Immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment and are increasingly associated with cardiovascular toxicities, including myocarditis and accelerated atherosclerosis. While ICI myocarditis has received substantial attention, thrombotic complications remain underrecognized and may be difficult to distinguish from immune-mediated cardiac inflammation and cancer-related hypercoagulable state. We present a case of non-bacterial thrombotic endocarditis (NBTE) and myocardial microthrombi mimicking ICI myocarditis.

Cardiac masses identified on echocardiography can pose significant diagnostic challenges, particularly when differentiating between thrombi and vegetations, which require markedly different management approaches. We present the case of a 57-year-old postmenopausal woman with a history of thymic cancer and recent pulmonary embolism (PE), who presented with abdominal pain, weight loss, and laboratory findings consistent with disseminated intravascular coagulation (DIC). Abdominal ultrasound and magnetic resonance imaging (MRI) revealed a large fibroid uterus with multiple masses concerning for leiomyosarcoma or leiomyoma, and transthoracic echocardiography (TTE) showed a large echo density on the tricuspid valve and a bicuspid aortic valve with mild-to-moderate stenosis. Further evaluation with transesophageal echocardiography (TEE) confirmed a large mass on the tricuspid valve and also revealed multiple echo densities on the mitral and aortic valves. Cardiac MRI (CMR) demonstrated thickened, mobile tricuspid valve leaflets with moderate regurgitation; mild-to-moderate mitral regurgitation was also seen, along with thickening of the mitral valve leaflets. However, the nature of the masses remained unclear. Despite negative blood cultures, the clinical and imaging findings raised suspicion for non-bacterial thrombotic endocarditis (NBTE), though thrombi remained a differential consideration. Given the patient's hypercoagulable state, a multidisciplinary team initiated anticoagulation and arranged close outpatient follow-up. A cervical lymph node biopsy subsequently confirmed metastatic, poorly differentiated carcinoma with immunohistochemistry positive for CKAE1/AE3, HMWCK, and PAX8, suggesting either recurrent thymic malignancy or a primary uterine origin. A few months later, repeat TTE showed reduced severity of mitral and tricuspid regurgitation, and the valvular masses were less apparent. The patient is currently undergoing palliative chemotherapy with carboplatin, paclitaxel, and dostarlimab, continues on lifelong anticoagulation, and receives comprehensive pain management. This case underscores the diagnostic complexity of cardiac masses, particularly in patients with malignancy. It highlights the critical role that multimodality imaging plays in resolving complex diagnostic dilemmas and emphasizes the importance of a collaborative approach in managing such patients.

Thrombosis is a significant complication of childhood acute lymphoblastic leukemia (ALL) associated with both the disease itself and its treatment. This study aimed to predict the thrombotic process with TGA performed at diagnosis and during induction therapy in pediatric ALL cases, to assess the contribution of hereditary risk factors, ALL, and treatment to thrombophilia, and to compare the thrombosis tendency according to ALL risk group. The study included 24 ALL patients and 23 healthy children. TGA was performed before the start of induction chemotherapy (ALL BFM-2009 protocol) and on days 8, 15, and 33 of treatment for ALL patients and once for healthy controls. TGA was conducted using a Thrombinoscope (Calibrated Automated Thrombogram; Maastricht, Netherlands) device and kits from the same company. We found the frequency of thrombosis to be 12.5% in children with ALL. Although the number of thrombosis was small (n = 3), the association of peak thrombin and ETP with thrombosis was encouraging: patients who developed thrombosis had higher mean ETP and peak thrombin values on days 8 and 15 of induction therapy compared to patients without thrombosis, with TGA profiles more comparable to those of the healthy control group. Patients' lag time and time to peak thrombin on days 8, 15, and 33 of induction therapy were significantly longer, in addition peak thrombin and ETP values were significantly lower compared to the control group. The results of this study indicate that changes in hemostatic balance did not cause an increase in the thrombin generation potential, and thrombin generation remained low compared to the healthy control group. Although these findings seem to contradict those of studies showing thrombophilia in ALL patients, our study does not support hypercoagulability alone. Considering the absence of signs of hypercoagulability, thrombophilia in these patients may be secondary to endothelial damage caused by the disease and cytotoxic therapy. Comprehensive studies are needed to elucidate the etiology of thrombosis in ALL.

Aging is recognized as a highly complex process mediated by multiple mechanisms. It affects all body systems, including the cardiovascular system. The severity of age-related changes in the body is often associated with the severity of vascular aging. It remains crucial to analyze current data on vascular aging, tracing the available cause-and-effect relationships of molecular and genetic interactions that are significant for vascular aging. Various studies have confirmed the contribution of various processes and substances to aging, forming a reliable foundation for further gerontological research. Vascular aging is largely associated with the progressive deterioration of endothelial cell function in the vascular intima, leading to impaired production of biologically active substances, causing thrombophilia and increased vascular tone. Endothelial cell aging is largely due to changes in their DNA structure, including telomere shortening and an increase in gene mutations. A comprehensive study of these processes could help us better understand the mechanisms that initiate vascular aging. Furthermore, it is clear that a detailed study of the fundamental intracellular mechanisms underlying vascular aging could help us understand approaches to reducing the incidence of cardiovascular disease with age.

Thrombin generation assay (TGA) is a tool to assess bleeding and thrombotic risk in citrated plasma, either in the presence or absence of platelets, and several different commercial assays have been developed and actively marketed. TGA can be used for various research and clinical applications, including the identification of patients at risk of bleeding or thrombosis, as well as monitoring of treatment in at risk patients. Though current implementation is limited to specialized laboratories in university hospitals and research centers, wider implementation will require additional, large clinical trials.

Thrombophilia testing is a critical aspect of managing venous thromboembolism, a condition affecting approximately 1 in 1000 individuals annually and causing significant morbidity, mortality, and health care costs. This document provides an in-depth overview of current best practices in thrombophilia testing, including clinical guidelines, assay methodologies, and advances in molecular diagnostics, with the aim of optimizing diagnosis, treatment, and prevention strategies.

Portal vein thrombosis (PVT) is a rare but serious complication of hypercoagulable states or conditions that increase portal pressure, such as liver cirrhosis, inherited or acquired coagulation cascade abnormalities, myeloproliferative disorders, malignancy, inflammation, or infection. COVID-19 has been associated with a prothrombotic state, leading to both arterial and venous thromboses. Here, we present a patient with minimal hypercoagulable risk factors who presented with PVT and acute-on-chronic cholecystitis with bacteremia, likely provoked by residual hypercoagulability from a "long COVID-19" syndrome. An 81-year-old male developed PVT as a complication of acute-on-chronic cholecystitis, with contributing factors potentially including hypercoagulability related to prior COVID-19 infection more than 4 months prior. PVT should remain a diagnostic consideration in patients with various hypercoagulable risk factors, including long COVID-19, who present with relevant clinical findings. There should be a low threshold for the pursuit of further diagnostic imaging, given the serious consequences of delayed diagnosis.

Over the last few decades, the increase in medically assisted reproduction has led to a significant increase in the frequency of twin and higher-order multiple pregnancies (defined as triplets or more). A critical element of this trend is the increased risk of preterm birth and infant mortality in twin and higher-order pregnancies. Fetal reduction (FR) was initially established as an option to reduce these adverse outcomes. Indications for FR have now expanded, with literature indicating clear improvement of outcomes after reduction to twins or singletons from triplet pregnancies, although physiological adaptations during pregnancy following FR have not been thoroughly investigated. One clinically relevant research gap is the effect of FR on coagulation and fibrinolysis, given that pregnancy is associated with a hypercoagulable state. In this novel case study, our objective was to characterize the hemostatic impact of FR. We employed a functional assay, thromboelastography (TEG), to compare the maternal hemostatic function in a triplet pregnancy that was sequentially reduced to a singleton pregnancy with uncomplicated singleton pregnancies. Patient 611 became pregnant during her fourth cycle of intrauterine insemination, and a dating ultrasound confirmed a trichorionic triamniotic triplet pregnancy. After counseling, the patient chose to undergo fetal reduction to a singleton pregnancy. Both reductions were achieved via the injection of potassium chloride. TEG was performed on blood samples taken during pregnancy, and patient 611 was compared with patients with singleton pregnancies who had also undergone ovulation induction at similar gestational ages. We observed an overall decrease in coagulability across all TEG parameters from prepregnancy to term in patient 611 compared with that in control singleton pregnancies. These data suggest that fetal reduction may limit the pregnancy-associated hypercoagulable states.