Objectives. The aim of this study is to assess the prevalence and predictive factors for developing chronic access-site (A-S) pain after percutaneous coronary intervention (PCI) via radial artery access. Methods. Data of selected patients (n = 161) who underwent elective PCI were collected prospectively and analysed in 2020. Verbal analogue scale was used to evaluate pain intensity after 12, 24, and 48 h and 3 months after PCI. The univariate logistic regression analysis was used. Results. Pain prevalence decreased from 29% straight after PCI and 54% two hours later to 3.7% following 3 months after procedure. The predictors for A-S pain chronicity are diabetes (OR = 5.77 95% CI (1.07-31.08), p=0.041), hematoma (OR = 6.48, 95% CI (1.06-39.66), p=0.043), A-S hand neuropathy (OR = 19.93 95% CI (1.27-312.32), p=0.033), A-S pain immediately after PCI (OR = 14.60 95% CI (1.63-130.27), p=0.016), after 12 h (OR = 17.2 95% CI (1.60-185.27), p=0.019), 24 h (OR = 48 95% CI (4.87-487), p=0.01), and 48 h (OR = 23.46 95% CI (3.81-144.17), p=0.001), and pain intensity immediately after procedure (OR = 3.30 95% CI (1.65-6.60), p=0.001), after 2 h (OR = 2.56 95% CI (1.15-5.73), p=0.022), after 12 h (OR = 3.02 95% CI (1.70-5.39), p<0.001), after 24 h (OR = 3.58 95% CI (1.90-6.74), p<0.001), and after 48 h (OR = 2.89 95% CI (1.72-4.87), p<0.001). Pain control was performed with Ketoprofen and Ibuprofen as most used NSAIDs. 10 mg of Morphine intravenously was the choice from strong opioids if necessary. Conclusions. The prevalence of chronic A-S pain is 3.7%. Main predictive factors for the A-S pain chronicity are diabetes, hematoma, and persistent pain and pain intensity during 48 h period after PCI.

Context. Approximately 1 in 20 patients undergoing the percutaneous cardiac intervention (PCI) experience severe procedure-related access-site (A-S) pain. The multimodal pain management model (MPM) can reduce the intensity and prevalence of pain and this approach was not investigated in the postprocedural pain management area. To address this, a randomized controlled trial was conducted in Hospital of Lithuanian University of Health Sciences Kauno klinikos in 2018. Methods. 137 patients who underwent PCI procedure via radial artery were randomly assigned (1 : 1) to the control (CG, n = 68) and intervention (IG, n = 65) groups. IG received MPM (paracetamol, ibuprofen, and the arm physiotherapy), CG received pain medication “as needed.” Outcomes were assessed immediately after, 2, 12, 24, and 48 h, 1 week, and 1 and 3 months after PCI. The primary outcome was A-S pain prevalence and pain intensity numeric rating scale (NRS) 0–10. Results. Results showed that A-S pain prevalence during the 3-month follow-up period was decreasing. Statistically significant difference between the groups (CG versus IG) was after 24 h (41.2% versus 18.5, $p=0.005$ ), 48 h (30.9% versus 1.5%, $p\le 0.001$ ), 1 week (25% versus 10.8%, $p=0.042$ ), 1 month (23.5% versus 7.7%, $p=0.017$ ) after the procedure. The mean of the highest pain intensity was after 2 h (IG-2.17 ± 2.07; CG-3.53 ± 2.69) and the lowest 3 months (IG-0.02 ± 0.12; CG-0.09 ± 0.45) after the procedure. A-S pain intensity mean scores were statistically significantly higher in CG during the follow-up period (Wilks’ λ = 0.84 F (7,125) = 3.37, $p=0.002$ ). Conclusion. In conclusion, MPM approach can reduce A-S pain prevalence and pain intensity after PCI. More randomized control studies are needed.

Hypercholesterolemia, characterized by elevated levels of low-density lipoprotein cholesterol (LDL-C), along with inflammation, is a well-known risk factor for developing atherosclerosis and coronary artery disease (CAD). Many patients with hypercholesterolemia may carry inherited genetic variants that are not part of the commonly recognized mutations in the LDLR, APOB, LDLRAP1, and PCSK9 genes. These genetic variants may have cumulative effects that contribute to increased LDL-C levels and CAD development. The polygenic risk score (PRS) may provide an essential tool for evaluating an individual’s genetic predisposition to these conditions. This pilot study aimed to investigate the impact of the PRS calculated from specific single nucleotide polymorphisms (SNPs) associated with LDL cholesterol (LDL-C)—namely, CELSR2 rs629301, APOB rs1367117, ABCG8 rs6544713, LDLR rs6511720, APOE rs429358, and rs7412—on LDL-C levels in both healthy individuals with elevated LDL-C levels (>2.6 mmol/L) and those diagnosed with ST-segment elevation myocardial infarction (STEMI). A total of 61 healthy individuals with high LDL-C levels (>2.6 mmol/L) and 93 STEMI patients were selected for the study. The High-Resolution Melting Polymerase Chain Reaction (HRM PCR) method was adopted and sequencing techniques were employed to identify the specific single nucleotide polymorphisms (SNPs) of interest. The patient group exhibited a PRS of 0.824 (with a range of −0.62 to 1.174) compared to 0.674 (range: −0.176 to 0.974) in healthy individuals, indicating a higher genetic predisposition to elevated LDL-C levels (p = 0.001) in patients. Interestingly, patients had lower LDL-C concentrations than healthy individuals. Additionally, a more significant number of patients were past smokers and statin users. The PRS calculations revealed that patients with a higher PRS had increased odds of experiencing an MI, with an odds ratio of 12.044 (95% confidence interval: 1.551–93.517, p = 0.017). Similarly, smokers showed even higher odds, with an odds ratio of 24.962 (95% CI: 7.171–86.890, p < 0.001). Among healthy individuals, those with a higher PRS had increased odds of having an LDL-C concentration greater than 4.9 mmol/L (odds ratio: 20.391, 95% CI: 1.116–358.486, p = 0.039). However, no significant association was found between the PRS and LDL-C levels in the patient group during hospitalization (p = 0.782). This pilot study shows that PRS can be employed to evaluate the risk of MI and to estimate concentrations greater than 4.9 mmol/L LDL-C in healthy individuals.

Background: A rare but serious complication of heart valve replacement, prosthetic valve thrombosis carries significant risks of morbidity and mortality. Effective management depends on prompt diagnosis and the appropriate treatment, often involving fibrinolytic agents. Protocols using slower infusion rates and lower doses of these agents have led to improved therapy outcomes.Clinical case: We report a case of a 56-year-old man admitted to the Lithuanian University of Health Sciences Kaunas Clinics due to mechanical mitral valve prosthesis thrombosis complicated by a respiratory failure and atrial fibrillation. The patient was treated with ultraslow thrombolysis with alteplase. The function of the mechanical valve prosthesis became normal, and the patient was discharged from the hospital.Discussion and Conclusions: Managing prosthetic valve thrombosis is challenging due to overlapping clinical features with other diagnoses and the lack of consensus on the treatment methods. Slow-infusion, low-dose thrombolytic therapy with alteplase can be a life-saving intervention with a high success rate.

The formation of extracellular traps (ETs) through ETosis has emerged as a key mechanism in immunothrombosis. However, the temporal dynamics and clinical significance of ETosis in coronary thrombi of ST-elevation myocardial infarction (STEMI) patients remain incompletely understood. We investigated whether ETosis burden increases with thrombus age and is associated with DNASE1 and TREX1 genetic variants as well as impaired myocardial reperfusion. Thrombus aspirates from 81 STEMI patients undergoing primary percutaneous coronary intervention were histologically classified as fresh (n = 41) or lytic (n = 40). ETosis was quantified by citrullinated histone H3 (CitH3) immunohistochemistry and digital image analysis, complemented by multiplex staining for myeloperoxidase (MPO), CD68, caspase 3, and CD61. Plasma ET-related markers and genotyping of DNASE1 (rs1053874) and TREX1 (rs11797) were also performed. CitH3-positive cells were present in all thrombi but were more abundant in lytic (older) thrombi compared with fresh thrombi (1348 vs. 591 cells/mm², p < 0.001). Increased ETosis was associated with neutrophil and macrophage infiltration, apoptosis, prolonged ischemia time, elevated systemic inflammation (neutrophil–lymphocyte ratio and C-reactive protein), and impaired myocardial reperfusion (lower TIMI flow grades). Moreover, the DNASE1 GG genotype was associated with higher densities of MPO- and CD68-positive cells, whereas the TREX1 CC genotype was associated with increased densities of CitH3-, MPO-, and CD68-positive cells. This study demonstrates that ETosis increases with coronary thrombus maturation and is associated with local inflammation and impaired reperfusion in STEMI. Genetic variants in DNASE1 and TREX1 may modulate inflammatory cell accumulation within thrombi. These findings suggest ETosis as a potential therapeutic target, particularly in patients with delayed presentation.