Search Results (1,228)

Background/Objectives: Naringin, a major flavonoid found in citrus fruits, has garnered significant attention over the past two decades for its potential cardiovascular benefits. This systematic review evaluates the effects of naringin on endothelial function and myocardial performance, with particular emphasis on ischemia-reperfusion (I/R) injury, based on the literature published from January 2000 to June 2025. Methods: The review was conducted in accordance with PRISMA 2020 guidelines. A comprehensive search of PubMed, Scopus, EMBASE, and Web of Science databases was performed using key terms including “naringin”, “cardiovascular”, “endothelial function”, “atherosclerosis”, and “ischemia-reperfusion.” A total of 62 studies were included and categorized into three domains: cellular models, animal studies, and human trials. Risk of bias assessments were conducted for each study type using appropriate tools. Results: Naringin consistently exhibited antioxidant, anti-inflammatory, and vasoprotective effects across all study types. Mechanistic studies highlighted the modulation of key signaling pathways, including PI3K/Akt, NF-κB, Nrf2, the renin-angiotensin system (RAS), and enhancement of KATP channel expression, as well as its ability to inhibit apoptosis, autophagy, and ferroptosis. In animal models, naringin improved endothelium-dependent vasorelaxation, reduced infarct size, and preserved myocardial function. Although limited, human trials reported beneficial effects on lipid profiles, arterial stiffness, and adiponectin levels. Conclusions: Naringin demonstrates strong potential as a dietary adjunct for cardiovascular protection, especially in the context of ischemic injury and vascular dysfunction. Further well-designed clinical trials are needed to define optimal dosing strategies and improve its bioavailability in humans. Full article

Background: Sepsis-induced myocardial injury (SIMI) significantly contributes to sepsis-related mortality, yet effective therapies remain limited. This study investigated the cardioprotective potential of isopropyl 3-(3,4-dihydroxyphenyl)-2-hydroxypropanoate (IDHP), a bioactive metabolite from Salvia miltiorrhiza, focusing on its mechanism via the GAS6/Axl signaling axis in lipopolysaccharide (LPS)-induced myocardial injury. Methods: Using an in vitro HL-1 cardiomyocyte model, IDHP’s cytotoxicity was assessed (0–20 μM). Cells were pretreated with IDHP (10 μM, optimal concentration) before LPS exposure. Inflammatory cytokines (IL-6/TNF-α/IL-1β/IL-18), chemokines (CCL2/CCR2, CCL25/CCR9), ROS levels (Nrf2 pathway), and apoptosis markers (Bax) were quantified. GAS6/Axl-AMPK signaling was evaluated via GAS6 knockout experiments. Results: IDHP (≤20 μM) showed no cytotoxicity. At 10 μM, it exhibited anti-inflammatory effects by reducing LPS-induced cytokine/chemokine release, demonstrated antioxidant activity through lowering ROS via Nrf2 activation, and exerted anti-apoptotic action by downregulating Bax. Mechanistically, IDHP restored GAS6/Axl-AMPK phosphorylation, an effect abolished in GAS6-knockout cells. Conclusions: IDHP mitigates LPS-induced cardiomyocyte injury by concurrently targeting inflammation, oxidative stress, and apoptosis via GAS6/Axl-AMPK signaling, proposing a novel therapeutic avenue for SIMI. Full article

The growing success of oncologic therapies has led to a significant improvement in patient survival; however, this has been accompanied by an increasing incidence of cardiovascular adverse events, particularly cancer therapy-related cardiac dysfunction (CTRCD). Among these, left ventricular impairment represents a major concern due to its potential to compromise both cardiac and oncologic outcomes. This review provides an in-depth overview of the cardiotoxic adverse events associated with several classes of anticancer agents. Particular focus is given to the molecular mechanisms involved in myocardial injury, such as oxidative stress, mitochondrial dysfunction, calcium dysregulation, endothelial reticulum stress, autophagy, and apoptosis. In parallel, established and emerging cardioprotective strategies, from conventional to newer therapeutic approaches, are explored. The role of advanced imaging modalities, as well as cardiac biomarkers, is discussed in the context of early detection and monitoring of subclinical cardiac injury. Finally, the integration of pharmacogenomics and epigenetics is considered as a promising avenue to personalize risk stratification and preventive therapy. By elucidating the complex interplay between cancer treatments and cardiovascular health, this review underscores the importance of a multidisciplinary, precision medicine approach to optimizing the care of patients undergoing potentially cardiotoxic therapies. Full article

Background: Elevated cardiac troponin (cTn) levels in patients with paroxysmal supraventricular tachycardia (PSVT) often prompt coronary artery disease evaluation, though the clinical relevance of this finding remains unclear. This study aimed to identify risk factors for cTn elevation after a PSVT episode and assess its clinical significance, including the role of coronary artery disease (CAD) and long-term outcomes. Methods: We retrospectively collected data on demographics, presenting symptoms, comorbidities, chronic antiarrhythmic medication use, tachycardia duration, admission systolic blood pressure (SBP), heart rate (HR), laboratory findings, and cardioversion method in patients presenting to the Emergency Department (ED) with PSVT over a 4-year period. Patients were stratified into two groups based on the presence or absence of troponin elevation. Individuals with elevated cTn levels and at least one cardiovascular risk factor were further evaluated for CAD. One-year outcomes included SVT recurrence, rehospitalization, ablation, and mortality. Results: Among 120 patients with PSVT, 58 (48.3%) exhibited elevated cardiac troponin (cTn) levels. Independent predictors of cTn elevation included retrosternal chest pain, absence of prior SVT history, higher admission HR, and lower SBP. A heart rate cut-off of 165 bpm was identified as optimal for predicting cTn elevation (sensitivity 62.1%, specificity 72.6%). Of the 58 cTn (+) patients, 25 underwent CAD evaluation, with only 1 case (4%) confirming significant coronary disease. At one-year follow-up (n = 118), troponin elevation was not associated with increased SVT recurrence, rehospitalization, ablation, or mortality. Similarly, CAD evaluation in troponin-positive patients did not predict outcomes. Conclusions: Troponin elevation after PSVT is frequent but not prognostically significant. It is likely due to transient myocardial stress rather than CAD, supporting a conservative, individualized approach to further testing. Full article

Doxorubicin (Dox) is a potent anthracycline antitumor drug whose clinical utility is significantly restricted by its dose-dependent, cumulative cardiotoxicity, driven by increased oxidative stress, impaired antioxidant defenses, and apoptosis-mediated cardiomyocyte loss. Methylene blue (MB), a phenothiazine derivative with well-documented redox-modulating properties, is being explored as a viable cardioprotective agent due to its antioxidant and anti-apoptotic effects. This study evaluated the protective role of MB against Dox-induced cardiotoxicity in rats by examining its impact on oxidative stress markers (Kelch-like ECH-associated protein 1; KEAP1, nuclear factor erythroid 2-related factor 2; NRF2, Glutathione peroxidase 4; GPX-4, 8-hydroxy-2′-deoxyguanosine; 8-OHdG), neurohormonal indicators (noradrenaline), cardiac injury biomarkers (troponin I), and apoptotic mediators (p53, Caspase-3). Forty male albino rats were divided equally into four groups: control, Dox (15 mg/kg, i.p.), MB alone (4 mg/kg/day, p.o. for 7 days), and Dox plus MB. Dox administration significantly increased serum troponin I and noradrenaline levels, elevated cardiac KEAP1 and 8-OHdG, and reduced NFE2L2, NRF2, and GPX-4 expression. It also upregulated p53 and Caspase-3 and caused marked myocardial degeneration, necrosis, and inflammatory infiltration. MB co-treatment significantly reduced troponin I and noradrenaline levels, restored KEAP1/NFE2L2 (NRF2)/GPX-4 pathway balance, decreased oxidative DNA damage, and attenuated p53 and Caspase-3 activation, preserving myocardial architecture with minimal inflammatory changes. These findings demonstrate that MB confers potent cardioprotection against Dox-induced cardiac injury by enhancing antioxidant defenses, limiting oxidative DNA damage, suppressing apoptosis, and normalizing neurohormonal imbalance, suggesting its promise as an adjunctive strategy to mitigate anthracycline-associated cardiotoxicity. Full article

Background: The coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, has had a profound impact on global health, extending beyond pulmonary complications. Cardiovascular involvement in COVID-19 is multifactorial and may be influenced by viral load, inflammatory response, and pre-existing comorbidities. Discussion: Acute complications include myocardial injury, arrhythmias, acute coronary syndromes (ACS), heart failure, Takotsubo cardiomyopathy, myopericarditis, and cardiac arrest. Notably, atrial fibrillation (AF) emerges as a frequent arrhythmic complication, particularly among critically ill patients, and is associated with increased mortality. COVID-19-patients with concomitant ACS present more severe clinical profiles and higher rates of thrombotic events, including stent thrombosis. Cardiac arrest predominantly presents with non-shockable rhythms and is associated with dismal outcomes. COVID-19 also exacerbates heart failure, both by aggravating existing cardiac dysfunction or by precipitating de novo heart failure. Takotsubo cardiomyopathy and myocarditis, although less frequent, have been reported and are often underdiagnosed due to subtle clinical presentations. Right ventricular dysfunction, linked to pulmonary involvement, has emerged as a key prognostic marker. Post-COVID-19 syndrome include persistent cardiac abnormalities such as reduced ventricular function and myocardial inflammation. Cardiac magnetic resonance imaging and strain echocardiography have proven useful in identifying subclinical cardiac involvement. Conclusions: Early recognition and monitoring of cardiovascular complications are crucial for improving outcomes in patients affected by COVID-19. This review summarizes current evidence regarding cardiovascular manifestations associated with COVID-19. Full article

Sepsis-induced myocardial injury is age-related and leads to increased mortality. Considering the importance of mitochondrial dysfunction in cardiac impairment, we aimed to investigate whether aging exacerbates the cardiac mitochondrial metabolic response to inflammation, thus leading to increased cardiac dysfunction in the elderly. Cecal ligation and puncture (CLP) was conducted in young adult (12–18 weeks) and aged (19–21 months) male C57BL/6 mice. Cardiac function was detected 20 h post-CLP. Additionally, cardiomyocytes isolated from young adult and aged male mice were used for assessments of mitochondrial respiratory function +/– TNFα or LPS. Protein levels of oxidative phosphorylation (OXPHOS), NADPH oxidase (NOX)2, NOX4, phosphor-STAT3 and STAT3 were determined in mouse hearts 24 h post-CLP and in cardiomyocytes following inflammatory stimuli. CLP significantly reduced cardiac contractility in both young and aged mice, with a higher incidence and greater severity of cardiac functional depression in the older group. Mitochondrial respiratory capacity was decreased in cardiomyocytes derived from aged mice, with increased susceptible to inflammatory toxic effects compared to those from young adult mice. The age-dependent changes were observed in myocardial OXPHOS complexes and NOX4. Importantly, CLP led to a significant increase in OXPHOS protein levels in the hearts of older mice, suggesting a possible compensatory response to decreased mitochondrial metabolic function and a greater potential for reactive oxygen species (ROS) generation. Our findings highlight that the response of aging-impaired mitochondria to inflammation may underlie the worsened cardiac functional depression in the aged group during sepsis. Full article

Background/Objectives: Heart failure with preserved ejection fraction (HFpEF) has increased in prevalence as the population ages and associated comorbidities increase. Remote ischemic preconditioning (RIPC) has been shown to provide protection against ischemic injury to the heart and other organs. Therefore, the aim of this project will be to analyse the effectiveness of RIPC in terms of arterial stiffness, endothelial function, diastolic function, and exercise capacity in patients with HFpEF. Methods: The PIRIC-FEp study will be a parallel, randomised controlled trial with two groups conducted at the Faculty of Nursing in Cuenca, University of Castilla-La Mancha. Individuals who are diagnosed with HFpEF and are older than 40 years, with a left ventricular ejection fraction ≥50% and a sedentary lifestyle, will be included. The exclusion criteria will include, among others, patients with noncardiac causes of heart failure symptoms, significant pulmonary disease, diabetes, peripheral vascular disease, or myocardial infarction within the previous three months. A sample size of 48 patients was estimated, with 24 for each group. Participants will be randomly allocated (1:1) to either the RIPC intervention group or the control group to evaluate the effects on arterial stiffness, endothelial function, diastolic function, and exercise capacity. Assessments will be conducted at baseline and after a three-month follow-up period. Results: The findings will be published in a peer-reviewed journal article. Conclusions: This study is important for daily clinical practice because it provides a new approach for the treatment of HFpEF patients via RIPC. Full article

Background and Objectives: Effective myocardial protection is essential for successful cardiac surgery outcomes, especially in complex and prolonged procedures. To this end, Del Nido (DN) and histidine-tryptophan-ketoglutarate (HTK) cardioplegia solutions are widely used; however, their comparative efficacy in adult surgeries with prolonged aortic cross-clamp (ACC) times remains unclear. This study aimed to compare the efficacy and safety of DN and HTK for myocardial protection during prolonged ACC times in adult cardiac surgery and to define clinically relevant thresholds. Materials and Methods: This retrospective study included a total of 320 adult patients who underwent cardiac surgery under cardiopulmonary bypass (CPB) with an aortic cross-clamp time ≥ 90 min. Data were collected from the medical records of elective adult cardiac surgery cases performed at a single center between 2019 and 2025. Patients were categorized into two groups based on the type of cardioplegia received: Del Nido (n = 160) and HTK (n = 160). The groups were compared using 1:1 propensity score matching. Clinical and biochemical outcomes—including troponin I (TnI), CK-MB, lactate levels, incidence of low cardiac output syndrome (LCOS), and need for mechanical circulatory support—were analyzed between the two cardioplegia groups. Subgroup analyses were performed according to ACC duration (90–120, 120–150, 150–180 and >180 min). The predictive threshold of ACC duration for each complication was determined by ROC analysis, followed by the analysis of independent predictors of each endpoint by multivariate logistic regression. Results: Intraoperative cardioplegia volume and transfusion requirements were lower in the DN group (p < 0.05). HTK was associated with lower TnI levels and less intra-aortic balloon pump (IABP) requirement at ACC times exceeding 180 min. Markers of myocardial injury were lower in patients with an ACC duration of 120–150 min in favor of HTK. The propensity for ventricular fibrillation after ACC was significantly lower in the DN group. Significantly lower postoperative sodium levels were observed in the HTK group. Prolonged ACC duration was an independent risk factor for LCOS (odds ratio [OR]: 1.023, p < 0.001), VIS > 15 (OR, 1.015; p < 0.001), IABP requirement (OR: 1.020, p = 0.002), and early mortality (OR: 1.016, p = 0.048). Postoperative ejection fraction (EF), troponin I, and CK-MB levels were associated with the development of LCOS and a VIS > 15. Furthermore, according to ROC analysis, HTK cardioplegia was able to tolerate ACC for up to a longer duration in terms of certain complications, suggesting a higher physiological tolerance to ischemia. Conclusions: ACC duration is a strong predictor of major adverse outcomes in adult cardiac surgeries. Although DN cardioplegia is effective and economically advantageous for shorter procedures, HTK may provide superior myocardial protection in operations with long ACC duration. This study supports the need to individualize cardioplegia choice according to ACC duration. Further prospective studies are needed to establish standard dosing protocols and to optimize cardioplegia selection according to surgical duration and complexity. Full article

Background/Objectives: Acute kidney injury (AKI) is a common and severe complication in patients with acute myocardial infarction (AMI). Very elderly patients are at a heightened risk of developing AKI. Fibrinogen and albumin are well-known biomarkers of inflammation and nutrition, which are highly related to AKI. We aim to explore the predictive value of the fibrinogen-to-albumin ratio (FAR) for AKI in very elderly patients with AMI. Methods: A retrospective cohort of AMI patients ≥ 75 years old hospitalized at the First Affiliated Hospital of Xi’an Jiaotong University between January 2018 and December 2022 was established. Clinical data and medication information were collected through the biospecimen information resource center at the hospital. Univariate and multivariable logistic regression models were used to analyze the association between FAR and the risk of AKI in patients with AMI. FAR was calculated as the ratio of fibrinogen (FIB) to serum albumin (ALB) level (FAR = FIB/ALB). The primary outcome is acute kidney injury, which was diagnosed based on KDIGO 2012 criteria. Results: Among 1236 patients enrolled, 66.8% of them were male, the median age was 80.00 years (77.00–83.00), and acute kidney injury occurred in 18.8% (n = 232) of the cohort. Comparative analysis revealed significant disparities in clinical characteristics between patients with or without AKI. Patients with AKI exhibited a markedly higher prevalence of arrhythmia (51.9% vs. 28.1%, p < 0.001) and lower average systolic blood pressure (115.77 ± 25.96 vs. 122.64 ± 22.65 mmHg, p = 0.013). In addition, after adjusting for age, sex, history of hypertension, left ventricular ejection fraction (LVEF), and other factors, FAR remained an independent risk factor for acute kidney injury (OR = 1.47, 95%CI: 1.36–1.58). ROC analysis shows that FAR predicted stage 2–3 AKI with superior accuracy (AUC 0.94, NPV 98.6%) versus any AKI (AUC 0.79, NPV 93.0%), enabling risk-stratified management. Conclusions: FAR serves as both a high-sensitivity screening tool for any AKI and a high-specificity sentinel for severe AKI, with NPV-driven thresholds guiding resource allocation in the fragile elderly. Full article

Background: Breast and hematological cancer treatments, especially with anthracyclines, have been shown to be associated with an increased risk of cardiotoxicity (CTX). An accurate prediction of cardiotoxicity risk and early detection of myocardial injury may allow for effective cardioprotection to be instituted and tailored to reverse cardiac dysfunction and prevent the discontinuation of essential cancer treatments. Objectives: The PRoactive Evaluation of Function to Evade Cardio Toxicity (PREFECT) study sought to evaluate the ability of fast-strain-encoded (F-SENC) cardiac magnetic resonance imaging (CMR) and 2D echocardiography (2D Echo) to stratify patients at risk of CTX prior to initiating cancer treatment, detect early signs of cardiac dysfunction, including subclinical CTX (sub-CTX) and CTX, and monitor for recovery (REC) during cardioprotective therapy. Methods: Fifty-nine patients with breast cancer or lymphoma were prospectively monitored for CTX with F-SENC CMR and 2D Echo over at least 1 year for evidence of cardiac dysfunction during anthracycline based chemotherapy. F-SENC CMR also monitored myocardial deformation in 37 left ventricular (LV) segments to obtain a MyoHealth risk score based on both longitudinal and circumferential strain. Sub-CTX and CTX were classified based on pre-specified cardiotoxicity definitions. Results: CTX was observed in 9/59 (15%) and sub-CTX in 24/59 (41%) patients undergoing chemotherapy. F-SENC CMR parameters at baseline predicted CTX with a lower LVEF (57 ± 5% vs. 61 ± 5% for all, p = 0.05), as well as a lower MyoHealth (70 ± 9 vs. 79 ± 11 for all, p = 0.004) and a worse global circumferential strain (GCS) (−18 ± 1 vs. −20 ± 1 for all, p < 0.001). Pre-chemotherapy MyoHealth had a higher accuracy in predicting the development of CTX compared to CMR LVEF and 2D Echo LVEF (AUC = 0.85, 0.69, and 0.57, respectively). The 2D Echo parameters on baseline imaging did not stratify CTX risk. F-SENC CMR obtained good or excellent images in 320/322 (99.4%) scans. During cancer treatment, MyoHealth had a high accuracy of detecting sub-CTX or CTX (AUC = 0.950), and the highest log likelihood ratio (indicating a higher probability of detecting CTX) followed by F-SENC GLS and F-SENC GCS. CMR LVEF and CMR LV stroke volume index (LVSVI) also significantly worsened in patients developing CTX during cancer treatment. Conclusions: F-SENC CMR provided a reliable and accurate assessment of myocardial function during anthracycline-based chemotherapy, and demonstrated accurate early detection of CTX. In addition, MyoHealth allows for the robust identification of patients at risk for CTX prior to treatment with higher accuracy than LVEF. Full article

Background/Objectives: Blunt cardiac injury (BCI) is a severe medical condition that may arise as a result of various traumas, including motor vehicle accidents and falls. The main objective of this study was to explore the role and underlying mechanisms of the TRPV4 gene in BCI. Elucidating the function of TRPV4 in BCI may reveal potential novel therapeutic targets for the treatment of this condition. Methods: Rats in each group, including the SD control group (SDCON), the SD blunt-trauma group (SDBT), the TRPV4 gene-knockout control group (KOCON), and the TRPV4 gene-knockout blunt-trauma group (KOBT), were all freely dropped from a fixed height with a weight of 200 g and struck in the left chest with a certain energy, causing BCI. After the experiment, the levels of serum IL-6 and IL-1β were detected to evaluate the inflammatory response. The myocardial tissue structure was observed by HE staining. In addition, cardiac transcriptome analysis was conducted to identify differentially expressed genes, and metabolomics studies were carried out using UHPLC-Q-TOF/MS technology to analyze metabolites. The results of transcriptomics and metabolomics were verified by qRT-PCR and Western blot analysis. Results: Compared with the SDCON group, the levels of serum IL-6 and IL-1β in the SDBT group were significantly increased (p < 0.001), while the levels of serum IL-6 and IL-1β in the KOBT group were significantly decreased (p < 0.001), indicating that the deletion of the TRPV4 gene alleviated the inflammation induced by BCI. HE staining showed that myocardial tissue injury was severe in the SDBT group, while myocardial tissue structure abnormalities were mild in the KOBT group. Transcriptome analysis revealed that there were 1045 upregulated genes and 643 downregulated genes in the KOBT group. These genes were enriched in pathways related to inflammation, apoptosis, and tissue repair, such as p53, apoptosis, AMPK, PPAR, and other signaling pathways. Metabolomics studies have found that TRPV4 regulates nucleotide metabolism, amino-acid metabolism, biotin metabolism, arginine and proline metabolism, pentose phosphate pathway, fructose and mannose metabolism, etc., in myocardial tissue. The combined analysis of metabolic and transcriptional data reveals that tryptophan metabolism and the protein digestion and absorption pathway may be the key mechanisms. The qRT-PCR results corroborated the expression of key genes identified in the transcriptome sequencing, while Western blot analysis validated the protein expression levels of pivotal regulators within the p53 and AMPK signaling pathways. Conclusions: Overall, the deletion of the TRPV4 gene effectively alleviates cardiac injury by reducing inflammation and tissue damage. These findings suggest that TRPV4 may become a new therapeutic target for BCI, providing new insights for future therapeutic strategies. Full article

Background/Objectives: Acute kidney injury (AKI) worsens outcomes in COPD exacerbation (COPDe), yet limited data compare the demographics and mortality risk factors of COPDe admissions with and without AKI. Understanding this association may enhance risk stratification and management strategies. The aim of this study was to identify demographic differences and mortality risk factors in COPDe admissions with and without AKI. Methods: We conducted a retrospective cohort study using the National Inpatient Sample (NIS) from 1 January 2016 to 1 January 2021. Patients aged ≥ 35 years with a history of smoking and a diagnosis of COPDe were included. Patients with CKD stage 5, end-stage kidney disease (ESKD), heart failure decompensation, urinary tract infections, myocardial infarction, alpha-1 antitrypsin deficiency, or active COVID-19 infection were excluded. Baseline demographics were analyzed using descriptive statistics. Multivariate logistic regression analysis was used to measure the odds ratio (OR) of mortality. Statistical analyses were conducted using IBM SPSS Statistics V.30, with statistical significance at p < 0.05. Results: Among 405,845 hospitalized COPDe patients, 13.6% had AKI. These patients were older, had longer hospital stays, and included fewer females and White patients. AKI was associated with significantly higher mortality (OR: 2.417), more frequent acute respiratory failure (OR: 4.559), intubation (OR: 10.262), and vasopressor use (OR: 2.736). CVA, pneumonia, and pulmonary hypertension were significant mortality predictors. Hypertension, CAD, and diabetes were associated with lower mortality. Conclusions: AKI in COPDe admissions is associated with worse outcomes. Protective effects from certain comorbidities may relate to renoprotective medications. Study limitations include coding errors and retrospective design. Full article

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. Full article