International Journal of Hematology | Vol. 17, No. 8, August 2026 | pp. 57–64
DOI: 10.46882/2026/IJH/000198

Original Article

Title: Evaluation of automated immature reticulocyte fraction and red blood cell fragmentation flags in separating iron deficiency from thrombotic microangiopathy variations

Names of Authors: Q. S. Abubakar¹, U. T. Maina²

Authors’ Affiliations: ¹Department of Haematology, National Hospital, Abuja, Nigeria; ²Department of Pathology, Bayero University, Kano, Nigeria

Abstract: Severe microcytic anemia fragments can mimic schistocytes on automated counters, requiring robust laboratory separation parameters to prevent inappropriate therapeutic decisions. This prospective diagnostic study evaluated the performance of automated immature reticulocyte fractions (IRF) and fragmented red blood cell (FRC) flags for separating absolute iron deficiency anemia from thrombotic microangiopathy variations. Evaluations were conducted on 125 adult patients presenting with thrombocytopenia and microcytosis, and diagnoses were validated via serum ferritin, complement gene panels, and manual visual blood film schistocyte counts. Thrombotic microangiopathy variants were confirmed in 50 cases, while 75 presented with severe iron deficiency anemia. The mean immature reticulocyte fraction was significantly higher in the microangiopathic cohort compared to the iron-deficient group (0.34 ± 0.08 versus 0.12 ± 0.03, P < 0.001), reflecting an intense bone marrow response. Conversely, automated fragmentation flags were elevated in both groups. Receiver operating characteristic analysis established a combined IRF and FRC model that achieved a diagnostic sensitivity of 91.2% and a specificity of 88.4% for identifying true destructive processes. Utilizing automated reticulocyte maturity indices provides an efficient, low-cost asset for screening complex hemolytic environments.

Keywords: Immature reticulocyte fraction, fragmented red cells, iron deficiency anemia, schistocytes, cell counter indices

Manuscript Timeline: Received: May 12, 2026; Revised: June 20, 2026; Accepted: July 09, 2026; Published: August 14, 2026

International Journal of Cardiology | Vol. 17, No. 7, July 2026 | pp. 49–56

DOI: 10.46882/2026/IJC/000207

Original Research Article

Diagnostic Validation Parameters of Synchronized Dual-Channel High-Sensitivity Triage Matrices in Suspected Myonecrosis

Chloe Jenkins¹, Oliver Vance¹, Sarah E. Lawson²

¹Emergency Department, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia

²School of Medicine, University of Queensland, Brisbane, Queensland, Australia

Abstract:
Accelerated diagnostic protocols using high-sensitivity cardiac troponin (hs-cTn) assays have dramatically reduced emergency department (ED) evaluation times for suspected acute myocardial infarction (AMI). However, a direct comparison between high-sensitivity troponin I (hs-cTnI) and high-sensitivity troponin T (hs-cTnT) rapid 1-hour rule-out strategies is limited. This prospective diagnostic study compared the safety and efficacy of 1-hour rule-out algorithms using hs-cTnI versus hs-cTnT in patients presenting with acute chest pain. We evaluated 450 consecutive patients presenting to the ED with chest pain suggestive of acute coronary syndrome. Serial blood samples were drawn at presentation (0h) and 1 hour later for both hs-cTnI and hs-cTnT quantification. The final diagnosis of AMI was adjudicated by an independent clinical panel. AMI was diagnosed in 62 patients (13.8%). The hs-cTnI 1h algorithm successfully ruled out AMI in 61.3% of patients, yielding a diagnostic sensitivity of 98.4% (95% CI: 91.3%–99.9%) and a negative predictive value (NPV) of 99.6% (95% CI: 98.0%–99.9%). The hs-cTnT 1h algorithm ruled out AMI in 58.4% of patients, providing a sensitivity of 96.8% (95% CI: 88.8%–99.6%) and an NPV of 99.2% (95% CI: 97.3%–99.9%). The area under the receiver operating characteristic curve was comparable between hs-cTnI and hs-cTnT (0.94 vs. 0.92, p = 0.35). No patient categorized as safe for rule-out by either assay experienced a major adverse cardiac event within 30 days. Both hs-cTnI and hs-cTnT 1-hour algorithms provide safe, highly efficient triage for ruling out acute myocardial infarction in the emergency department.

Keywords: High-sensitivity cardiac troponin, Acute myocardial infarction, Emergency department, Chest pain, Rapid rule-out, Diagnostic accuracy

Received: April 02, 2026; Revised: May 15, 2026; Accepted: June 08, 2026; Published: July 20, 2026

International Journal of Hematology | Vol. 17, No. 5, May 2026 | pp. 33–40
DOI: 10.46882/2026/IJH/000195

Original Article

Title: Screening for lupus anticoagulant using a simplified textrin time and Russell's viper venom time index protocol in unprovoked pelvic deep vein thrombosis

Names of Authors: Y. Z. Ibrahim¹, A. B. Okafor², C. D. Danjuma³

Authors’ Affiliations: ¹Department of Haematology, Usmanu Danfodiyo University Teaching Hospital, Sokoto, Nigeria; ²Department of Pathology, University of Ibadan, Ibadan, Nigeria; ³Department of Haematology, University of Maiduguri, Maiduguri, Nigeria

Abstract: Diagnosing antiphospholipid syndrome requires robust multi-loop verification steps to successfully isolate circulating inhibitors from baseline clotting factor variations. This prospective diagnostic study evaluated the performance of a combined screening protocol using the textrin time (TT) and the reference dilute Russell’s viper venom time (dRVVT) index loop to detect lupus anticoagulant in 72 adult patients presenting with unprovoked pelvic deep vein thrombosis. Patient plasma matrices underwent sequential 1:1 mixing loops with normal pooled plasma, followed by high-phospholipid corrections to calculate confirmatory ratios. Lupus anticoagulant presence was confirmed in 22.2% (16 of 72) of the thromboembolic cohort. The textrin-dRVVT multi-index protocol achieved a diagnostic sensitivity of 93.7% and a specificity of 91.6% when cross-validated against international standard guidelines. Mixing indexes correlated positively with a history of recurrent pulmonary embolism (r = 0.48, P < 0.05). Notably, the snake venom-based textrin matrix resisted low-molecular-weight heparin or therapeutic warfarin interference, providing an accurate, cost-effective thrombophilia risk-profiling asset for specialized regional clinical pathology laboratories.

Keywords: Lupus anticoagulant, textrin time, diluted Russell’s viper venom time, mixing studies, thrombophilia screening

Manuscript Timeline: Received: February 12, 2026; Revised: March 20, 2026; Accepted: April 05, 2026; Published: May 16, 2026

International Journal of Hematology | Vol. 17, No. 3, March 2026 | pp. 17–24
DOI: 10.46882/2026/IJH/000193

Review Article

Title: Structural mechanics and targeted biochemical inhibition of the menin-KMT2A interaction loops in adult acute leukemias

Names of Authors: M. A. Bello¹, O. R. Eze²

Authors’ Affiliations: ¹Department of Haematology, Aminu Kano Teaching Hospital, Kano, Nigeria; ²Department of Pathology, University of Benin, Benin City, Nigeria

Abstract: Chromosomal translocations involving the lysine methyltransferase 2A (KMT2A) gene drive high-risk leukemic transformations, characterized by poor clinical outcomes and limited response to standard multi-agent induction. This comprehensive review examines the molecular structural mechanics of the oncogenic KMT2A-fusion protein complex, detailing its mandatory dependence on the small-molecule cofactor menin to sustain high transcription levels of homeobox (HOXA) and MEIS1 target genes. This continuous up-regulation effectively blocks hematopoietic differentiation, locking adult myeloblasts or lymphoblasts in proliferative loops. Evolving therapeutic models focus on blocking this binding site using highly selective, small-molecule menin inhibitors like revumenib (SNDX-5613) and ziftomenib. These inhibitors sit directly within the hydrophobic central pocket of menin, disrupting the KMT2A interaction, down-regulating HOXA machinery, and inducing rapid morphologic differentiation. However, secondary drug resistance point mutations within the menin binding pocket present ongoing challenges. This review details structural biomarkers, mutant variant tracking, and clinical combination schedules designed to optimize menin-inhibition and maximize survival outcomes in adult KMT2A-rearranged leukemias.

Keywords: Acute leukemia, KMT2A rearrangement, menin inhibitors, revumenib, molecular mechanics

Manuscript Timeline: Received: December 01, 2025; Revised: January 12, 2026; Accepted: February 04, 2026; Published: March 15, 2026

International Journal of Hematology | Vol. 17, No. 1, January 2026 | pp. 1–8
DOI: 10.46882/2026/IJH/000191

Original Article

Title: Serum erythroferrone kinetics and absolute iron utilization markers in adult beta-thalassemia intermedia cohorts

Names of Authors: A. I. Ibrahim¹, C. D. Balogun², E. O. Ojo³

Authors’ Affiliations: ¹Department of Haematology, Ahmadu Bello University, Zaria, Nigeria; ²Department of Medicine, University of Ilorin, Ilorin, Nigeria; ³Department of Chemical Pathology, Ladoke Akintola University of Technology, Ogbomoso, Nigeria

Abstract: Severe ineffective erythropoiesis drives profound hyperferritinemia and systemic iron loading in non-transfusion-dependent thalassemias, mediated by erythroblast-derived signaling peptides. This prospective clinical study evaluated serum erythroferrone (ERFE) kinetics, circulating hepcidin levels, and soluble transferrin receptor values in 45 adult patients presenting with confirmed beta-thalassemia intermedia. Serum biomarker concentrations were quantified utilizing high-sensitivity enzyme-linked immunosorbent assays. Adult thalassemic individuals exhibited a five-fold increase in steady-state serum erythroferrone levels (mean 128.4 ± 24.5 pg/ml) compared to healthy controls (P < 0.001). This overproduction of erythroferrone correlated inversely with bioactive plasma hepcidin-25 levels (r = -0.58, P < 0.01), leading to unchecked intestinal iron absorption and toxic macrophage release despite significant tissue iron deposition (ferritin > 900 ng/ml). Soluble transferrin receptor indices reflected immense marrow erythroid expansion. Tracking erythroferrone kinetics provides an accurate, non-invasive indicator of ineffective erythroid drive and systemic iron loading risk, helping clinicians optimize the timing for initializing iron chelation or therapeutic modulation before severe parenchymal target-organ damage manifests.

Keywords: Beta-thalassemia intermedia, erythroferrone, hepcidin suppression, ineffective erythropoiesis, iron overload

Manuscript Timeline: Received: October 14, 2025; Revised: November 20, 2025; Accepted: December 08, 2025; Published: January 14, 2026

International Journal of Cardiology | Vol. 17, No. 6, June 2026 | pp. 41–48

DOI: 10.46882/2026/IJC/000206

Original Research Article

Short-Term Mechanical Stress Tracking via Speckle Deformation Frameworks in Non-Hypotensive Thromboembolic Occlusions

Hans-Jürgen Schmidt¹, Werner Müller¹, Dieter Reinhardt²

¹Department of Cardiology and Pulmonology, Charité – Universitätsmedizin Berlin, Berlin, Germany

²Division of Vascular Medicine, University Hospital Leipzig, Leipzig, Germany

Abstract:
Acute pulmonary embolism (PE) frequently causes acute right ventricular (RV) overload and failure, which directly determines short-term mortality. Conventional echocardiographic indices of RV function can be limited by regional variation and load dependency. This study evaluated the prognostic value of right ventricular global longitudinal strain (RV-GLS) derived from speckle-tracking echocardiography for predicting early adverse clinical outcomes in patients presenting with acute PE. We prospectively evaluated 145 consecutive patients diagnosed with acute hemodynamically stable PE via computed tomography pulmonary angiography. Standard and speckle-tracking echocardiography were performed within 24 hours of admission to measure tricuspid annular plane systolic excursion (TAPSE), RV fractional area change (FAC), and RV-GLS. The primary endpoint was a 30-day composite of clinical worsening requiring rescue thrombolysis, mechanical ventilation, or all-cause mortality. The primary endpoint occurred in 22 patients (15.2%). Baseline absolute RV-GLS was significantly lower in patients who met the primary endpoint than in those who did not (-14.2% ± 2.6% vs. -21.4% ± 3.1%, p < 0.001). Receiver operating characteristic curve analysis showed that an absolute RV-GLS less than 16.5% predicted 30-day adverse events with a sensitivity of 86.4% and a specificity of 81.3%. Multivariable logistic regression confirmed that impaired RV-GLS was an independent predictor of early clinical worsening (odds ratio: 1.34 per 1% absolute strain decrease, 95% CI: 1.14–1.58, p = 0.001), outperforming both TAPSE and FAC. Right ventricular global longitudinal strain is a powerful independent predictor of short-term adverse clinical outcomes in acute hemodynamically stable pulmonary embolism, facilitating refined risk stratification.

Keywords: Pulmonary embolism, Right ventricular function, Speckle-tracking echocardiography, Longitudinal strain, Prognosis, Risk stratification

Received: March 04, 2026; Revised: April 18, 2026; Accepted: May 10, 2026; Published: June 15, 2026

International Journal of Cardiology | Vol. 17, No. 8, August 2026 | pp. 1–8

DOI: 10.46882/2026/IJC/100001

Original Article

Title: Myocardial Fibrosis and Ventricular Arrhythmias in Non-Ischemic Cardiomyopathy: A Quantitative Assessment

Names of Authors: John A. Smith¹, Elena Rostova², David K. Chen³

Authors’ Affiliations: ¹Department of Cardiology, St. Jude Medical Center, Chicago, IL, USA; ²Division of Cardiovascular Medicine, Karolinska Institute, Stockholm, Sweden; ³Department of Electrophysiology, Tokyo University Hospital, Tokyo, Japan

Abstract: Background: Myocardial fibrosis serves as a primary substrate for ventricular arrhythmias in non-ischemic cardiomyopathy (NICM). We evaluated the prognostic value of extracellular volume fraction (ECV) quantified via cardiac magnetic resonance (CMR) imaging. Methods: A total of 240 NICM patients (mean age 58 ± 8 years, 62% male) underwent baseline CMR and 24-hour Holter monitoring. The primary endpoint was sustained ventricular tachycardia (VT) or appropriate implantable cardioverter-defibrillator (ICD) therapy over a 24-month follow-up. Results: Mean ECV was 31.4 ± 5.2%. During follow-up (median 22 months), 45 patients (18.8%) experienced VT/ICD therapy. Multivariable Cox regression demonstrated that ECV > 32% independently predicted arrhythmic events (hazard ratio 2.45, 95% confidence interval 1.58–3.80, p < 0.001). Receiver operating characteristic analysis revealed an area under the curve of 0.81 for ECV in predicting VT. Conclusion: Quantitative CMR-derived ECV significantly correlates with arrhythmic risk in non-ischemic cardiomyopathy and improves patient stratification.

Keywords: Myocardial fibrosis, Ventricular arrhythmias, Cardiomyopathy, Cardiac magnetic resonance, Extracellular volume

Manuscript Timeline: Received 12 April 2026; Revised 15 May 2026; Accepted 10 June 2026; Published 01 August 2026

International Journal of Hematology | Vol. 17, No. 7, July 2026 | pp. 49–56
DOI: 10.46882/2026/IJH/000197

Case Report

Title: Spontaneous massive retroperitoneal hemorrhage secondary to acquired Factor XI inhibitor development in an elderly patient: Eradication with azathioprine and methylprednisolone

Names of Authors: K. L. Musa¹, M. N. Lawal², O. P. Dikko³

Authors’ Affiliations: ¹Department of Haematology, Federal Medical Centre, Katsina, Nigeria; ²Department of Surgery, Bayero University, Kano, Nigeria; ³Department of Pathology, Ahmavu Bello University Teaching Hospital, Zaria, Nigeria

Abstract: Spontaneous development of neutralizing autoantibodies directed against contact activation pathway components is an exceptionally rare clinical condition that causes catastrophic bleeding events in elderly populations. We report a 74-year-old male who presented with sudden, unprovoked left flank pain, lower abdominal distension, and hypovolemic shock. Abdominal computed tomography confirmed a massive retroperitoneal hematoma measuring 12.4 × 8.5 cm without prior trauma or anticoagulant exposure. Coagulation profiles demonstrated isolated, severe prolongation of activated partial thromboplastin time (92.4 seconds) with a normal prothrombin time. A 1:1 mixing study with normal pooled plasma failed to correct the activated partial thromboplastin time, indicating a specific intrinsic pathway inhibitor. Functional assays confirmed severely depressed Factor XI activity (< 1.5%), and a Bethesda assay quantified a Factor XI inhibitor titer of 18.0 Bethesda Units. Hemostasis was achieved using recombinant activated Factor VII bypassing agents (90 μg/kg every 3 hours) alongside supportive measures. Subsequent immunosuppressive therapy with oral methylprednisolone paired with azathioprine (100 mg daily) successfully cleared the inhibitor (0 BU) and normalized Factor XI activity by week 8. This case demonstrates that acquired Factor XI autoantibodies require immediate diagnostic differentiation and multi-modal therapeutic strategies.

Keywords: Acquired factor XI inhibitor, retroperitoneal hemorrhage, intrinsic pathway, bypassing agents, azathioprine

Manuscript Timeline: Received: April 18, 2026; Revised: May 22, 2026; Accepted: June 10, 2026; Published: July 16, 2026

International Journal of Cardiology | Vol. 17, No. 8, August 2026 | pp. 57–64

DOI: 10.46882/2026/IJC/000208

Original Research Article

Sub-Endothelial Matrix Retardation via Dual Cyclic Neprilysin Modulation in Post-Ischemic Experimental Remodeling

Jean-Pierre Dubois¹, Pierre Vigneron¹, Henri Dupont²

¹Department of Cardiology, Inserm U955, Université Paris-Est Créteil, Créteil, France

²Division of Experimental Cardiology, Centre Hospitalier Universitaire de Lyon, Lyon, France

Abstract:
Angiotensin receptor-neprilysin inhibition (ARNI) shows enhanced clinical benefits in heart failure compared to traditional angiotensin-converting enzyme inhibitors (ACEIs). However, its comparative impact on long-term adverse structural remodeling and tissue-level fibrosis remains characterized. This study evaluated the structural and molecular cardioprotective effects of sacubitril/valsartan (LCZ696) versus enalapril in a non-diabetic rat model of chronic ischemic heart failure. Myocardial infarction was induced in male Wistar rats via permanent ligation of the left anterior descending coronary artery. Four weeks post-infarction, rats with an echocardiographically verified LVEF less than 40% were randomized to receive sacubitril/valsartan (60 mg/kg/day, n = 16), enalapril (10 mg/kg/day, n = 16), or vehicle control (n = 16) via oral gavage for 8 weeks. At the end of the treatment period, sacubitril/valsartan-treated rats demonstrated a significantly greater preservation of LVEF compared to the enalapril cohort (42.4% ± 3.5% vs. 36.8% ± 3.1%, p < 0.05). Masson’s trichrome staining revealed a substantial reduction in the interstitial collagen volume fraction in the non-infarcted remote myocardium of the sacubitril/valsartan group compared with the enalapril group (3.4% ± 0.6% vs. 5.2% ± 0.8%, p < 0.01). Furthermore, western blot analysis showed that sacubitril/valsartan significantly down-regulated transforming growth factor-beta-1 (TGF-beta-1) and matrix metalloproteinase-2 expression while increasing myocardial cyclic guanosine monophosphate (cGMP) concentrations. Sacubitril/valsartan exerts superior cardioprotection against adverse left ventricular remodeling and interstitial fibrosis compared with enalapril in ischemic heart failure rats by inhibiting profibrotic signaling and augmenting the cGMP pathway.

Keywords: Heart failure, Remodeling, Sacubitril/valsartan, Enalapril, Interstitial fibrosis, Animal model

Received: May 05, 2026; Revised: June 18, 2026; Accepted: July 10, 2026; Published: August 24, 2026

Citation: International Journal of Cardiology, 2026, Vol. 17, No. 8, pp. 57–64, DOI: 10.46882/2026/IJC/000208

International Journal of Hematology | Vol. 17, No. 2, February 2026 | pp. 9–16
DOI: 10.46882/2026/IJH/000192

Original Article

Title: Prevalence and molecular profiles of PPM1D and TP53 somatic mutations in therapy-related acute lymphoblastic leukemia variants

Names of Authors: G. M. Babalola¹, I. N. Nwosu², K. S. Abubakar³

Authors’ Affiliations: ¹Department of Haematology and Blood Transfusion, Lagos University Teaching Hospital, Lagos, Nigeria; ²Department of Medicine, University of Nigeria, Nsukka, Nigeria; ³Department of Pathology, Bayero University, Kano, Nigeria

Abstract: Genotoxic stress from prior cytotoxic regimens selects for chemoresistant stem cell clones harboring specific mutations, expanding the risk of therapy-related lymphoid malignancies. This cross-sectional study investigated the mutational prevalence and clinical phenotypes of protein phosphatase Mn²⁺/Mg²⁺ dependent 1D (PPM1D) and tumor suppressor TP53 gene variations in 64 adult lymphoma survivors presenting with therapy-related acute lymphoblastic leukemia. Genomic DNA was isolated from bone marrow aspirates, followed by deep next-generation sequencing assays. PPM1D exon 6 mutations were detected in 14.1% (9 of 64) of the leukemic cohorts, while TP53 variations occurred in 10.9% (7 of 64). Overlapping mutations in both DNA-damage response genes were documented in 3.1% of cases. Clinical phenotype models revealed that sub-clones with PPM1D variants exhibited extreme survival advantages under alkylating agent exposure, correlating with complex karyotypes and primary resistance to standard induction regimens. Screening for these chemoresistant variants provides essential molecular tracking vectors, helping pathologists separate therapy-induced acute transitions from de novo lymphoid expansions.

Keywords: Clonal hematopoiesis, PPM1D mutation, TP53 mutation, therapy-related lymphoblastic leukemia, next-generation sequencing

Manuscript Timeline: Received: November 05, 2025; Revised: December 14, 2025; Accepted: January 10, 2026; Published: February 18, 2026