Cardiac regenerative therapies seek to replace damaged tissue following myocardial infarction to prevent heart failure. Human pluripotent stem-cell derived cardiomyocyte (hPSC-CM) injection can be used to remuscularize the heart and improve function but also cause ventricular tachycardia (VT). Electrical mapping studies suggest this VT is focal (i.e., driven by spontaneous excitations), but true mechanisms remain unknown. Computational approaches can provide new insights into these arrhythmias, but current simulation frameworks have not replicated focal VT. In this study, we conducted simulations with biophysically plausible representations of cell injection and the formation of gap junctions between hPSC-CM grafts and host tissue. We examined hPSC-CM ionic models with slow (1.1 Hz) and accelerated (2.5, 4 Hz) beating rates and assessed if these conditions could produce focal VT that is adequately rapid and robust to overpower sinus rhythm. For simulations conducted in human ventricular slice geometries with non-human primate graft patterns, we assessed susceptibility to focal VT. For the slow ionic model, focal VT was seen only at bradycardic heart rates (40 bpm); at faster heart rates (60 or 80 bpm), ectopic activity from the graft could not out-compete Purkinje-like endocardial excitations. In contrast, focal VT was seen for all tested heart rates when faster ionic models were used. Doubling graft size to cover larger infarct areas increased focal VT susceptibility in all cases. Thus, we conclude that post-injection increase in hPSC-CM spontaneous beating rate is a potential mechanism for focal VT, with applications in safer cell injection methods following experimental validation.

Cow's milk is widely considered a fundamental component of early childhood nutrition in India and frequently represents the primary daily beverage for toddlers. However, cow's milk contains minimal bioavailable iron and may inhibit intestinal iron absorption, thereby increasing the risk of iron deficiency. Iron deficiency remains the most prevalent micronutrient deficiency in India and is the leading cause of anemia among young children. Despite national nutrition initiatives, anemia prevalence in this age group continues to be substantial, largely driven by inadequate dietary iron intake, prolonged milk-dominant feeding, suboptimal complementary feeding practices, and socioeconomic determinants. In urban and semi-urban Indian populations, excessive cow's milk consumption has emerged as a clinically relevant yet frequently overlooked contributor to iron deficiency in toddlers. In addition to its low iron content, high intake of cow's milk may impair iron utilization and predispose children to occult gastrointestinal blood loss. We describe five Indian children (age range: 48-84 months) presenting with severe iron deficiency anemia (IDA) associated with high daily intake of cow's milk (≥600 to 1,000 mL) and inadequate consumption of iron-rich complementary foods. All patients presented with marked pallor and lethargy. Three children had poor weight gain, while two demonstrated tachycardia with clinical features suggestive of early cardiac decompensation. Hematologic investigations revealed severe microcytic hypochromic anemia with markedly reduced serum ferritin and elevated total iron-binding capacity. Three children required hospital admission, and one required pediatric intensive care unit management with packed red blood cell transfusion due to hemodynamic instability. Management included blood transfusion when clinically indicated, therapeutic oral iron supplementation, dietary modification, and restriction of cow's milk intake to age-appropriate levels. Follow-up at 8-12 weeks demonstrated substantial hematologic recovery in all cases. This case series highlights the ongoing burden of nutritional IDA among Indian toddlers and underscores the importance of caregiver education, routine dietary assessment during pediatric visits, and counseling on appropriate milk intake to prevent severe anemia and its complications.

Antithyroid drug-induced agranulocytosis is a rare but potentially life-threatening complication, particularly in patients with limited therapeutic options. This case illustrates the complexity of managing uncontrolled thyrotoxicosis in the context of a patient with decompensated heart failure, chronic obstructive pulmonary disease (COPD), and adverse reactions to both methimazole and propylthiouracil. A 54-year-old male patient with a 2-year history of Graves' disease presented with worsening dyspnea and tachycardia in the setting of thyrotoxicosis with a TSH of 0.0007 mIU/L. He had previously developed agranulocytosis (ANC 180 cells/µL) subsequent to treatment with methimazole, and subsequently developed febrile agranulocytosis (ANC 190 cells/µL) upon initiation of propylthiouracil, thereby exhausting all antithyroid drug options. A bridging therapy of Lugol's iodine and granulocyte colony-stimulating factor (G-CSF) was utilized, which enabled successful total thyroidectomy. Right heart catheterization confirmed the patient's suitability for surgery despite a left ventricular ejection fraction of 35%. This case highlights the importance of interdisciplinary collaboration in managing complex endocrine-cardiac-hematology presentations.