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Journal of Clinical Medicine Research May 2024Acute myocardial infarction (AMI) in young patients is an important issue because of its impact on health and social life. The mechanisms and disease courses of...
Acute myocardial infarction (AMI) in young patients is an important issue because of its impact on health and social life. The mechanisms and disease courses of ST-elevation myocardial infarction (STEMI) in young individuals may differ from those in the elderly. Behcet disease (BD) is a multisystem autoimmune disorder of unknown etiology. Cardiac involvement is rare, yet it was reported to affect 6% of patients, with 17% of the cases presenting as the first manifestation. We present the case of a 33-year-old male heavy smoker with negative medical history, who presented with acute inferior myocardial infarction. His coronary angiography showed huge thrombosis in proximal right coronary artery. He was treated with primary coronary intervention and implantation of drug-eluting stent, with subsequent intervention and implantation of two more drug-eluting stents due to acute stent thrombosis within 48 h. Rheumatologic assessment revealed the history of four different attacks of oral ulcers and one attack of genital ulcer. His workup showed positive human leukocyte antigen (HLA) allele (B51) which is strongly associated with BD. AMI in young adults due to arterial thrombosis can be attributed to hypercoagulable state related to early manifestation of BD. Increased knowledge of AMI in young adults and its presentation in BD is necessary to reduce morbidity and mortality. Corticosteroids and colchicine may improve cardiac manifestations in BD.
PubMed: 38855780
DOI: 10.14740/jocmr5132 -
Theranostics 2024Myocardial infarction (MI) as a consequence of atherosclerosis-associated acute thrombosis is a leading cause of death and disability globally. Antiplatelet and...
Platelet-targeted thromboprophylaxis with a human serum albumin fusion drug: Preventing thrombosis and reducing cardiac ischemia/reperfusion injurywithout bleeding complications.
Myocardial infarction (MI) as a consequence of atherosclerosis-associated acute thrombosis is a leading cause of death and disability globally. Antiplatelet and anticoagulant drugs are standard therapies in preventing and treating MI. However, all clinically used drugs are associated with bleeding complications, which ultimately limits their use in patients with a high risk of bleeding. We have developed a new recombinant drug, targ-HSA-TAP, that combines targeting and specific inhibition of activated platelets as well as anticoagulation. This drug is designed and tested for a prolonged circulating half-life, enabling unique thromboprophylaxis without bleeding complications. Targ-HSA-TAP combines a single-chain antibody (scFv) that targets activated glycoprotein IIb/IIIa on activated platelets, human serum albumin (HSA) for prolonged circulation, and tick anticoagulant peptide (TAP) for coagulation FX inhibition. A non-binding scFv is employed as a non-targeting control (non-targ-HSA-TAP). Its efficacy was investigated using murine models of acute thrombosis and cardiac ischemia-reperfusion (I/R) injury. Our experiments confirmed the targeting specificity of targ-HSA-TAP to activated platelets and demonstrated effective prevention of platelet aggregation and thrombus formation, as well as FXa inhibition . Thromboprophylactic administration of targ-HSA-TAP subcutaneously in mice prevented occlusion of the carotid artery after ferric chloride injury as compared to non-targ-HSA-TAP and PBS-control treated mice. By comparing the therapeutic outcomes between targ-TAP and targ-HSA-TAP, we demonstrate the significant improvements brought by the HSA fusion in extending the drug's half-life and enhancing its therapeutic window for up to 16 h post-administration. Importantly, tail bleeding time was not prolonged with targ-HSA-TAP in contrast to the clinically used anticoagulant enoxaparin. Furthermore, in a murine model of cardiac I/R injury, mice administered targ-HSA-TAP 10 h before injury demonstrated preserved cardiac function, with significantly higher ejection fraction and fractional shortening, as compared to the non-targ-HSA-TAP and PBS control groups. Advanced strain analysis revealed reduced myocardial deformation and histology confirmed a reduced infarct size in targ-HSA-TAP treated mice compared to control groups. The inclusion of HSA represents a significant advancement in the design of targeted therapeutic agents for thromboprophylaxis. Our activated platelet-targeted targ-HSA-TAP is a highly effective antithrombotic drug with both anticoagulant and antiplatelet effects while retaining normal hemostasis. The long half-life of targ-HSA-TAP provides the unique opportunity to use this antithrombotic drug for more effective, long-lasting and safer anti-thrombotic prophylaxis. In cases where MI occurs, this prophylactic strategy reduces thrombus burden and effectively reduces cardiac I/R injury.
Topics: Animals; Serum Albumin, Human; Mice; Thrombosis; Humans; Hemorrhage; Blood Platelets; Disease Models, Animal; Male; Anticoagulants; Single-Chain Antibodies; Myocardial Reperfusion Injury; Myocardial Infarction; Mice, Inbred C57BL; Recombinant Fusion Proteins
PubMed: 38855181
DOI: 10.7150/thno.97517 -
The Journal of International Medical... Jun 2024Coexistence of pulmonary embolism (PE) and arterial thrombosis in a single patient is rare. Management of such cases is challenging because there is no unified standard...
Coexistence of pulmonary embolism (PE) and arterial thrombosis in a single patient is rare. Management of such cases is challenging because there is no unified standard on how to treat this type of disease. We herein report a case involving a 73-year-old man who was admitted to the hospital because of a 2-day history of chest tightness. Pulmonary computed tomography angiography revealed a filling defect of the main pulmonary artery and bilateral branches as well as a left subclavian artery embolism. AngioJet mechanical thrombectomy (Boston Scientific, Marlborough, MA, USA) was used to treat the PE, and this was combined with left brachial artery incision and thrombectomy for treatment of the left subclavian artery embolism. The patient recovered well after the operation. The prognosis was good after 9 months of regular follow-up. AngioJet mechanical thrombectomy combined with left brachial artery incision thrombectomy may be a feasible treatment option for cases of PE combined with left subclavian artery embolism.
Topics: Humans; Male; Aged; Pulmonary Embolism; Thrombectomy; Subclavian Artery; Computed Tomography Angiography; Treatment Outcome; Embolism
PubMed: 38853428
DOI: 10.1177/03000605241258141 -
International Journal of Surgery Case... Jul 2024Tibial exostosis (osteochondroma) represents a prevalent benign bone tumor typically identified in young adults. Uncommonly, vascular complications can emerge,...
INTRODUCTION AND IMPORTANCE
Tibial exostosis (osteochondroma) represents a prevalent benign bone tumor typically identified in young adults. Uncommonly, vascular complications can emerge, encompassing vessel perforation, thrombosis and arterial thromboembolic events. Rare instances of popliteal vein thrombosis resulting from tibial osteochondroma have been documented.
CASE PRESENTATION
We report a rare case of a 25-year-old patient who presented with a red and swollen leg, and the diagnosis of deep venous thrombosis (DVT) of the left popliteal vein was established. The patient also exhibited a painless, hard swelling in the popliteal fossa. Radiography revealed an exostosis on the posterior aspect of the proximal tibia. An angioscan demonstrated close relations with the popliteal vessels, leading to venous compression. The patient underwent resection through a posterior knee approach. Histopathological analysis of the exostosis ruled out malignant transformation.
CLINICAL DISCUSSION
The discussion emphasizes the need for prompt diagnostic measures when signs indicate a vascular concern in a young patient, initiating with a radiograph followed by Doppler ultrasound and/or angiography to diagnose complications and precisely delineate their relationships with the tumor. Surgical intervention is underscored as urgent, particularly in cases involving arterial thrombosis, where immediate measures such as thrombectomy or bypass with a venous graft may be necessary.
CONCLUSION
Vascular complications associated with bone exostoses are rare but require prompt surgical treatment. However, it should prompt the performance of an angioscan in the presence of any abnormalities during clinical examination or an appearance raising concerns about potential vascular conflict.
PubMed: 38851065
DOI: 10.1016/j.ijscr.2024.109839 -
Auris, Nasus, Larynx Jun 2024Idiopathic sudden sensorineural hearing loss (ISSNHL) is characterized by abruptly appearing hearing loss, sometimes accompanied by vertigo. Vascular pathologies (e.g.,... (Review)
Review
Idiopathic sudden sensorineural hearing loss (ISSNHL) is characterized by abruptly appearing hearing loss, sometimes accompanied by vertigo. Vascular pathologies (e.g., cochlear ischemia, or cochlear infarction) are one of the most likely causes of ISSNHL. This review aims to present current understanding of inner ear anatomy, clinical features of ISSNHL, and its treatment strategies. The labyrinthine artery is the only end artery supplying blood to the inner ear, and it has three branches: the anterior vestibular artery, the main cochlear artery, and the vestibulo-cochlear artery (VCA). Occlusion of the VCA can be caused by a variety of factors. The VCA courses through a narrow bone canal. ISSNHL is usually diagnosed after excluding retrocochlear pathologies of sudden sensorineural hearing loss (SSNHL), such as vestibular schwannoma. Therefore, a head MRI or assessing auditory brainstem responses are recommended for patients with SSNHL. Severe SSNHL patients with high CHADS scores, an index of stroke risk, have a significantly lower rate of vestibular schwannoma than severe SSNHL patients with low CHADS scores, suggesting that severe ISSNHL in individuals at high risk of stroke is caused by vascular impairments. Intralabyrinthine hemorrhage causes SSNHL or vertigo, as in ISSNHL. The diagnosis of intralabyrinthine hemorrhage requires careful interpretation of MRI, and a small percentage of patients diagnosed with ISSNHL may in fact have intralabyrinthine hemorrhage. Many studies have reported an association between ISSNHL and atherosclerosis or cardiovascular risk factors (e.g., diabetes mellitus, hypertension, dyslipidemia and cardiovascular disease), and subsequent risk of stroke in patients with ISSNHL may be elevated compared to controls. Increased hearing level on the healthy ear side, high Framingham risk score, high neutrophil-to-lymphocyte ratio, high platelet-to-lymphocyte ratio, and severe white matter lesions may be poor prognostic factors for patients with ISSNHL. The association between thrombosis-related genes and susceptibility to ISSNHL has been reported in many studies (e.g., coagulation factor 2, coagulation factor 5, plasminogen activator inhibitor-1, platelet-associated genes, a homocysteine metabolism-related enzyme gene, endothelin-1, nitric oxide 3, phosphodiesterase 4D, complement factor H, and protein kinase C-eta). Treatment of ISSNHL with the aim of mitigating the vascular impairment in the inner ear includes systemically administered steroids, intratympanic steroid injections, hyperbaric oxygen therapy, prostaglandin E1, defibrinogenation therapy, and hydrogen inhalation therapy, but there is currently no evidence-based treatment for ISSNHL. Breakthroughs in the unequivocal diagnosis and treatment of ISSNHL due to vascular impairment are crucial to improve quality of life.
PubMed: 38850720
DOI: 10.1016/j.anl.2024.05.009 -
Biomedicine & Pharmacotherapy =... Jul 2024Intracranial atherosclerotic stenosis (ICAS) is a pathological condition characterized by progressive narrowing or complete blockage of intracranial blood vessels caused... (Review)
Review
Intracranial atherosclerotic stenosis (ICAS) is a pathological condition characterized by progressive narrowing or complete blockage of intracranial blood vessels caused by plaque formation. This condition leads to reduced blood flow to the brain, resulting in cerebral ischemia and hypoxia. Ischemic stroke (IS) resulting from ICAS poses a significant global public health challenge, especially among East Asian populations. However, the underlying causes of the notable variations in prevalence among diverse populations, as well as the most effective strategies for preventing and treating the rupture and blockage of intracranial plaques, remain incompletely comprehended. Rupture of plaques, bleeding, and thrombosis serve as precipitating factors in the pathogenesis of luminal obstruction in intracranial arteries. Pericytes play a crucial role in the structure and function of blood vessels and face significant challenges in regulating the Vasa Vasorum (VV)and preventing intraplaque hemorrhage (IPH). This review aims to explore innovative therapeutic strategies that target the pathophysiological mechanisms of vulnerable plaques by modulating pericyte biological function. It also discusses the potential applications of pericytes in central nervous system (CNS) diseases and their prospects as a therapeutic intervention in the field of biological tissue engineering regeneration.
Topics: Pericytes; Humans; Animals; Intracranial Arteriosclerosis; Vasa Vasorum; Cerebral Arteries
PubMed: 38850658
DOI: 10.1016/j.biopha.2024.116870 -
Ugeskrift For Laeger May 2024Individuals with antiphospholipid syndrome (APS) have antibodies directed against phospholipid-binding proteins (aPL). The condition is most associated with an increased... (Review)
Review
Individuals with antiphospholipid syndrome (APS) have antibodies directed against phospholipid-binding proteins (aPL). The condition is most associated with an increased risk of thromboembolism and obstetric complications. The 2023 classification criteria for APS include six clinical domains (venous thromboembolism, arterial thrombosis, microvascular events, obstetric events, cardiac valve, thrombocytopaenia) and two laboratory domains (lupus anticoagulant, and anti-cardiolipin or anti-β2-glycoprotein-I antibodies). Diagnosis and treatment of APS are specialist tasks and are summarised in this review.
Topics: Antiphospholipid Syndrome; Humans; Antibodies, Antiphospholipid; Pregnancy; Female; Anticoagulants; Thrombosis
PubMed: 38847311
DOI: 10.61409/V11230715 -
Indian Journal of Pathology &... Jun 2024Cortical necrosis of the renal allograft is an extremely rare but serious complication of renal transplantation and can lead to graft failure. Few cases have been...
Cortical necrosis of the renal allograft is an extremely rare but serious complication of renal transplantation and can lead to graft failure. Few cases have been reported in the literature to date. We present a rare case of a 28-year-old woman with chronic kidney disease for the past four years who was on biweekly hemodialysis and referred to our tertiary care center for a living-related renal transplant. The patient developed tacrolimus toxicity on the second day post-transplant. The renal biopsy performed on third day after transplant showed ischemic acute tubular injury. C4d and donor-specific antibodies were negative. On day 12 post-transplant, USG Doppler of the renal allograft showed thrombosis of the renal vein, and an open wedge biopsy was performed that showed extensive renal cortical necrosis. A month and half later, the patient developed pus collection anterior to the transplanted kidney and a fistula from the perinephric space up to the skin with persistent pus discharge. Two months later, a graft nephrectomy was performed, and diffuse cortical necrosis of renal allograft with a thick band of exudate on the capsule was diagnosed on histopathology. Ureteral necrosis and thrombosis of both renal artery and renal vein were also seen. In this case, the etiology of graft cortical necrosis is multifactorial and includes acute ischemia, urologic complications, and sepsis. To prevent graft failures, it is critical to differentiate thrombosis caused by surgical complications from hyperacute or acute humoral rejection.
PubMed: 38847210
DOI: 10.4103/ijpm.ijpm_662_23 -
European Journal of Case Reports in... 2024Anomalous bronchial artery origins may have clinical implications beyond their anatomical curiosity. In this case, identification of such an anomaly led to the diagnosis...
UNLABELLED
Anomalous bronchial artery origins may have clinical implications beyond their anatomical curiosity. In this case, identification of such an anomaly led to the diagnosis of chronic thromboembolic pulmonary hypertension (CTEPH). A 49-year-old male with a history of recurrent deep vein thrombosis (DVT) and pulmonary embolism (PE) on anticoagulation presented with chest pain and shortness of breath. Laboratory analysis was remarkable for a troponin peak of 14.74 ng/ml, a brain natriuretic peptide level of 602 pg/ml and a D-dimer level of 0.62 μg/ml. Electrocardiogram showed non-specific ST elevation in the anterolateral and inferior leads. Computed tomography angiography (CTA) of the chest was positive for PE involving the right lower lobe pulmonary arterial tree. Echocardiogram showed reduced left ventricular function (ejection fraction 38%) and akinesis of the antero-apical and infero-apical segments. Cardiac catheterization revealed non-obstructive coronary arteries, and an anomalous origin of a right bronchial artery from the right coronary artery. The right bronchial hypertrophied as it supplied collateral flow to the occluded right pulmonary artery. This anomaly and the patient's history of multiple DVT/PEs while on therapeutic levels of warfarin with near normal D-dimer levels raised suspicion for a false positive PE. Pulmonary angiogram revealed chronic occlusion in branches of the right pulmonary artery, mean pulmonary artery pressure of 36 mmHg and no acute thrombus. Ventilation-perfusion scan confirmed the diagnosis of CTEPH. The patient underwent successful pulmonary thromboendarterectomy and subsequently had normalization of mean pulmonary artery pressure. This case underscores the importance of a comprehensive diagnostic approach, and consideration of alternative explanations for imaging findings, that unveiled the diagnosis of a complex and life-threatening condition such as CTEPH.
LEARNING POINTS
This case underscores the diagnostic significance of identifying anomalous bronchial artery origin which played a crucial role in the diagnosis of the underlying chronic thromboembolic pulmonary hypertension (CTEPH).It is important to understand the limitations of computed tomography angiography (CTA) chest for diagnosis of CTEPH.
PubMed: 38846648
DOI: 10.12890/2024_004616 -
CJC Open May 2024Ongoing debate remains regarding optimal antithrombotic therapy in patients with atrial fibrillation (AF) and coronary artery disease. (Review)
Review
BACKGROUND
Ongoing debate remains regarding optimal antithrombotic therapy in patients with atrial fibrillation (AF) and coronary artery disease.
METHODS
We performed a systematic review and meta-analysis to synthesize randomized controlled trials (RCTs) comparing the following: (i) dual-pathway therapy (DPT; oral anticoagulant [OAC] plus antiplatelet) vs triple therapy (OAC and dual-antiplatelet therapy) after percutaneous coronary intervention (PCI) or acute coronary syndrome (ACS), and (iii) OAC monotherapy vs DPT at least 1 year after PCI or ACS. Following a 2-stage process, we identified systematic reviews published between 2019 and 2022 on these 2 clinical questions, and we updated the most comprehensive search for additional RCTs published up to October 2022. Outcomes of interest were major adverse cardiovascular events (MACE), death, stent thrombosis, and major bleeding. We estimated risk ratios (RRs) and 95% confidence intervals (CIs) using a random-effects model.
RESULTS
Based on 6 RCTs (n = 10,435), DPT reduced major bleeding (RR 0.62, 95% CI 0.52-0.73) and increased stent thrombosis (RR 1.55, 95% CI 1.02-2.36), vs triple therapy after PCI or medically-managed ACS, with no significant differences in MACE and death. In 2 RCTs (n = 2905), OAC monotherapy reduced major bleeding (RR 0.66, 95% CI 0.49-0.91) vs DPT in AF patients with remote PCI or ACS, with no significant differences in MACE or death.
CONCLUSIONS
In patients with AF and coronary artery disease, using less-aggressive antithrombotic treatment (DPT after PCI or ACS, and OAC alone after remote PCI or ACS) reduced major bleeding, with an increase in stent thrombosis with recent PCI. These results support a minimalist yet personalized antithrombotic strategy for these patients.
PubMed: 38846448
DOI: 10.1016/j.cjco.2024.01.001