Browse
Submit Data
Databases
API
Help

Dataset Information

29 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Native coronary artery thrombosis in the setting of heparin-induced thrombocytopenia: a case report.

ABSTRACT:

Background

Heparin-induced thrombocytopenia (HIT) is a rare complication of heparin therapy. Its pathogenesis includes thrombotic events that can rarely affect the coronary arteries.

Case summary

We report a 67-year-old woman who presented with extensive lower extremities deep venous thrombosis. After being treated with heparin, she developed an ST-elevation myocardial infarction secondary to an acute thrombus formation. The patient's platelets dropped within 6?days from the procedure and her heparin-PF4 IgG antibody and serotonin release assay were positive confirming the diagnosis of HIT.

Discussion

Prothrombotic states, such as HIT, are associated with increased risk for coronary thrombosis and ischaemia. Heparin-induced thrombocytopenia can cause coronary complications usually in previously disrupted coronary vessels and bypass grafts. Here, we demonstrate that spontaneous thrombosis can occur in a previously untreated native coronary artery in a patient with HIT.

SUBMITTER: Almeqdadi M

PROVIDER: S-EPMC6426051 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

"Spontaneous" Heparin-Induced Thrombocytopenia and Thrombosis After Total Knee Arthroplasty: A Report of 2 Cases.

Project description:"Spontaneous" heparin-induced thrombocytopenia is a rare and virulent form of heparin-induced thrombocytopenia that occurs in the absence of exposure to any drug of the heparin class of anticoagulants. Most reported cases have occurred after knee replacement surgery. Herein we report 2 additional cases following total knee replacement. Clinical suspicion and immediate initiation of appropriate nonheparin anticoagulation are essential to avoid potentially devastating thrombotic complications.

| S-EPMC8121995 | biostudies-literature

Heparin 'flush' induced thrombocytopenia triggered by total hip replacement: a case report.

Project description:Background:Heparin-induced thrombocytopenia (HIT) typically responds to heparin termination. Some types of HIT can persist after heparin discontinuation. Case summary:A 95-year-old woman was referred to the cardiology from orthopaedics because of acute limb ischaemia (ALI) 1?day after surgery of a femoral neck fracture. Despite thrombectomy, ALI relapsed the next day. She had been treated with intravenous antibiotics with a diagnosis of aspiration pneumonia for 1?week until 3?days before surgery, together with heparin flush twice a day. Of note, no intra-/post-operative heparin was administered, no cell salvage device, central venous, nor arterial catheters were used before development of ALI. The patient and her family refused reattempting invasive therapies; consequently, the patient continued to worsen and died on post-operative day 3. Diagnosis of autoimmune HIT, which was prompted by surgery without re-exposure to heparin, was confirmed posthumously. Discussion:This case emphasizes the significance of suspecting autoimmune HIT in any patient presenting with thrombosis, even if the heparin exposure dates back more than a few days or even without heparin exposure.

| S-EPMC7180709 | biostudies-literature

Arterial and Venous Thrombosis From Delayed-Onset Heparin-Induced Thrombocytopenia.

Project description:Heparin Induced Thrombocytopenia (HIT) is a life threatening condition which is caused due to antibody formation following exposure to heparin or heparin products. It occurs due to the formation of Platelet Factor 4 antibodies (PF4). HIT is classified into 3 categories based on the duration between heparin exposure and onset of drop in platelet counts. A less common form of HIT is delayed onset HIT which occurs more than 9 days after exposure to heparin or heparin products. In this report we would like to present a rare case of delayed onset HIT which occurred in our patient who presented with rhabdomyolysis and Non ST elevation myocardial infraction (NSTEMI); which resulted in limb ischemia which needed to be treated by amputation of the affected area. We also highlight further management of patients who have thrombotic disease in the setting of HIT and review literature of how heparin or heparin products can be reintroduced in such patient who cannot be managed by other anticoagulation.

| S-EPMC9533806 | biostudies-literature

Subacute right coronary artery thrombosis treated by using Excimer Laser Coronary Angioplasty: a case report.

Project description:BackgroundManaging high thrombotic burden in the context of myocardial infarction remains a challenging scenario.Case summaryA 51-year-old male was admitted for a subacute inferior myocardial infarction with persistent chest pain. Emergent coronary angiography showed an ostial-proximal thrombotic occlusion of a large ectatic right coronary artery. Several balloon inflations were performed that were not able to improve distal TIMI flow beyond II. With the intent of vaporizing the remaining thrombus, Excimer Laser Coronary Angioplasty was performed with a favourable outcome.DiscussionThe present case constitutes an opportunity to revisit percutaneous and non-percutaneous strategies to tackle persistent coronary thrombus showing a contemporary approach to niche technologies such as laser angioplasty.

| S-EPMC10587994 | biostudies-literature

Setting things "right": right internal mammary artery on anomalous right coronary artery - a case report.

Project description:Anomalous aortic origin of a coronary artery (AAOCA) is a rare pathology that may cause episodic ischemia owing to possible vessel compression during systolic expansion of the aortic root. This anomaly can lead to myocardial infarction, malignant arrhythmias and sudden cardiac death (SCD). Several surgical techniques have been described; however, there are no defined guidelines regarding the treatment of AAOCA. We report the case of a 47-year-old woman with ectopic origin of the right coronary artery (RCA) from the left sinus of Valsalva, with an interarterial course of the proximal segment of the artery, running between the aorta and the pulmonary trunk. Revascularization was accomplished by harvesting the right internal mammary artery (RIMA) and anastomosing it to the anomalous RCA, given the small portion of the RCA following an intramural course and our familiarity with the procedure. The RCA was ligated proximal to the anastomosis to avoid the string sign phenomenon. This procedure is safe and fast and can be considered an alternative to coronary reconstruction.

| S-EPMC8573513 | biostudies-literature

Accelerated heparin-induced thrombocytopenia in a COVID-19 patient; a case report with literature review.

Project description:IntroductionHeparin-induced thrombocytopenia (HIT) is a rare and serious immune-mediated complication of heparin therapy which is seldom reported in association with COVID-19. This report aims to present a case of accelerated HIT in a severe COVID-19 patient.Case reportA 63-year-old man presents with symptoms of COVID-19 for one week. He was conscious, ordinated, feverish, and had diffused chest crackles. Initial laboratory tests revealed elevated C-reactive protein of 87.66 mg/dL, elevated D-dimmer of 1258.9 ng/ml, elevated ferritin of 1020 ng/ml, and his platelet count was within the normal range. Polymerase chain reaction (PCR) confirmed the diagnosis of COVID-19. On the 9th day of admission, he developed a progressive worsening of dyspnea. His D-dimmer level significantly increased to 7020 ng/ml, and his interleukin-6 was 27.3 pg/ml. Hence, we started him on unfractionated heparin (UFH) for thromboprophylaxis. On the 12th day of hospitalization, the platelet count dropped from 258000 to 111000 cells/μL. He had a high probability of HIT (4Ts score = 6). As a result, we discontinued UFH and switched him to apixaban. His platelet count normalized (174000 cells/μL) within two weeks of ceasing UHF.DiscussionHIT results from the production of antibodies against platelet factor 4/heparin complexes. It is associated with a diminished platelet count within 5-10 days post heparin initiation. Because thrombocytopenia can occur in COVID-19 patients, HIT is seldom suspected.ConclusionHIT should be considered a differential diagnosis in COVID-19 patients with thrombocytopenia.

| S-EPMC9090824 | biostudies-literature

Inhibition of NADPH oxidase blocks NETosis and reduces thrombosis in heparin-induced thrombocytopenia.

Project description:Heparin-induced thrombocytopenia (HIT) is associated with severe and potentially lethal thrombotic complications. NETosis was recently shown to be an important driver of thrombosis in HIT. We investigated the role of reactive oxygen species (ROS) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) and their contributions to thrombus development in HIT. We showed that neutrophil activation by HIT immune complexes induced ROS-dependent NETosis. Analysis of thrombi formed in a microfluidics system showed ROS production in both platelets and neutrophils, and abundant neutrophil extracellular traps (NETs) and ROS distributed throughout the clot. Neutrophil-targeted ROS inhibition was sufficient to block HIT-induced NETosis and thrombosis using human blood. Inhibition of NOX2 with diphenyleneiodonium chloride or GSK2795039 abrogated HIT-induced thrombi in vivo using FcγRIIa+/hPF4+-transgenic mice. Thrombocytopenia in mice remained unaffected by ROS inhibition. Increased ROS production in activated neutrophils was also confirmed using fresh blood from patients with active HIT. Our findings show that ROS and NOX2 play a crucial role in NETosis and thrombosis in HIT. This enhances our understanding of the processes driving thrombosis in HIT and identifies NOX2 as a potential new therapeutic target for antithrombotic treatment of HIT.

| S-EPMC9153028 | biostudies-literature

Neutrophil activation and NETosis are the major drivers of thrombosis in heparin-induced thrombocytopenia.

Project description:Heparin-induced thrombocytopenia/thrombosis (HIT) is a serious immune reaction to heparins, characterized by thrombocytopenia and often severe thrombosis with high morbidity and mortality. HIT is mediated by IgG antibodies against heparin/platelet factor 4 antigenic complexes. These complexes are thought to activate platelets leading to thrombocytopenia and thrombosis. Here we show that HIT immune complexes induce NETosis via interaction with FcγRIIa on neutrophils and through neutrophil-platelet association. HIT immune complexes induce formation of thrombi containing neutrophils, extracellular DNA, citrullinated histone H3 and platelets in a microfluidics system and in vivo, while neutrophil depletion abolishes thrombus formation. Absence of PAD4 or PAD4 inhibition with GSK484 abrogates thrombus formation but not thrombocytopenia, suggesting they are induced by separate mechanisms. NETs markers and neutrophils undergoing NETosis are present in HIT patients. Our findings demonstrating the involvement of NETosis in thrombosis will modify the current concept of HIT pathogenesis and may lead to new therapeutic strategies.

| S-EPMC6428879 | biostudies-literature

Coronary subclavian steal syndrome due to thrombosis of the left subclavian artery aneurysm: a case report

Project description:Abstract Background Coronary subclavian steal syndrome (CSSS) is an often easily overlooked cause of angina that may occur after a coronary artery bypass graft (CABG) procedure. The onset of CSSS several years after coronary revascularization has been described in case reports, and in the few retrospective reviews that compare the endovascular approach with surgical treatment. Subclavian stenosis can naturally coincide with coronary artery disease and may already be present during the initial CABG. Case summary A 59-year-old male with a history of three-vessel disease who had a left internal mammary artery (LIMA) bypass graft, exhibited a gradual worsening of angina that coincided with numbness and impaired function of the left fingers, hand, and arm. Myocardial perfusion imaging showed reversible ischaemia, and coronary angiography suggested a thrombotic lesion proximal to the LIMA ostium. Calcified and partially thrombosed proximal left subclavian artery (LSA) aneurysm was visualized using computed tomography imaging, whereas Doppler ultrasound revealed a partially reversed vertebral flow. The lowest risk treatment was a bypass between the left common carotid artery and the LSA. The procedure was immediately successful, with cessation of symptoms and a favourable medium-term outcome. Discussion As no guidelines exist for such cases, the importance of multidisciplinary co-operation in diagnostics and devising a treatment plan is underlined. Moreover, screening for subclavian artery stenosis in CABG candidates should be warranted as part of the initial preoperative assessment.

| S-EPMC9883703 | biostudies-literature

Arterial intracranial thrombosis as the first manifestation of vaccine-induced immune thrombotic thrombocytopenia (VITT): a case report.

Project description:ObjectiveWe describe a severe case of vaccine-induced immune thrombotic thrombocytopenia (VITT) after the first dose of the ChAdOx1 nCoV-19 vaccine leading to massive ischemic stroke.MethodsA 42-year-old woman developed acute left hemiparesis (NIHSS 12) 9 days after the first vaccine dose.ResultsThe blood tests revealed low platelets (70 103/μL) and severe increment of D-dimer (70,745 ng/mL FEU). Brain non-contrast computed tomography and multiphasic CT angiography demonstrated a right middle cerebral artery occlusion. The patient was treated with primary thrombectomy, steroids, immunoglobulin, and fondaparinux. Despite the treatment, the neurological status deteriorated and underwent decompressive hemicraniectomy. She was transferred to the rehab's unit 52 days after the onset.DiscussionHealthcare providers should be aware of the possibility of ischemic stroke as a manifestation of VITT. Awareness on this very rare and possibly fatal complication should be reinforced on both the vaccine recipients and general practitioners.

| S-EPMC8754523 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data