Human immunodeficiency virus (HIV) infection is associated with an increased cardiovascular risk through chronic inflammation, immune dysregulation, endothelial dysfunction, and prothrombotic mechanisms. However, the mechanisms underlying acute coronary events in young patients with newly diagnosed advanced HIV infection remain incompletely understood. We report the case of a 36-year-old man with newly diagnosed HIV infection and severe immunosuppression who was initially evaluated for suspected systemic vasculitis and subsequently diagnosed with Pneumocystis jirovecii pneumonia. His initial CD4 cell count was 13.56 cells/mm³, and his HIV RNA level was 14,095,323 copies/mL. Twenty-five days after the initiation of antiretroviral therapy, he developed an acute anterior ST-segment elevation myocardial infarction. Peak high-sensitivity cardiac troponin T was 1051 ng/L. Coronary angiography demonstrated a 90-99% thrombotic lesion at the ostium of the left anterior descending artery with preserved TIMI 3 flow. Given his clinical stability, preserved coronary flow, and potential procedural risks, percutaneous coronary intervention was deferred, and treatment with abciximab, unfractionated heparin, aspirin, and ticagrelor was continued. Repeat angiography after 72 hours demonstrated marked regression of the thrombotic lesion without significant residual stenosis, and no coronary intervention was required. Antiphospholipid antibody testing was negative; however, a comprehensive evaluation for inherited and acquired thrombophilia was not performed. The coexistence of profound immunosuppression, active opportunistic infection, systemic inflammation, and acute coronary thrombosis raises the possibility of a multifactorial prothrombotic state. However, causality cannot be established based on a single case. This case highlights the importance of considering acute coronary thrombosis in young patients with severe HIV-related immunosuppression and active opportunistic infection while recognizing alternative thrombotic mechanisms.

Headache attributed to fasting is a recognized secondary headache in the International Classification of Headache Disorders, 3rd edition (ICHD-3), defined as a diffuse, non-pulsating headache developing during fasting and relieved after eating. It is especially relevant during Ramadan, when large populations undergo predictable daily periods of food and fluid abstinence lasting up to 20 hours. Despite the high number of individuals potentially affected, the evidence on fasting-induced headache during Ramadan remains fragmented and has never been systematically summarized.

Livedoid vasculopathy (LV) is a rare, chronic vascular disorder marked by painful, recurrent ulcerations that primarily affect the lower extremities. It is frequently associated with hypercoagulable states, although its pathophysiology remains incompletely understood. We present the case of a 25-year-old woman with a longstanding history of LV, elevated factor VIII, increased lipoprotein(a), recurrent kidney stones, and iron deficiency anemia who presented with worsening lower-extremity ulcerations. An extensive workup excluded other hypercoagulable and connective-tissue conditions, leaving elevated factor VIII and lipoprotein(a) as the most likely contributors to her disease. Although her symptoms initially resolved with treatment, they recurred over time, and management was further complicated by her desire for future pregnancy, which precluded the use of several standard anticoagulant therapies. Her regimen was ultimately centered on pentoxifylline and low-dose aspirin to control symptoms while minimizing risk to a future pregnancy. This case illustrates the importance of individualized treatment planning in LV, particularly when hypercoagulable risk factors intersect with reproductive goals.

Thromboembolic complications remain among the most serious complications of childhood idiopathic nephrotic syndrome (INS). Although their incidence is considerably lower than in adults, venous thromboembolism continues to cause substantial morbidity and occasional mortality, including pulmonary embolism, cerebral venous sinus thrombosis, and extensive deep venous thrombosis. Preventive management remains controversial because most affected children may not develop thrombosis, whereas pharmacological prophylaxis exposes many low-risk patients to potential overtreatment. Current recommendations are largely based on retrospective studies, expert opinions, and extrapolation from adult nephrotic syndrome, while prospective pediatric evidence remains scarce. This review examines the contemporary understanding of thrombogenesis in childhood INS, emphasizing that hypercoagulability extends beyond urinary antithrombin loss to involve hepatic overproduction of procoagulant factors, impaired fibrinolysis, platelet activation, endothelial dysfunction, and hemoconcentration. We also discuss the possibility that historical thrombotic risk may have been amplified by prolonged corticosteroid exposure and consider whether the widespread adoption of steroid-sparing immunosuppressive therapies and earlier relapse detection may have modified the epidemiology of thromboembolism in the modern therapeutic era. Current preventive strategies-including no routine prophylaxis, biomarker-guided individualized approaches, aspirin, and prophylactic low-molecular-weight heparin (LMWH)-are critically reviewed. We argue that increasingly complex biomarker-based algorithms have not demonstrated clear clinical superiority over simple, pragmatic decision-making. Severe hypoalbuminemia provides a pragmatic surrogate of nephrotic severity and may therefore help identify children in whom the overall prothrombotic state is likely to be substantial. We are not proposing albumin <20 g/L as a validated predictor of thrombosis. We are proposing it as a pragmatic clinical trigger for considering prophylaxis in a disease in which no validated predictive model currently exists. We propose a pragmatic risk-stratified approach in which routine pharmacological prophylaxis is unnecessary for early biochemical relapses with minimal clinical manifestations but should be strongly considered in children and adolescents with clinically significant active nephrotic syndrome associated with severe hypoalbuminemia (approximately <20 g/L), provided no major contraindications exist. Where feasible, LMWH appears to be the most appropriate prophylactic agent. Until prospective pediatric studies better define thrombotic risk and validate prediction models, practical consistency based on clinically meaningful risk thresholds may provide a more rational framework than theoretical precision for thromboprophylaxis in childhood INS.

Summary: Background: Cardiovascular physiology exhibits circadian rhythms, including a morning surge in platelet reactivity and cardiovascular events. Aligning the timing of antiplatelet therapy with these rhythms may be a simple, cost-effective approach to improve clinical efficacy. This systematic review evaluates the diurnal variability in platelet reactivity among individuals receiving aspirin, clopidogrel, ticagrelor, and prasugrel and explores the potential for timed administration to optimise platelet inhibition and other surrogate cardiovascular markers. Patients and methods: PubMed, Embase, Cochrane Central Register of Controlled Trials, and trial registries (e.g., ClinicalTrials.gov) were searched from 1980 to August 2025 for randomised controlled trials and observational studies in adults investigating morning versus evening dosing or diurnal efficacy. Results: Of 2,340 records, 25 studies were included (17 on aspirin, seven on clopidogrel, one on ticagrelor, and three overlapping with prasugrel). For aspirin, the data showed a tendency that evening administration achieved greater reductions in morning Cyclooxygenase-1 (COX-1)-dependent platelet reactivity in healthy volunteers and cardiovascular disease patients, although there were mixed effects on ambulatory blood pressure. Clopidogrel exhibited diurnal variability, with peaks in Adenosine Diphosphate (ADP)-induced aggregation occurring in the morning, while prasugrel provided more consistent inhibition than clopidogrel or ticagrelor. No studies directly compared evening versus morning dosing for P2Y12-Inhibitors, and clinical outcomes such as major adverse cardiac events were only assessed in one included study. Conclusions: While evening aspirin may enhance chronopharmacological efficacy, the available evidence is limited due to heterogeneity and variable quality. The limited number of studies on agents beyond aspirin highlights a critical research gap, with robust Randomised Controlled Trials needed to evaluate clinical benefits and inform chronotherapeutic strategies.