Background: Pulsed field ablation (PFA) is a novel non-thermal modality for pulmonary vein isolation (PVI) in atrial fibrillation (AF), offering myocardial selectivity through irreversible electroporation while sparing surrounding structures. However, concerns have emerged regarding potential subclinical hemolysis, reflected by alterations in biochemical markers such as lactate dehydrogenase (LDH). Methods: We conducted a retrospective, single-center study involving 249 patients undergoing PVI: 121 treated with PFA (PulseSelect or FARAPULSE) and 128 with radiofrequency (RF) ablation (PVAC catheter). Laboratory parameters were assessed at baseline, post-procedure, and at discharge, including hemoglobin, hematocrit, red blood cell (RBC) count, platelet count, creatinine, and LDH. The primary endpoint was the variation in blood cell indices; the secondary endpoint was the evaluation of LDH and hematocrit changes. Statistical analysis included t-tests and chi-square tests. Results: Baseline characteristics and pre-procedural labs did not differ significantly between groups. No significant changes in hemoglobin, hematocrit, RBC count, platelet count, or creatinine were observed post-ablation or at discharge. However, LDH levels significantly increased in the PFA group both post-procedurally and at discharge (p < 0.001), without concurrent changes in other blood cell parameters. Conclusions: PFA and RF ablation yield comparable hematological profiles after PVI, with no significant impact on key blood cell parameters. Nonetheless, the consistent rise in LDH levels in the PFA group suggests mild, subclinical hemolysis or tissue injury due to more extensive lesions. While supporting the hematologic safety of PFA, these findings underscore the need for further studies to assess the clinical significance of these biochemical alterations, particularly in high-risk patients or extensive ablation settings.

Background/Objectives: Vulnerable coronary plaques are strongly associated with acute coronary events, posing significant therapeutic challenges despite statin therapy. This case report evaluates the impact of Evolocumab, a PCSK-9 inhibitor, on stabilizing high-risk plaques and promoting phenotypic transformation, assessed through coronary CT angiography (CCTA). Methods: A 50-year-old male with chronic coronary syndrome and a history of myocardial infarction underwent a CCTA, revealing a high-risk plaque (approximately 50%) in the proximal LAD. Despite achieving LDL-C targets with statin therapy, the plaque showed vulnerability features. Evolocumab (140 mg subcutaneously every two weeks) was added to therapy, combined with dietary counseling and dual antiplatelet therapy. Results: A follow-up CCTA at 24 months demonstrated significant reductions in plaque volume and positive remodeling, with a transformation from a mixed phenotype to a predominantly calcified plaque. LDL-C levels decreased from 71 mg/dL to 18 mg/dL. The patient remained asymptomatic, with no cardiovascular events reported during the follow-up. Conclusions: This case highlights the role of PCSK-9 inhibitors in stabilizing high-risk plaques, achieving structural changes that promote stability beyond LDL-C reduction. Advanced imaging techniques such as CCTA proved essential for risk stratification and monitoring therapy efficacy. Evolocumab offers a promising adjunctive treatment for high-risk patients unsuitable for elective revascularization, potentially redefining the standard of care for plaque stabilization in this setting.