Coronary Artery Thrombosis Research Articles

Paroxysmal atrial fibrillation complicated with thrombosis of coronary and mesenteric artery: a case report

Paroxysmal atrial fibrillation complicated with thrombosis of coronary and mesenteric artery: a case report

Neutrophil Extracellular Traps Induce Endothelial Cell Activation and Tissue Factor Production Through Interleukin-1α and Cathepsin G

Objective- Coronary artery thrombosis can occur in the absence of plaque rupture because of superficial erosion. Erosion-prone atheromata associate with more neutrophil extracellular traps (NETs) than lesions with stable or rupture-prone characteristics. The effects of NETs on endothelial cell (EC) inflammatory and thrombogenic properties remain unknown. We hypothesized that NETs alter EC functions related to erosion-associated thrombosis. Approach and Results- Exposure of human ECs to NETs increased VCAM-1 (vascular cell adhesion molecule 1) and ICAM-1 (intercellular adhesion molecule 1) mRNA and protein expression in a time- and concentration-dependent manner. THP-1 monocytoid cells and primary human monocytes bound more avidly to NET-treated human umbilical vein ECs than to unstimulated cells under flow. Treatment of human ECs with NETs augmented the expression of TF (tissue factor) mRNA, increased EC TF activity, and hastened clotting of recalcified plasma. Anti-TF-neutralizing antibody blocked NET-induced acceleration of clotting by ECs. NETs alone did not exhibit TF activity or acceleration of clotting in cell-free assays. Pretreatment of NETs with anti-interleukin (IL)-1α-neutralizing antibody or IL-1Ra (IL-1 receptor antagonist)-but not with anti-IL-1β-neutralizing antibody or control IgG-blocked NET-induced VCAM-1, ICAM-1, and TF expression. Inhibition of cathepsin G, a serine protease abundant in NETs, also limited the effect of NETs on EC activation. Cathepsin G potentiated the effect of IL-1α on ECs by cleaving the pro-IL-1α precursor and releasing the more potent mature IL-1α form. Conclusions- NETs promote EC activation and increased thrombogenicity through concerted action of IL-1α and cathepsin G. Thus, NETs may amplify and propagate EC dysfunction related to thrombosis because of superficial erosion.

ST segment elevation myocardial infarction with normal coronary arteries

Case presentationA middle-aged patient presented to the emergency department with intermittent chest pain of 4-hour duration. The patient had been recently diagnosed with metastatic adenocarcinoma of the colon and was...

Assess the Clinical Efficacy of Streptokinase in Thrombolysed Patients of Acute ST Segment Elevation Myocardial Infarction

: Introduction: Acute myocardial infarction is the most important and feared consequence of coronary artery disease. STEMI is the one of that kind and it occurs by formation of a vulnerable plaque from atherosclerosis and transforms into coronary artery thrombosis in the end. Streptokinase has been used as a thrombolytic agent in patients with acute STEMI. It combines with the circulatory plasminogen to form an activator complex and it converts into plasmin, where, the plasmin breaks the fibrin complex in the blood clot. Streptokinase can be given as 1,500,000U a slow I.V infusion over 30 min. Each STEMI subject is different with the aetiology, pain, ST segment elevation. By considering these factors the clinical efficacy of streptokinase will be evaluated. Materials and Methods: A total number of 75 subjects presenting with acute STEMI to the department of cardiology, King George Hospital, Visakhapatnam, and, those were thrombolysed with streptokinase are included in the study. pain was assessed before and 90 min after administration of streptokinase on numerical pain rating scale from 0-10. ST segment resolution was assessed as percentage reduction in ST segment elevation before administration of streptokinase and the reduction of ST segment elevation 90 min after administration of streptokinase. Student t-test and chi-square test were applied to evaluate the results by using software SPSS. Results: A significant resolution in the pain and ST segment elevation were identified by comparing the numerical pain rating scale and ST segment elevation on pre and post streptokinase administration. Conclusion: Streptokinase has been shown to have significant effect on pain resolution and ST segment resolution in subjects with acute ST segment elevation myocardial infarction.Key words: Acute ST segment elevation myocardial infarction, Clinical efficacy, Pain, Streptokinase, ST segment elevation, Thrombolysed subjects.

DEFERRED STENT IMPLANTATION IN PATIENTS WITH ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION AND MASSIVE CORONARY THROMBOSIS

By researches it is proved that the phenomenon of no-reflow is an independent predictor of remodeling of the left ventricle at the moment. Particular importance in formation of this phenomenon is the fragmentation of a thrombus with distal embolization of small vessels, which often arise as a complication of the percutaneous coronary intervention during the destruction of a thrombus. Attempts to prevent the development of microvascular obstruction led to the creation of delayed stenting.The Purpose:assessing the efficacy and safety of deferred stent implantation in patients with ST-segment elevation myocardial infarction and massive coronary thrombosis.Material and Methods.12 patients with STEMI are included in a research. In the course of emergency coronary angiography was performed a massive thrombosis of the infarct-related coronary artery was observed with TIMI 2–3 blood flow. The emergency stenting wasn’t carried out to these patients, but continued anti-thrombotic therapy within 24 hours. After one day, repeated the coronary angiography was performed and, according to the indications, performed stenting of residual stenosis.Results.Development of the phenomenon of no-reflow, deaths and coronary events due to reocclusion of the infarctrelated coronary artery at all patients wasn’t observed. Also, all patients had a positive angiographic result in the form of regurgitation of the thrombus as a result of repeated the coronary angiography.Conclusion.Two-stage revascularization with delayed-on-day stenting with massive thrombosis of the infarct-related coronary artery in patients with acute myocardial infarction combined with aggressive antithrombotic therapy may be use in clinical practice to reduce the risk of developing the no-reflow phenomenon.

OBESITY AS ENVIRONMENTAL RISK FACTOR FOR REPEATED PREGNANCY LOSS IN PATIENTS WITH ANTIPHOSPHOLIPID SYNDROME

Introduction: Antiphospholidsyndrome (APS) is an autoimmune hypercoagulablestate caused by antiphospholid antibodies. Primary antiphospholipidsyndrome occurs in absence of any other related disease. Secondary antiphospholipid syndrome occurs with other autoimmune disease as systemic lupus erythrematosis. The clinical features of the APS are various, but the most common clinical presentation is pregnancy loss, DVT. Pulmonary thromboembolism, the cardiac manifestations of APS include myocardial infarction, pericardial effusion, myocardiopathy, and coronary artery thrombosis, but the most common manifestation is valvular abnormalities. Aim: to investigate the influence of obesity in women diagnosed as an antiphospholipid cases according to Sydney’s criteria on pregnancy morbidities, vascular events, pulmonary thromboemboism and laboratory criteria. Methods: A case control study was conducted that include women attending obstetric outpatient clinic. These women were previously diagnosed as antiphospholipid cases according to (Sydney’s criteria).A total of 60 women have been equally divided into two groups: First group corresponds to control group which includes 30 women with normal body mass index (BMI) i.e. 30Kg/m2). Results: Obesity is independent predictor for preterm birth intrauterine fetal death and pulmonary thromboembolism. Conclusion: Obesity is associated with worth pregnancy outcomes in patients with primary antiphospholipid syndrome.

Coronary Artery Aneurysms and Thrombosis in Kawasaki Disease.

Coronary Artery Aneurysms and Thrombosis in Kawasaki Disease.

TCTAP C-115 Successful Bailout of Iatrogenic Left Main Coronary Artery Thrombosis by "Pushing Method" with an Extension Catheter

TCTAP C-115 Successful Bailout of Iatrogenic Left Main Coronary Artery Thrombosis by "Pushing Method" with an Extension Catheter

Spontaneous thrombosis in an ectatic right coronary artery

A 73-year-old man presented to our cardiology service with intense central chest pain as an ST-segment elevation myocardial infarction (STEMI) call. His ECG showed inferior ST-segment elevation with reciprocal anterior...

A BENTALL DEBACLE: THROMBUS OR DISSECTION?

In coronary angiography, differentiating coronary artery (CA) dissection and thrombosis can be difficult creating diagnostic equipoise and impacting clinical care. We report a case of a 39 year old male with history of Marfan's syndrome and ascending aortic aneurysm status post Bentall

RLj-RGD3, a novel recombinant toxin protein from Lampetra japonica, prevents coronary thrombosis-induced acute myocardial infarction by inhibiting platelet functions in rats

Recombinant Lampetra japonica RGD-peptide (rLj-RGD3), a soluble protein containing three RGD sequences, was acquired from the oral salivary glands of Lampetra japonica using recombinant DNA technology. The aim of this study was to investigate the protective effects of rLj-RGD3 against acute myocardial infarction (AMI) induced by coronary artery thrombosis, as well as the underlying mechanisms. A rat model of AMI caused by ferric chloride-induced thrombosis on the surface of the left anterior descending (LAD) coronary artery was successfully established. Rats were given various doses of rLj-RGD3 (12 μg/kg, 24 μg/kg and 48 μg/kg) via sublingual intravenous delivery 10 min before AMI. ST segment elevation was recorded by electrocardiogram (ECG) until the end of the model. Left ventricular Evans blue content and histopathological changes were examined. Blood samples were collected to determine 5-hydroxytryptamine (5-HT), β-thromboglobulin (β-TG), platelet factor 4 (PF4) and cAMP levels. The effects of rLj-RGD3 on platelet aggregation, adhesion and intracellular calcium concentrations were also measured. rLj-RGD3 significantly reduced ST segment elevation, prevented thrombus formation in the coronary artery and decreased Evans blue content in the left ventricular myocardium. Meanwhile, rLj-RGD3 exerted an inhibitory effect on adenosine diphosphate (ADP)-induced platelet aggregation and blocked platelet adhesion to collagen. Treatment with rLj-RGD3 prevented 5-HT, β-TG and PF4 release and significantly elevated intracellular cAMP levels in a dose-dependent manner but decreased the level of cytosolic-free Ca2+, an aggregation-inducing molecule. These results show that rLj-RGD3 can effectively reduce coronary thrombosis in AMI rats by strongly inhibiting platelet function, indicating that the recombinant RGD toxin protein rLj-RGD3 may serve as a potent clinical therapeutic agent for AMI.

Рідкісний випадок спонтанного тромболізису у пацієнтки з гострим інфарктом міокарда з елевацією сеґмента ST

In the pathogenesis of acute myocardial infarction an important role belongs to coronary sclerosis and coronary artery thrombosis. Endothelium plays an important role in a regulation of vascular tone, local inflammation, hemostasis, neovascularisation. An impairment of endothelial barrier function occurs after direct damage of endothelial cells as a result of an atherosclerotic plaque destabilization, injury, chronic inflammation or exposure to hazardous substances. Breakage of the endothelial surface causes an exposure of subendothelial collagen and triggers expression of adhesive proteins (e.g. tissue factor and von Willebrand factor) and decreases synthesis of prostacyclin and nitric oxide. In case of its damage and activation, thrombocytes adhere and aggregate to each other which leads to thrombosis and can cause an acute myocardial infarction.  Aim. Our aim was to evaluate a cellular mechanisms of thrombosis as well as conditions that leads to spontaneous thrombolysis in acute myocardial infarction for treatment optimisation of acute coronary syndrome.   Material and Methods. The case of acute myocardial infarction with ST segment elevation in 79 years old patient is presented that showed spontaneous coronary blood flow recovery.  Results and Discussion. In described case in a patient with acute myocardial infarction a rapid regression of ECG changes were documented after medical treatment at home was provided. Those changes were most likely a results of spontaneous thrombolysis with subsequent recovery of coronary blood flow in infarct-related artery due to rarely occurring activation of fibrinolytic system. The fibrinolysis system was triggered by the release of plasminogen activator and affected newly formed thrombus. However unstable atherosclerotic plaque was thrombogenic enough and leaded to recurrence of myocardial infarction. Thus the patient received coronary artery stenting. Clinical and morphological data has shown that in those patients a major role in development of acute coronary syndrome plays not a coronary artery spasm but a coronary thrombosis with subsequent spontaneous thrombolysis and restoration of coronary blood flow which happened upon timely application of antiaggregants, anticoagulants and antianginals drugs. Coronary artery spasm typically occurs more distal from the obstruction place as a result of exposure to vasoconstrictors released after thrombocyte degranulation. Spontaneous thrombolysis by acute myocardial infarction is untypical, hence myocardial infarction with pathological Q wave develops.  Conclusions. Patients with acute coronary syndrome, which exhibit spontaneous thrombolysis require angiography and stenting of coronary arteries as soon as possible to prevent recurrence of coronary thrombosis and development of acute myocardial infarction.

Recurrent and concurrent subacute stent thrombosis of two coronary arteries in a schizophrenic patient.

Subacute stent thrombosis after acute coronary syndrome and concurrent thrombosis of multiple coronary arteries are rare complications. Schizophrenia and antipsychotic drugs cause hypercoagulability, and rates of cardiovascular mortality are higher in schizophrenic patients compared with the normal population. We want to discuss a case of recurrent and concurrent subacute left anterior descending artery and right coronary artery stent thrombosis after acute myocardial infarction in a schizophrenic patient. Learning Objectives: Schizophrenia and antipsychotic medications should be considered risk factors for acute and subacute stent thrombosis in patients treated with percutaneous coronary stent implantation. Intensive antiplatelet therapy should be considered for patients with schizophrenia on antipsychotic treatment who undergo percutaneous coronary intervention.

Immediate Rupture of Another Coronary Plaque After PCI of the Culprit Lesion in ST Segment Elevation Myocardial Infarction

ST-segment elevation myocardial infarction (STEMI) is usually the result of thrombosis in the single coronary artery. The incidence of multiple coronary artery thrombosis in acute phase is very low. The etiology of multivessel coronary thrombosis is still unclear. Observational studies have shown that plaque instability underlying thrombosis is not due to local vascular causes alone. These pathophysiological processes such as inflammation, sympathic activity and catecholamines discharge act across the entire coronary network and cause multiple plaque instability.1,2 We think that the pathogenesis of multiple coronary occlusive lesions may be explained by multiple atherosclerotic plaque rupture during the acute phase of myocardial infarction. In our case, the first percutaneous coronary intervention was performed on the left anterior descending artery due to anterior STEMI. At the second hour of follow-up, inferior STEMI developed and percutaneous coronary intervention was performed on optus marginalis.

ИНФАРКТ МИОКАРДА В ПОСТПАРТАЛЬНОМ ПЕРИОДЕ У МОЛОДОЙ ЖЕНЩИНЫ С ДЕФИЦИТОМ ПРОТЕИНА С

Women of childbearing age without cardiovascular risk factors have low risk of acute myocardial infarction. Pregnancy has been shown to increase the risk of myocardial infarction compared to the risk in non-pregnant women of similar age. Acute myocardial infarction during pregnancy or postpartum period as a rule develops due to coronary spasm or non-atherogenic thrombosis or spontaneous coronary dissection. Thrombosis is most likely related to hypercoagulable state of pregnancy and postpartum period. It is worth considering the importance of defects of coagulation, such as Leiden factor, protein C, protein S, antithrombin III and mutations of propter genes. There is also the significant role of antiphospholipid antibodies in young women. We present the clinical case of acute ST-elevation myocardial infarction in 34-years old woman without traditional cardiovascular risk factors, which was developed after childbirth due to non-atherogenic left anterior coronary artery thrombosis. Her coagulation profile showed normal results for antithrombin III, protein S, prothrombin gene mutation, factor V Leiden and antiphospholipid antibody syndrome. At the same time the protein C activity decreased to 43 % as well as trombophilia genetic markers MTHFRC677T, MTRR 66A>G, ITGA2:807 C>T and ITGB:1565 T>C genetic polymorphisms were revealed.

Pre-clinical model of severe glutathione peroxidase-3 deficiency and chronic kidney disease results in coronary artery thrombosis and depressed left ventricular function.

Chronic kidney disease (CKD) patients have deficient levels of glutathione peroxidase-3 (GPx3). We hypothesized that GPx3 deficiency may lead to cardiovascular disease in the presence of chronic kidney disease due to an accumulation of reactive oxygen species and decreased microvascular perfusion of the myocardium. Methods. To isolate the exclusive effect of GPx3 deficiency in kidney disease-induced cardiac disease, we studied the GPx3 knockout mouse strain (GPx3-/-) in the setting of surgery-induced CKD. Results. Ribonucleic acid (RNA) microarray screening of non-stimulated GPx3-/- heart tissue show increased expression of genes associated with cardiomyopathy including myh7, plac9, serpine1 and cd74 compared with wild-type (WT) controls. GPx3-/- mice underwent surgically induced renal mass reduction to generate a model of CKD. GPx3-/- + CKD mice underwent echocardiography 4 weeks after injury. Fractional shortening (FS) was decreased to 32.9 ± 5.8% in GPx3-/- + CKD compared to 62.0% ± 10.3 in WT + CKD (P < 0.001). Platelet aggregates were increased in the myocardium of GPx3-/- + CKD. Asymmetric dimethylarginine (ADMA) levels were increased in both GPx3-/- + CKD and WT+ CKD. ADMA stimulated spontaneous platelet aggregation more quickly in washed platelets from GPx3-/-. In vitro platelet aggregation was enhanced in samples from GPx3-/- + CKD. Platelet aggregation in GPx3-/- + CKD samples was mitigated after in vivo administration of ebselen, a glutathione peroxidase mimetic. FS improved in GPx3-/- + CKD mice after ebselen treatment. These results suggest GPx3 deficiency is a substantive contributing factor to the development of kidney disease-induced cardiac disease.

A Mysterious Case of ST-Elevation Myocardial Infarction; an Old Man with Weight Loss and Dyspepsia

We present a 65-year-old man who developed retrosternal compressive chest pain. A 12-lead electrocardiography demonstrated ST-segment elevation in leads II, III and aVF. Emergent coronary angiography showed significant thrombus in the distal portion of the left main coronary artery. Abdomino-pelvic computed tomography scan, which was performed the next day, confirmed a pancreatic mass with peritoneal seedings, compatible with peritoneal carcinomatosis. This case underscores the importance of malignancies that may lead to a catastrophic ST-elevation myocardial infarction due to a hypercoagulable state and following thrombosis in the left main coronary artery.

Echocardiographic and clinical retrospective study of 35 patients with Kawasaki disease combined with coronary artery thrombosis

Objective To summarize the echocardiographic findings and clinical characteristics of Kawasaki disease(KD) complicated with coronary artery thrombosis(CAT). Methods Thirty-five patients with KD combined with CAT were enrolled, who were admitted to Beijing Children's Hospital, Capital Medical University between July 2005 and August 2016. The clinical characteristics and echocardiographic findings during follow-ups were retrospectively studied. According to whether the childrenhad been complicated with myocardial ischemia, the patients were divided into 2 groups: ischemic group and non-ischemic group.The duration of fever, the time when the intravenous immunoglobulin(IVIG) was first injected, the time when coronary artery aneurysms(CAA) was formed, the maximum diameter of CAA and inflammatory index inthe acute phase were compared between 2 groups. Results All of the 35 children diagnosed as KD combined with CAT suffered from CAA, and the coronary thrombosis was detected in all the cases with aneurysms. Thirty-five patients had 99 branches of CAA, of which the maximum diameter of CAA was (9.6±3.1) mm(4.0-19.0 mm). Fifty-four plots of CAT were detected in the aneurysms. The diameter of CAA that thrombosis located was larger than that of which the thrombosis was not located[(10.9±2.8) mm vs.(7.9±2.6) mm], and the difference was significant(P<0.01). During 4 months to 10 years and 8 months [(39.2±29.5) months]follow-ups, CAA regressed in 32 branches [32.3%(32/99 branches)], of which 4 branches[4.0%(4/99 branches)] completely regressed to the normal diameter. The maximum diameter of CAA regressed was smaller than the maximum diameter of CAA consistence [(7.3±1.9) mm vs.(10.6±3.0) mm ], and the difference was significant(P<0.01). Out of 35 patients, 15 cases [42.9%(15/35 cases) had myocardial ischemia , while the other 20 cases[57.2%(20/35 cases)] didn't have.Among 15 cases with myocardial ischemia, 6 cases[17.1%(6/35 cases)]had myocardial infarction, 4 cases[11.4%(4/35 cases)]had heart failure, and 1 case[2.9%(1/35 cases)] died of acute heart failure complicated with severe ventricular arrhythmia. Compared with non-ischemic group, the children in the ischemic group had longer duration of fever[( 19.1±7.8) d vs.(12.1±3.3) d], higher white blood cell account in the acute phase[(24.8±13.5)×1012/L vs.(19.7±4.0) × 1012/L], later treatment of IVIG [(13.9±5.5) d vs.(9.8±3.8) d], and earlier CAA formation [(16.0±4.9) d vs.(20.9±14.5) d], and the differences were statistically significant (all P<0.05). Conclusions CAT of children with KD commonly originates from CAA. Patients who have more serious inflammatory reaction in the acute phase, earlier formation, heavy severity and longer consistence of CAA are prone to have myocardial ischemia. Echocardiographic study plays an important role in monitoring CAA, detecting the CAT and finding the early left ventricle dysfunction, which is of clinical significance. Key words: Kawasaki Disease; Coronary artery thrombosis; Coronary artery aneurysm; Myocardial ischemia; Follow-up

Effects of antiretroviral treatment and nadir CD4 count in progression to cardiovascular events and related comorbidities in a HIV Brazilian cohort: a multi-stage approach

ABSTRACTThe use of highly active antiretroviral therapy has resulted in changes of comorbidity profile in people living with HIV (PLHIV), increasing non-AIDS-related events. The occurrence of cardiovascular events is greater in PLHIV, but the mechanism responsible for it is still controversial. This article aimed to investigate factors associated with the progression to cardiovascular events in PLHIV using HAART. A 15-years cohort study with 1135 PLHIV was conducted in Rio de Janeiro-Brazil. Clinical progression was stratified in five states: No comorbidities (s1), arterial hypertension (s2), lipid abnormalities (s3), hypertension and lipid abnormalities (s4) and major cardiovascular events (stroke, coronary artery disease, thrombosis or death) (s5). Semi-Markov models evaluated the effects of cardiovascular traditional factors, treatment and clinical covariates on transitions between these states. Hazard Ratios (HR) and 95% confidence intervals (CI) were provided. In addition to traditional factors (age, sex, educational level and skin color), the development of one comorbidity (lipid abnormalities or hypertension) increased in patients with low nadir CD4 (<50 cells/mm3), (HR = 1.59, CI 1.11–2.28 and 1.36, CI 1.11–1.66, respectively). The risk to experience a second comorbidity (s3→s4) increased 75% with low nadir CD4. Age was the only factor that increased the risk of major cardiovascular events once having lipid abnormalities with or without hypertension (s3,s4→s5). The prolonged use of certain antiretroviral drugs (abacavir, didanosine, ritonavir, lopinavir, amprenavir and fosamprenavir) increased the risk of direct transition (s1→s5) to major cardiovascular events (HR = 5.29, CI 1.16–24.05). This analysis suggests that prolonged use of certain antiretroviral drugs led directly to major cardiovascular events, while low nadir CD4 only affected the occurrence of lipid abnormalities and hypertension. Management strategies, including rational use of complex exams (such as, computed-tomography angiography), statins and antihypertensives, should be developed based on the distinct roles of antiretroviral use and of HIV infection itself on the progression to cardiovascular events.

A Rare Case of Varicella Pneumonia with Acute Coronary Syndrome and Lower Limb Arterial Thrombosis

A Rare Case of Varicella Pneumonia with Acute Coronary Syndrome and Lower Limb Arterial Thrombosis