in prasugrel-treated patients (p < 0.05). High on-treatment residual platelet reactivity (HRPR) in response to AA was detected in four patients, and HRPR ADP was seen in seven patients, with no significant differences between female and male ACS patients (both p > 0.05). Low on-treatment residual platelet reactivity (LRPR) in response to AA was identified in 153 patients and LRPR ADP was present in 80 patients, with a higher prevalence of LRPR ADP in men (p = 0.01). Conclusions: Female ACS patients on prasugrel exhibited higher ADP-inducible platelet aggregation than male patients, while no sex-related differences were observed in patients on ticagrelor. Full article

Background: Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most common malignancies associated with thrombotic events. While there is research present on various techniques of portal vein reconstruction, there is limited published data on the techniques and/or considerations of reconstruction in the setting of complete portal vein occlusion. We therefore sought to analyze and present our experience of this clinical scenario. Methods: This was a retrospective analysis of a prospectively collected database. All patients who underwent portal vein resection and/or reconstruction during a pancreatic resection were included. Post-operatively, all patients underwent a contrast-enhanced CT scan on post-operative day 1 to assess for any portal vein thrombus. Results: Pancreatic resection with portal vein reconstruction was performed in 183 patients. Complete PV occlusion was seen in 12 patients at the time of surgery. In those patients with an occluded PV, reconstruction options included primary repair with end-end anastomosis (n = 2) or use of an interposition graft (n = 9). Interposition graft conduits included the left renal vein (n = 6), tubularized bovine pericardium (n = 3), and femoral vein (n = 1). Post-operative portal vein thrombus was seen in 4/12 patients. The majority of patients (n = 7) were discharged on therapeutic anticoagulation, 4 were discharged on an antiplatelet, and 1 patient received neither. Conclusions: Based on our series, we would recommend attempting PV reconstruction in these patients with an interposition graft (with autologous left renal vein or bovine pericardium). We believe that with this technique, the post-operative thrombosis risk is similar to PV reconstructions in non-occluded patients. Full article

Introduction: A direct head-to-head comparison between potent P2Y12 inhibitors: prasugrel versus ticagrelor is still lacking. Purpose: In this single-center study, we sought to address the efficacy and safety of these two third-generation antiplatelet drugs, after about a decade of practical use. Methods: A retrospective observational study included all patients who were admitted with acute coronary syndrome between January 2010 and December 2019 and were discharged with aspirin and either prasugrel or ticagrelor after percutaneous coronary intervention. Patients were divided into two groups based on the dual antiplatelet drugs prescribed. Primary endpoint: A composite endpoint of cardiovascular death, recurrent coronary syndrome, or ischemic stroke at one year. Secondary endpoint: Significant bleeding according to the BARC classification (types 3, 4, or 5). Results: During this period, 746 patients met the inclusion criteria. The primary endpoint was reached in 70 patients (9.4%): 24 patients (8.0%) in the group treated with ticagrelor and 46 patients (10.3%) in the group treated with prasugrel (p-value = 0.303). In terms of safety events, significant bleeding was not statistically different between the ticagrelor and prasugrel groups: 13 (2.9%) vs. 9 (3%), respectively (p-value = 0.9). More patients discontinued their treatment before the end of the year among those treated with ticagrelor compared to those treated with prasugrel (16.7% vs. 9.6%, p-value = 0.003). Conclusions: There was no significant difference in the occurrence of recurrent cardiac events, stroke, or cardiovascular death, nor significant bleeding among ACS patients treated either with prasugrel or ticagrelor. Full article

Background/Objectives: Patients with atrial fibrillation and mitral regurgitation (MR) undergoing transcatheter edge-to-edge mitral valve repair (M-TEER) often have concomitant indications for left atrial appendage occlusion (LAAO), mandating a more personalized treatment approach. This study aimed to examine the effectiveness and safety of combining M-TEER/LAAO in one procedure. Methods: MEDLINE (PubMed), Scopus, and Cochrane were searched through 21 March 2025 for studies examining M-TEER/LAAO with or without control (M-TEER only). Double-independent study selection, extraction, and quality assessments were performed. Frequentist random-effects models were used to calculate mean differences (MDs) and risk ratios (RRs) with 95% confidence intervals (CIs). Results: Seven studies (223 participants) were included. For M-TEER/LAAO, the mean procedural time was 101.6 min (95% CI = [85.06, 118.13]), the mean radiation time was 29.97 min (95% CI = [23.85, 36.09]), the mean length of stay was 5.21 days (95% CI = [3.31, 7.12]), procedural success was achieved in 89.5% of cases (95% CI = [73.4, 96.3], and post-procedure MR > 2+ occurred in 14.8% of cases (95% CI = [3.6, 44.5]). Compared to M-TEER only, patients with M-TEER/LAAO had similar procedural (RR = 0.91, 95% CI = [0.71, 1.17]) and technical success (RR = 1, 95% CI = [0.94, 1.06]) with a similar risk of acute kidney injury (RR = 1, 95% CI = [0.07, 15.12]), bleeding (RR = 0.40, 95% CI = [0.01, 18.06]), and all-cause death (RR = 0.59, 95% CI = [0.22, 1.54]). M-TEER/LAAO was non-significantly associated with in-hospital death (RR = 3, 95% CI = [0.13, 70.23]), stroke (RR = 3, 95% CI = [0.13, 70.23]), and vascular complications (RR = 1.55, 95% CI = [0.43, 5.59]) compared to M-TEER only. Most patients (34.2%, 95% CI = [2.8, 90.4]) received dual antiplatelet therapy at discharge, followed by anticoagulation only (20.2%, 95% CI = [7.5, 44.3]). Conclusions: M-TEER/LAAO can be combined into a single procedure with good peri-procedural outcomes. Safety was also satisfactory; however, some concerns may arise regarding in-hospital death, stroke, and vascular complications. Further research is needed to explore the effectiveness and safety of this combined strategy and elucidate the risk–benefit profile of this personalized treatment approach. Full article

Background: Ischemic stroke (IS), a major cerebrovascular disease, is associated with high disability and mortality rates. Acute kidney injury (AKI) often complicates IS and increases in-hospital mortality. While antiplatelet agents are commonly used for IS treatment, their effectiveness in IS patients with AKI is unclear. Methods: This study, using data from the MIMIC-IV database, divided patients into non-combination (clopidogrel or ticagrelor alone) and combination (with aspirin) groups. The primary outcome was 28-day mortality, with secondary outcomes including 90-day, 1-year, and in-hospital mortality. Multivariable Cox and logistic regression models were used to analyze the relationship between antiplatelet regimens and mortality. Subgroup analyses and interaction tests were conducted. Results: Results showed the combination group had lower 28-day, 90-day, 1-year, and in-hospital mortality risks than the non-combination group (all p < 0.001). Subgroup analysis revealed an interaction effect by AKI stage, with combination therapy not significantly reducing mortality in severe AKI (stages 2 and 3, p = 0.743, p = 0.244). Conclusions: This study demonstrates that combination antiplatelet therapy significantly reduces 28-day, 90-day, 1-year, and in-hospital mortality risks of IS patients with AKI, suggesting its potential benefits in improving both short- and long-term clinical outcomes. However, this does not apply to patients with severe AKI, indicating heterogeneous survival benefits of combination therapy across AKI severity. Clinical decision-making should incorporate AKI stage stratification to evaluate the applicability of combination antiplatelet therapy. Further research is needed to explore the impact of AKI staging on antiplatelet therapy in IS patients. Full article

Background: Patients with no-option chronic limb-threatening ischemia (NoCLTI), lacking suitable distal arteries for conventional revascularization, face major limb amputation. The 1-year mortality rate after major amputation is 48.3%, increasing to 70.9% in 3 years. Open deep venous arterialization (DVA) offers a promising alternative for limb salvage, achievable through open, endovascular, or hybrid approaches. We aim to provide a comprehensive, step-by-step guide to performing open DVA in NoCLTI patients, addressing preoperative and postoperative considerations as well as the technical details of the procedure. Methods: Patient selection for open DVA focuses on individuals with NoCLTI at high risk for amputation. Preoperative assessments include evaluating risk factors, determining limb threat severity using the Wound, Ischemia, and foot Infection (WIfI) score, and mapping anatomical patterns via the Global Limb Anatomic Staging System (GLASS). The procedure involves identifying the target artery using Doppler ultrasound, performing microdissection to expose the artery and vein, ligating proximal vein branches, and creating a side-to-side anastomosis. Venous valves are disrupted with a valvulotome to allow antegrade flow. A proximal bypass graft may be applied if necessary. Results: Postoperatively, patients are monitored for 2–4 days with frequent Doppler assessments. Anticoagulation therapy begins with a heparin drip, transitioning to oral agents and/or dual antiplatelet therapy. Wound care includes deferred debridement for 2–4 weeks and may involve negative-pressure therapy. Follow-up involves weekly visits for the first month, and then at 3 months, and every 6 months thereafter, with surveillance using transcutaneous oxygen measurement, the toe–brachial index, and arterial duplex ultrasound. Conclusions: Open DVA represents a viable limb salvage option for patients with NoCLTI, potentially avoiding major amputations and improving quality of life. Success depends on careful patient selection, a meticulous surgical technique, and comprehensive postoperative care. Full article

Background and Objectives: Percutaneous coronary intervention (PCI) is a proven therapy for acute myocardial infarction (AMI) cardiogenic shock (CS). Dual anti-platelet therapy (i.e., aspirin plus an oral P2Y12 inhibitor) is recommended in patients treated with PCI. However, CS patients present severe hemodynamic instability, deranged hemostatic balance, and the need for invasive mechanical circulatory support (MCS) alongside invasive procedures, resulting in an increased risk of both bleeding and thrombotic complications, leaving uncertainty about the best anti-thrombotic treatment. Recently, the parenteral short-acting P2Y12 inhibitor has been increasingly used in the acute cardiac care setting, mainly in light of its favourable pharmacokinetic profile and organ-independent metabolism. Materials and Methods: In accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, we performed a systematic review and single-arm meta-analysis of the safety and efficacy outcomes (i.e., rates of major bleeding, occurrence of stent/any thrombosis, and hospital survival) of all existing original studies reporting on the intravenous administration of cangrelor in AMI-CS patients. Results: Ten studies (678 patients with CS) published between 2017 and 2023 were included in the present review: nine were observational and one had a randomized design. Percutaneous revascularization was performed in >80% of patients across the studies. Moreover, 26% of patients were treated with temporary MCS, and in all studies, concomitant systemic anticoagulation was performed. Cangrelor was administered intravenously at the dosage of 4 mcg/kg/min in 57% of patients, 0.75 mcg/kg/min in 37% of patients, and <0.75 mcg/kg/min in 6%. The pooled rate of major bleeding was 17% (11–23%, confidence interval [CI]), and the pooled rate of stent thrombosis and any thrombosis were 1% (0.3–2.3% CI) and 3% (0.4–7% CI), respectively. Pooled hospital survival was 66% (59–73% CI). Conclusions: Cangrelor administration in AMI-CS patients was feasible and safe with a low rate of thromboembolic complications. Haemorrhagic complications were more frequent than thrombotic events. Nevertheless, to date, the optimal dosage of cangrelor in this clinical context still remains not universally recognized. Full article

Background: Patients with a HeartMate 3 (HM3) left ventricular assist device (LVAD) typically receive anticoagulation and antiplatelet therapy. The HM3 has shown a marked reduction in hemocompatibility-related adverse events (HRAEs) like stroke, bleeding, and pump thrombosis. This study evaluated whether aspirin (ASA) response influences HRAE incidence and if ASA sensitivity changes over time in HM3 recipients. Methods: This single-center, cross-sectional study included 32 HM3 patients (age: 59.0 ± 10.0 years, 15.6% female). ASA sensitivity was assessed twice using the VerifyNow assay, with ASA resistance defined by ASA reactivity units (ARU) > 550. The primary endpoint was HRAE incidence in ASA responders vs. non-responders over two consecutive follow-ups; the secondary endpoint was temporal changes in ASA resistance. Results: At the first follow-up, 13 (40.6%) patients were ASA-resistant, and 8 (28.6%) were resistant at the second follow-up, without significant change (p = 0.22). ASA non-responders and responders had similar ASA doses and baseline characteristics. No significant difference in HRAE incidence was found between ASA non-responders and responders (0.0% vs. 15.8%, p = 0.14), and no additional HRAEs occurred during follow-up. Conclusions: ASA resistance varied considerably among HM3 patients without significant temporal changes, and the demonstrated excellent hemocompatibility supports recent evidence that ASA may have a limited role in the antithrombotic regimen for HM3 recipients. Full article