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Aims Current management of left ventricular (LV) thrombus relies on limited, non-contemporary, echocardiography-based studies. Data on LV thrombus evolution and the associated embolic risk are scarce. We aimed to describe the evolution of LV thrombus on serial cardiovascular magnetic resonance imaging (CMR)—the current reference standard for the detection of LV thrombus—and identify correlates of no resolution and the embolic risk associated with resolution status. Methods and results We conducted a retrospective cohort study of 107 consecutive patients with LV thrombus who had 213 serial CMRs at a median of 255 days after the index CMR. Of these, 97.2% were anticoagulated. At 3 months after detection by CMR, 75% (47/63) had no resolution of LV thrombus; at 6 months, 53% (35/66) had no resolution; and at 12 months, 37% (23/63) had no resolution. Correlates of no resolution at 6 months included a history of myocardial infarction, LV aneurysm, ischaemic aetiology of cardiomyopathy, and larger thrombus volume. Recurrence of LV thrombus was rare at 5.3%. On survival analysis using the landmark analysis method, embolic events often occurred beyond 6 months, more frequently in patients with unresolved LV thrombus. Conclusion Our findings challenge previous literature by demonstrating a lower rate of resolution of LV thrombus and substantial embolic risk beyond 6 months associated with unresolved LV thrombus on serial CMR. Our findings advocate for extended anticoagulation, particularly in patients with markers associated with no resolution. These findings have important implications for clinical practice and research into managing patients with LV thrombus. [ABSTRACT FROM AUTHOR]

Introduction: Advances in pharmacotherapy for coronary thrombosis treatment and prevention have transformed the clinical outcomes of patients with coronary artery disease but increased the complexity of therapeutic decision-making. Improvements in percutaneous coronary intervention techniques and stent design have reduced the incidence of thrombotic complications, which consequently has increased the challenge of adequately powering clinical trials of novel antithrombotic strategies for efficacy outcomes. Knowledge of the pathophysiology of coronary thrombosis and the characteristics of antithrombotic drugs can help with therapeutic decisions. Areas covered: This review covers the pathophysiology of coronary thrombosis and the mechanisms of action of drugs developed for its treatment, provides an overview of the key issues in decision-making, and highlights key areas for further work in order to guide clinicians on how to individualize risk management and address gaps in the evidence base. Expert opinion: Individualization of antithrombotic therapy regimens has become a vital part of optimizing risk management in people with coronary thrombosis. A critical appraisal of the strengths and limitations of available drugs and the evidence supporting the use of different antithrombotic combinations is intended to provide direction to clinicians and point the way toward further improvements in pharmacotherapy for coronary thrombosis treatment and prevention. [ABSTRACT FROM AUTHOR]

An 18-year-old teenager with significant atherosclerotic cardiovascular disease (ASCVD) risk factors developed acute chest pain. His electrocardiogram showed inferior ST-segment elevations. Emergent coronary angiogram revealed complete thrombotic occlusion of the right coronary artery. He underwent stenting of the culprit lesion with complete clinical recovery and resolution of his electrocardiographic abnormalities secondary to myocardial infarction. [ABSTRACT FROM AUTHOR]

Background/Objectives: Acute stent thrombosis (ST) is a rare yet severe complication following percutaneous coronary intervention (PCI). Herein, we investigated the possible association between routinely available coagulation and fibrinolysis markers with early ST. Methods: Within a single-center registry, we investigated the association between the preprocedural platelet count, plasma levels of fibrinogen and D-Dimer, and the incidence of early ST in the first 30 days after PCI. Results: Out of 10,714 consecutive patients who underwent PCI using drug-eluting stents (DESs), the preprocedural platelet count, fibrinogen, and D-Dimer measurements were available in 6337, 6155, and 956 patients, respectively. Fifty-eight patients (0.92%) experienced an early ST within 30 days after PCI. Compared with those without ST, patients with early ST showed significantly elevated preprocedural platelet counts (p < 0.05) and fibrinogen levels (p < 0.05). D-Dimer levels were not associated with early ST. Patients in the fifth quintile of platelet count had a significantly increased risk for early ST (HR 2.43; 95% CI 1.43–4.14; p = 0.001) compared with patients in the lower four quintiles. In addition, patients in the fifth quintile of fibrinogen also had a significantly increased risk for early ST (HR 1.86; 95% CI 1.07–3.26; p < 0.05) compared with patients in the lower four quintiles. These associations were independent of clinical risk factors, the number of stents, the presence of acute coronary syndromes, and white blood cell count. Conclusions: Preprocedural platelet counts and fibrinogen plasma levels can identify patients at elevated risk of early ST after implantation of DESs in addition to procedure-level and device-related risk factors. [ABSTRACT FROM AUTHOR]

Introduction: It has been shown that pregnancy can cause alterations in the severity of COVID-19 infection. We demonstrate an immediate post-partum patient diagnosed with severe COVID-19 and subsequently developed acute thrombosis of coronary artery. Case Summary: 35-year-old female unvaccinated for COVID-19 presented in labor and delivered on the same day. Several hours later, she was found to be in respiratory distress and tested positive for COVID-19. On day 7, computerized tomography (CT) of chest revealed bilateral pneumonia and pneumomediastinum. On day 8, she developed chest pain with electrocardiogram (EKG) showing inferior STelevations with troponin I of 0.6 ng/mL. She was intubated for airway protection and emergent diagnostic angiogram revealed thrombus occlusion of the third right posterolateral segment that resulted in thrombolysis in myocardial infarction (TIMI) 0 flow without evidence of underlying atherosclerotic disease in the remaining vessels. Intracoronary IIb/IIIa inhibitor was administered. Arterial blood gas in the lab revealed profound hypoxia despite being on 100% inspired oxygen. Multidisciplinary decision was made to cannulate patient for venovenous extracorporeal membrane oxygenation (ECMO) to treat severe COVID-19 pneumonia. She was finally decannulated from ECMO on day 65. After prolonged hospital stay, she eventually recovered and was discharged to rehabilitation. Conclusions: The center for disease control (CDC) surveillance has reported that pregnant patients with COVID-19 are more likely to require invasive ventilation and ECMO, and die given the immunological changes during pregnancy. Hypercoagulable state caused by combination of pregnancy and COVID-19 resulting in coronary thrombosis is rarely described in literature, our case demonstrated the paucity of this phenomenon. [ABSTRACT FROM AUTHOR]

Purpose of Review: Plaque erosion is the second leading cause of coronary thrombosis following plaque rupture and represents a key pathophysiological process underlying acute coronary syndromes that can culminate in sudden coronary death. While the precise mechanisms and risk factors driving plaque rupture are well-established, those for erosion have only recently been explored. This review summarizes current literature on the characteristics and risk factors favoring plaque erosion. Recent Findings: Plaque erosion is characterized by a defective endothelial layer in the intima, promoting thrombus formation in the presence of an intact fibrous cap. It is more common in younger women (< 50 years) and smokers. Pathologic intimal thickening or fibroatheroma are common underlying lesions. Risk factors include gender, age, smoking, and disturbances in shear flow. Advances in pathogenic and molecular mechanisms, such as endothelial shear stress, neutrophil activation, and toll-like receptor-2 pathways, are discussed. Summary: Understanding the major risk factors for plaque erosion can inform diagnostics and therapeutics to prevent the progression of arterial thrombosis. [ABSTRACT FROM AUTHOR]

Abstract Triple coronary artery thrombosis is a rare cause of acute myocardial infarction, and is associated with high mortality. Only a few cases of simultaneous multiple-vessel coronary thrombosis have been reported in the medical literature. This paper reports a unique case of sudden cardiac death in 36-year-old man without relevant risk factors who suffered from acute myocardial infarction due to simultaneous triple coronary artery thrombosis. Autopsy and histopathology examinations revealed near-total thrombotic occlusion in all three main coronary arteries. While the exact mechanism behind the simultaneous formation of these thrombi remains unclear, this paper discusses certain risk factors that may contribute to multiple coronary thrombosis. A review of previously reported cases of coronary thrombosis involving all three major coronary arteries in the literature is also provided to contribute to the understanding of this rare and potentially fatal condition. Obtaining a detailed medical and family history, collecting and saving blood samples for potential genetic analyses, and testing for Novel Coronavirus disease could be beneficial in cases of multiple coronary artery thrombosis to detect a potential underlying cause and provide prevention to family members at risk.

Background: ST-segment elevation myocardial infarction (STEMI) remains a leading cause of mortality worldwide, primarily caused by acute thrombosis over atherosclerotic plaques. Simultaneous acute thrombosis in two coronary arteries is an exceptionally rare event. This report highlights a unique case of STEMI associated with cardiogenic shock due to dual coronary artery thrombosis and provides insights from a literature review on this rare condition. Methods: We report the case of a 58-year-old male with a history of hypertension, type II diabetes, and heavy smoking, who presented with a two-day history of chest pain and cardiogenic shock. Diagnostic evaluation included an electrocardiogram showing ST-segment elevation in AVR and ischemia, along with echocardiography revealing severe left ventricular dysfunction (ejection fraction 20%). Emergency coronary angiography was performed to identify the underlying pathology. Additionally, a literature review was conducted to analyze the characteristics and outcomes of similar cases of dual coronary artery thrombosis. Results: Coronary angiography identified significant occlusions in the proximal circumflex branch and the left anterior descending artery (LAD), a combination rarely reported in the literature. Our review confirmed that dual thrombosis involving the LAD and right coronary artery (RCA) is the most frequently described presentation of this condition, while simultaneous CFX and LAD thrombosis is exceedingly rare. Most reported cases, including ours, were associated with cardiogenic shock, highlighting the severity of this clinical entity. Despite successful thrombus aspiration and stenting, our patient experienced severe complications, including infections, pleural effusions, and paralytic ileus, ultimately requiring evaluation for left ventricular assist device implantation. Conclusions: This case underscores the complexity and critical challenges of managing STEMI with cardiogenic shock due to simultaneous coronary thrombosis. The findings from our literature review suggest the need for heightened clinical awareness and tailored revascularization strategies. Further studies are warranted to optimize management approaches and improve outcomes in such rare and high-risk scenarios. [ABSTRACT FROM AUTHOR]

Background Sequential occurrences of acute ischaemic stroke in patients with acute myocardial infarction (MI) and vice versa have been reported, but not the simultaneous occurrence of both conditions. We report a case of simultaneous occurrence of MI and systemic embolism caused by a mechanism not reported to date. Case summary A 52-year-old female patient presented with concurrent chest pain, right arm weakness, and dysphasia. An electrocardiogram demonstrated ST-elevation MI. A computed tomography angiography ruled out aortic dissection and showed an ischaemic stroke and infarction in the right kidney and spleen. A right coronary thrombotic occlusion at the ostium was successfully recanalized. Transoesophageal echocardiography showed preserved left ventricular function with no intracardiac thrombi. Discussion The reported case presentation does not align with the mechanisms typically associated with simultaneous MI and stroke. The most plausible hypothesis is that the thrombus in the right coronary ostium extended into the aorta, resulting in a concurrent systemic embolism. [ABSTRACT FROM AUTHOR]

The structure of aspirated coronary thrombus in ST-segment elevation myocardial infarction (STEMI) is still being studied. Our aims were to characterize coronary thrombi of different ages, focusing on the appearance of activated protein C (APC/PC) and its relation to the elements of neutrophil extracellular traps (NETs), and the factors closely related to fibrin as factor XIII (FXIII) and α2 plasmin inhibitor (α2-PI). The thrombi of n = 24 male patients with atherosclerotic coronary plaque rupture related to native coronary artery occlusion were selected for histopathology analysis. Thrombus age was distinguished as fresh, lytic, and organized, and then analyzed by immunofluorescent staining and confocal microscopy. FXIII was present at a high level and showed a high degree of co-localization with fibrin in all stages of thrombus evolution. The amount of α2-PI was low in the fresh thrombi, which increased significantly to the lytic phase. It was evenly distributed and consistently associated with fibrin. APC/PC appeared in the fresh thrombus and remained constant during its evolution. The presence of NET marker and CD66b was most dominant in the lytic phase. APC/PC co-localization with the elements of NET formation shows its role in NET degradation. These observations suggest the importance of searching for further targeted therapeutic strategies in STEMI patients. [ABSTRACT FROM AUTHOR]

The article discusses a case of atypical myocardial infarction associated with airbag deployment, resulting in severe coronary injury and myocardial infarction in a 56-year-old woman involved in a car crash. The patient experienced dynamic electrocardiographic changes and intravascular imaging revealed a large intramural hematoma and luminal thrombosis in the right coronary artery. The case highlights the importance of serial electrocardiographic monitoring to detect latent coronary injury and emphasizes the necessity of wearing seat belts for both drivers and passengers to prevent such incidents. [Extracted from the article]

Background: Heparin rebound is a common observed phenomenon after cardiac surgery with CPB and is associated with increased postoperative blood loss. However, the administration of extra protamine may lead to increased blood loss as well. Therefore, we want to investigate the relation between heparin rebound and postoperative blood loss and the necessity to provide extra protamine to reverse heparin rebound. Methods: We searched PubMed, Cochrane, EMBASE, Google Scholar and Web of Science to review the question: "Does heparin rebound lead to postoperative blood loss in patients undergoing cardiac surgery with cardiopulmonary bypass." Combination of search words were framed within four major categories: heparin rebound, blood loss, cardiac surgery and cardiopulmonary bypass. All studies that met our question were included. Quality assessment was performed using the Cochrane risk of bias (RoB2) tool for randomized controlled trials and the risk of bias in non-randomized studies of intervention (ROBINS-I) for non-randomised trials. Results: 4 randomized and 17 non-randomized studies were included. The mean incidence of heparin rebound was 40%. The postoperative heparin levels, due to heparin rebound, were often below or equal to 0.2 IU/mL. We could not demonstrate an association between heparin rebound and postoperative blood loss or transfusion requirements. However the quality of evidence was poor due to a broad variety of definitions of heparin rebound, measured by various coagulation tests and studies with small sample sizes. Conclusion: The influence of heparin rebound on postoperative bleeding seems to be negligible, but might get significant in conjunction with incomplete heparin reversal or other coagulopathies. For that reason, it might be useful to get a picture of the entire coagulation spectrum after cardiac surgery, as can be done by the use of a viscoelastic test in conjunction with an aggregometry test. [ABSTRACT FROM AUTHOR]

Aim and background: To study an unusual presentation of coronary air embolism causing non-ST elevation myocardial infarction that occurred during a lung nodule biopsy procedure. Coronary air embolism can be a dreaded complication that may occasionally occur during cardiac catheterization, cardiac surgeries, and other cardiac procedures but is not so common during noncardiac procedures. The sequelae of this complication can range from being clinically insignificant to catastrophic coronary and/or cerebral air embolism. Case description: A 58-year-old male diagnosed with left-sided parotid carcinoma with suspected lung metastasis underwent a biopsy of lung lesion under local anesthesia. At the end of the procedure, the patient developed hemoptysis with unconsciousness. A cardiac code was activated, and the patient was immediately resuscitated. The patient developed a large pneumothorax with alveolar bleeding along with significant coronary air embolism. An electrocardiogram showed inferior wall myocardial ischemia. The patient was medically managed and made an uneventful recovery. Conclusion and clinical significance: The case highlights the unusual but catastrophic effects of coronary air embolism. It also shows that early recognition and timely treatment can improve outcomes. [ABSTRACT FROM AUTHOR]

Background Unroofed coronary sinus (UCS) is a rare congenital anomaly and is usually found incidentally. While coronary sinus thrombosis (CST) can occur following instrumentation of the coronary sinus, spontaneous CST is a rare occurrence and only a few cases have been reported to date. The presence of both rare entities concurrently has not been reported previously. Case summary A 57-year-old man presented with rectal bleeding and was in hypovolaemic shock. On computed tomography (CT), he was found to have ischaemic colitis as well as an incidental finding of a Type IV UCS with CST. He was initially managed with intravenous heparin infusion but developed life-threatening upper gastrointestinal bleeding, requiring endoscopic clipping of a gastric ulcer. The patient was recommenced on intravenous heparin and later transitioned to oral anticoagulant without further events. Discussion In UCS, the coronary sinus communicates with the left atrium. The majority of patients are asymptomatic, and the anomaly usually goes undetected. In this patient, UCS was found incidentally with concurrent spontaneous CST. The ischaemic colitis was likely due to cardioembolism from the CST. In the absence of evidence-based practice, we described our cautious approach to anticoagulation in this critically unwell patient. Furthermore, advances in cardiac intervention have seen an increasing need to instrument the coronary sinus and an increased awareness of coronary sinus anomalies is important. Cardiac CT provides an excellent imaging tool for assessing the coronary sinus anatomy (as demonstrated in this case) and can be helpful in pre-procedural planning. [ABSTRACT FROM AUTHOR]

Thrombosis is a major contributor to the pathophysiology of cardiovascular diseases. The involvement of platelets in the formation of thrombus has been studied extensively. Platelet aggregation inhibition is a promising strategy for the treatment of thrombosis. Artocarpus altilis is a medicinal plant containing 2-geranyl-2',3,4,4'-tetrahydroxydihydrochalcone (GTDC) with antiplatelet activity. A previous study showed that the plant extract and GTDC demonstrated antiplatelet activity in ADP-induced platelet aggregation. However, no data are available regarding its efficacy in platelet aggregation induced by other agonists. In addition, the antithrombotic activity of GTDC is unknown. This study evaluates the antithrombotic activity of GTDC and determines the antiplatelet specificity action of GTDC. Antithrombotic activity assay was done using FeCl3-induced arterial thrombosis in rats, whereas the antiplatelet assays were performed in vitro utilizing human platelet induced by several platelet receptor agonists. One-way ANOVA followed by the Tukey post-hoc test (p = 95%) in GraphPad Prism 8 software were used to analyze the data statistically. We found that GTDC (30 and 60 mg/kg) demonstrated antithrombotic activity by prolonging occlusion time due to thrombosis. GTDC showed its highest selectivity in the platelet aggregation pathway induced by ADP compared with thrombin, arachidonic acid, and epinephrine. [ABSTRACT FROM AUTHOR]

Coronary artery ectasia (CAE) is a rare vascular phenotype characterized by abnormal dilation of blood vessels and disruption of coronary artery blood flow, which may promote thrombosis and an inflammatory response. We performed a cross-sectional study to investigate the association of white blood cells to mean platelet volume ratio (WMR) with CAE. Consecutive eligible patients (n = 492) were divided into two groups: including 238 patients with CAE and 254 patients in the normal coronary artery (NCA) group. WMR, the systemic immune-inflammation index (SII), and neutrophil-to-lymphocyte ratio (NLR) were found to be significantly associated with CAE in both univariate and multivariate logistic regression analyses. In multivariate analysis, the presence of WMR was associated with CAE (the odds ratios (OR) = 1.002, 95% CI: 1.001–1.003, P <.001). In the ROC analysis, the statistics (Z-values) of WMR vs SII and WMR vs NLR were 2.427 and 2.670 and were statistically significant (P =.015 and P =.008), indicating that WMR was superior to SII and NLR in distinguishing WMR. The optimal cut-off value was calculated from the point of maximal sensitivity and specificity by using Youden's index, which was determined to be 635.50. WMR has the potential to be a cost-effective tool to monitor CAE. [ABSTRACT FROM AUTHOR]

Coronary artery aneurysms (CAAs) are morphologically classified as saccular and fusiform. There is still a great deal of clinical controversy as to which types of CAA are more likely to cause thrombosis. Therefore, the main objective of this study was to evaluate the trend of thrombus growth in CAAs with different morphologies and to assess the risk of possible long-term complications based on hemodynamic parameters. Utilizing computed tomography angiography (CTA) data from eight healthy coronary arteries, two distinct morphologies of coronary artery aneurysms (CAAs) were reconstructed. Distribution of four wall shear stress (WSS)-based indicators and three helicity indicators was analyzed in this study. Meanwhile, a thrombus growth model was introduced to analyze the thrombus formation in CAAs with different morphologies. The research results showed the distribution of most WSS indicators between saccular and fusiform CAAs was not statistically significant. However, due to the presence of a more pronounced helical flow pattern, irregular helical flow structure and longer time of flow stagnation in saccular CAAs during the cardiac cycle, the mean and maximum relative residence time (RRT) were significantly higher in saccular CAAs than in fusiform CAAs (P < 0.05). This may increase the risk of saccular coronary arteries leading to aneurysmal dilatation or even rupture. Although the two CAAs had similar rates of thrombosis, fusiform CAAs may more early cause obstruction of the main coronary flow channel where the aneurysm is located due to thrombosis growth. Thus, the risk of thrombosis in fusiform coronary aneurysms may warrant greater clinical concern. [ABSTRACT FROM AUTHOR]

Objective: Atherosclerosis is a chronic condition characterized by impaired lipid homeostasis and chronic inflammatory pathology in large and mid-sized arteries. Myocardial infarction is caused by coronary artery thrombosis in a ruptured or unstable atherosclerotic plaque. Despite the emphasis on known triggering factors, such as hypertension and dyslipidemia, adverse events following MI, such as recurrence and mortality, are still high. Therefore, it is imperative to assess potential determinants of plaque instability. We evaluated markers of inflammation, extracellular matrix (ECM) remodeling, thrombosis, and lipids in first-time and recurrent MI (RMI). Methods: Two hundred patients diagnosed with MI within the first 24 h of the event were included in the study and categorized as first-time or recurrent MI. Serum levels of NF-κB, hs-CRP, TNF-α, IFN ν, IL-6, VCAM-1, MMP-9, stromelysin, TIMP-1, MCP-1, PAPP-A, vWF, Ddimer, PLA2, PON-1, Apo-B, Apo-A1, ox-LDL, and anti-oxidized LDL antibodies were analyzed by ELISA. We performed a multivariate logistic regression analysis for risk stratification. Results: The mean age of first-time MI patients was 52.4±25 years and that of recurrent MI patients was 55.9±24.6 years. RMI patients showed significant (p<0.05) upregulation of markers of inflammation (TNF-a), endothelial adhesion (VCAM-1), ECM remodeling (MMP-9, PAPP-A), and antioxidant PON-1 enzyme. First-time MI patients had significantly higher serum IL-6 and D-dimer levels than RMI patients. Risk categorization for RMI was determined at 0.5 cut-off utilizing proteomic indicators at 95% confidence interval. Conclusion: Non-lipid factors provide substantial insights into plaque instability. Multiple markers of inflammation, thrombosis, extracellular matrix remodeling, and paroxonase-1 are reliable indicators of recurrent myocardial infarction. [ABSTRACT FROM AUTHOR]

Takotsubo cardiomyopathy (TCM) is a transient and reversible cardiomyopathy which exhibits regional wall motion abnormalities in the absence of obstructive coronary artery disease. While TCM is a rare condition (incidence <1%), its diagnosis has increased since its initial description in 1990. While many cases may follow an acute physical or emotional stressor, pathophysiology is likely multifactorial including factors such as catecholamine surges and microvascular dysfunction. On initial presentation, TCM often mimics acute coronary syndrome but may be differentiated with coronary angiography. Additional laboratory testing and imaging including transthoracic echocardiography may help with diagnosis and identification of complications such as left ventricular (LV) outflow obstruction and LV thrombus. Treatment is supportive, although medications such as angiotensin-converting enzyme inhibitors and beta-blockers have shown some benefit in improving long-term outcomes. Acute complications may include arrhythmia, LV or systemic thrombus, and cardiogenic shock, but most patients do well and experience rapid recovery. TCM continues to be an active area of research as there is still much to be learned regarding its pathogenesis, diagnosis, and treatment. This review analyzes the latest research to provide insight into the presentation, pathophysiology, diagnosis, and management of TCM. [ABSTRACT FROM AUTHOR]

Kounis or allergic vasospastic angina has been described after exposure to several foods, drugs, and insect bites and stings. Mast cell degranulation during a hypersensitivity allergic or anaphylactic reaction leads to inflammatory mediators causing coronary spasm and thrombosis. A 44-year-old female with no comorbidities presented with sweating, dizziness, rashes, chest tightness, and epigastric discomfort 1 h after oral amoxicillin clavulanate. Electrocardiogram (ECG) showed ST segment changes along with elevated troponin I. Suspecting Kounis syndrome, she was administered pheniramine maleate, hydrocortisone, and oral antiplatelets along with intravenous fluids. Chest tightness was better, and ECG improved in 60 min. Since systemic adrenaline was to be avoided for fear of coronary vasospasm, for airway edema, nebulized adrenaline was administered. She recovered completely and was discharged after 48 h. This case highlights coronary vasospasm during an ongoing allergic reaction and its management with antihistamines, steroids, and antiplatelet drugs. Nebulized adrenaline was safely given with ECG monitoring for airway edema. [ABSTRACT FROM AUTHOR]

Background: Coronary artery thrombosis and myocardial ischemia caused by giant coronary aneurysms are the main causes of death in children with Kawasaki disease. The use of thrombolytic therapy in children with Kawasaki disease who have coronary thrombosis is a controversial topic, especially with respect to the timing of treatment. Case presentation: In this article, we report a case of a child aged two years and nine months with Kawasaki disease whose coronary arteries had no involvement in the acute phase. However, by only one week after discharge, the patient returned because we found giant coronary aneurysms complicated by thrombosis via echocardiography. Despite aggressive thrombolytic therapy, the child developed myocardial ischemia during thrombolytic therapy. Fortunately, because of timely treatment, the child's thrombus has dissolved, and the myocardial ischemia has resolved. Conclusions: This case suggests that for patients at high risk of coronary artery aneurysms, echocardiography may need to be reviewed earlier. Low-molecular-weight heparin should be added to antagonize the early procoagulant effects of warfarin when warfarin therapy is initiated. In the case of first-detected coronary thrombosis, aggressive thrombolytic therapy may be justified, particularly during the acute and subacute phases of the disease course. [ABSTRACT FROM AUTHOR]

High-risk coronary plaques (HRP) are characterized in clinical radiological imaging by the presence of low plaque attenuation, a napkin-ring sign (NRS), spotty calcifications (SC) and a positive remodeling index (RI). To evaluate if these signs are detectable in postmortem imaging by a multi-phase postmortem CT angiography (MPMCTA), a retrospective study of a series of autopsy well-documented coronary plaques related to sudden cardiac death (SCD) was performed. Then correlations between histological and radiological findings were described. Fourty SCD cases due to acute coronary syndrome based on clinical history and confirmed at autopsy were selected (28 men and 12 women, age 53.3 ± 10.9). The culprit lesion was mainly situated in the proximal segments of coronary arteries, in the right coronary artery in 23 cases (57.5%), the left anterior descending artery in 13 cases (32.5%), the circumflex artery in 3 cases (7.5%) and in one case in the left main stem. MPMCTA showed a positive RI (≥ 1.1) in 75% of cases with a mean RI 1.39 ± 0.71. RI values were lower in cases with fibrotic plaques. NRS was observed in 40% of cases, low attenuation plaque in 46.3%, and SC in 48.7% of cases. There were significant correlations of the radiological presence of NRS for fibrolipid composition of the plaque (p-value 0.007), severe intraplaque inflammation (p-value 0.017), severe adventitial inflammation (p-value 0.021) and an increased vasa vasorum (p-value 0.012). A significant correlation (p-value 0.002) was observed between the presence of SC at radiological examination and the presence of punctuate/fragmented calcification at histology. In addition, in 58.3% of cases, plaque enhancement was observed, which correlated with plaque inflammation and the fibrolipid composition of the plaque. The coronary artery calcium score was 314 (± 455). There was a poor agreement between stenosis of the lumen at histology versus radiology. Our study shows that the various radiological signs of HRP can be detected in all plaques by MPMCTA, but individually only to a variable extent; plaque enhancement appeared as a new sign of vulnerability. In the postmortem approach, these radiological markers of HRP, should always be applied in combination, which can be useful for developing a predictive model for diagnosing coronary SCD. [ABSTRACT FROM AUTHOR]

Background: Respiratory infections were found to be connected with the incidence of acute coronary syndrome (ACS). The proposed pathway of this connection includes inflammation, oxidative stress, pro-coagulation, and atherosclerotic plaque destabilization. This can cause rapture and thrombus formation, leading to ACS. Our study aimed to assess the risk factors for coronary artery thrombosis as a manifestation of ACS and for lower respiratory tract infections (LRTIs) in patients with ACS. Methods: The study included 876 patients with ACS from January 2014 to December 2018. Both the clinical data and air pollution data were analyzed. Statistical tests used for analysis included Student's t-test, the Mann–Whitney U-test, the Chi-squared test, and the odds ratio Altman calculation. Results: LRTIs were found in 9.13% patients with ACS. The patients with LRTI had a higher risk of coronary artery thrombosis (OR: 2.4903; CI: 1.3483 to 4.5996). Moreover, they had increased values of inflammatory markers, were older, had a lower BMI, and a higher rate of atrial fibrillation. The average atmospheric aerosols with a maximum diameter of 2.5 μm (PM2.5 concentration) from three consecutive days before hospitalization for ACS were higher in patients with LRTI. Conclusions: The occurrence of coronary artery thrombosis was higher among the patients with LRTI during ACS. PM2.5 exposition was higher in the three consecutive days before hospitalization in patients with LRTI during ACS. [ABSTRACT FROM AUTHOR]

Objective: To verify the administration of a new nano delivery system coated with Tirofiban on preventing early thrombosis in vein graft. Methods: Forty New Zealand white rabbits were randomly divided into five groups with eight rabbits in each group. The rabbits of all groups underwent jugular vein transplantation, except group I with only neck opening and closing operation. Vein grafts of group II were preprocessed by intravenous injection of normal saline; group III were preprocessed by tirofiban alone; group IV were preprocessed by unloaded nanoparticles of PLGA-PEG; group V were preprocessed by PLGA-PEG coated with tirofiban. Coagulation and platelet function of peripheral and vein graft blood were detected at 1, 2, 4, 12 h and 1, 3, 7, 10, 14 days after operation. Patency rate of vein graft and blood flow index were measured by vascular ultrasound at third, seventh, 10th, and 14th days after operation; two rabbits in each group were randomly sacrificed at the corresponding time of detection. Pathological differences of vein grafts were observed by HE stainin. Results: The patency rate of vein grafts in group V was significantly higher than that in group II to IV. The platelet and platelet aggregation rate in group V were inhibited in vein graft blood significantly. The post-operative PT and APTT in vein graft blood in group V were increased obviously while the FBG, D-dimer and FDP were significantly inhibited. Except group I, the lumen loss rate of vein grafts in group V was significantly lower than that in other groups, and vein graft blood in group V had a significant lower expression of platelet P-selectin and GP IIb/IIIa receptor than that in other groups. Conclusion: This study proves that PEG-PLGA coated with tirofiban can effectively prevent early vein graft stenosis from thrombosis by inhibition of platelet function, coagulation function. [ABSTRACT FROM AUTHOR]

Background Amyloidosis can affect the heart, causing arrhythmia, thromboembolic events, and sudden cardiac death. Coronary sinus thrombosis is an uncommon though life-threatening condition which requires early identification and management. Case summary A 72-year-old Caucasian man, who recovered from out-of-hospital cardiorespiratory arrest, was diagnosed with coronary sinus thrombosis using cardiac imaging techniques. He had no history of invasive procedures and was diagnosed with cardiac amyloidosis based on an extra-cardiac biopsy positive for light chain amyloid, with consistent clinical, echocardiographic, and magnetic resonance criteria. Discussion A high frequency of intracardiac thrombosis is seen in amyloidosis. However, coronary sinus thrombosis is an uncommon complication. A multimodality imaging approach appears to be useful for the early diagnosis of coronary sinus thrombosis. The low specificity of the clinical signs, as well as the fast impairment of the patients, could result in fatal complications such as acute myocardial infarction, arrhythmia, and sudden death. Early screening, particularly in high-risk patients, as well as the use of early anticoagulant therapy, could reduce the associated morbidity and mortality. [ABSTRACT FROM AUTHOR]

Introduction: Cardiac arrests are traditionally classified according to the setting in which they occur, including out-of-hospital cardiac arrest (OHCA) and in-hospital cardiac arrest (IHCA). However, cardiac arrests that occur in the emergency department (EDCA) could constitute a third category, due to the peculiar characteristics of the emergency department (ED). In recent years, the need to study EDCAs separately from other intra-hospital events has emerged. The aim of this study was to describe the characteristics and outcomes of a cohort of patients experiencing EDCA in an Italian hospital over a 14-year period. Methods: This was a single-centre retrospective observational study conducted in the ED of the Santa Croce e Carle Hospital in Cuneo, Italy. All adult patients who experienced EDCA between 1 January 2010 and 30 June 2023 were included. OHCA patients, those arriving in the ED with on-going resuscitation measures, patients with EDCA not undergoing resuscitation, and patients with post-traumatic cardiac arrest were excluded from the study. The main outcome of the study was survival at hospital discharge with a favourable neurological outcome. Results: 350 cases of EDCA were included. The median age was 78 (63–85) years, and the median Charlson Comorbidity Index score was 5 (3–6). A total of 35 patients (10%) survived to hospital discharge with a cerebral performance category (CPC) Score of 1–2; survival in the ED was 28.3%. The causes of cardiac arrests were identified in 212 cases (60.6%) and included coronary thrombosis (35%), hypoxia (22%), hypovolemia (17%), pulmonary embolism (11%), metabolic (8%), cardiac tamponade (4%), toxins (2%) and hypothermia (1%). Variables associated with survival with a favourable neurological outcome were young age, a lower Charlson Comorbidity Index, coronary thrombosis as the primary EDCA cause, and shockable presenting rhythm; however, only the latter was associated with the outcome in a multivariate age-weighted model. Conclusions: In a cohort of patients with EDCA over a period of more than a decade, the most frequent cause identified was coronary thrombosis; 10% of patients survived with a good neurological status, and the only factor associated with the best prognosis was presenting a shockable rhythm. EDCA should be considered an independent category in order to fully understand its characteristics and outcomes. [ABSTRACT FROM AUTHOR]

The blood glucose level at admission indicates (with some limitations) poor prognosis and thrombus burden in patients with the acute coronary syndrome (ACS). Our study aimed to measure the predictive value of the stress hyperglycemia ratio (SHR), an indicator of stress hyperglycemia, showing increased thrombus burden in patients with ACS. Patients (n = 1222) with ACS were enrolled in this cross-sectional study. Coronary thrombus burden was classified as high and low. SHR was calculated by dividing the admission serum glucose by the estimated average glucose derived from HbA1c. Low thrombus burden was detected in 771 patients, while high thrombus burden (HTB) was detected in 451 patients. SHR was found to be significantly higher in patients with HTB (1.1 ±.3 vs 1.06 ±.4; P =.002). SHR was determined as a predictor of HTB (odds ratio (OR) 1.547 95% CI (1.139–2.100), P <.001) as a result of univariate analysis. According to multivariate analysis, SHR was determined as an independent risk factor for HTB (OR 1.328 CI (1.082–1.752), P =.001). We found that SHR predicted thrombus burden with higher sensitivity than admission glucose level in patients with ACS. [ABSTRACT FROM AUTHOR]

This article explores the role of electrocardiograms (ECGs) in diagnosing and localizing occlusions in the coronary arteries during acute myocardial infarction (heart attack). The study involved 112 patients and found that ECG criteria, such as ST segment elevation and depression in specific leads, can accurately predict the location of the occlusion. The results highlight the importance of ECGs in determining the need for early reperfusion therapy and assessing the extent of myocardial injury. The study's findings align with previous research in this area. [Extracted from the article]

Background ST elevation myocardial infarctions are usually a consequence of the occlusion of a single coronary artery, but in 2.5% of the cases, two or more culprit lesions are found. Simultaneous coronary artery occlusion is a potentially life-threatening condition that leads to cardiogenic shock or ventricular arrhythmias. Case summary We presented the case of a 74-year-old man presenting with chest pain and ST segment elevation (STE) in inferior leads and evidence of alternating STE in anterior leads in a pattern like Wellens syndrome type A in subsequent electrocardiogram (ECGs). Emergency coronary angiography (CA) revealed thrombotic occlusion of the proximal right coronary artery (RCA) and sub-occlusion of mid left anterior descending artery (LAD). During the CA, he became haemodynamically unstable requiring intravenous inotropes and vasopressors, and he underwent primary percutaneous coronary intervention of both RCA and LAD culprit lesions. His subsequent hospital stay was uneventful, and he was discharged 5 days later. Discussion ST elevation myocardial infarction with more than one culprit coronary artery is a rare but at high risk of haemodynamic decompensation. The causes of occlusion of multiple coronary arteries may be several: coronary embolism, coronary ectasia, simultaneous plaque disruption, coronary vasospasm, hypercoagulability states, smoking, and illicit drug abuse. The presumed mechanism behind the presented case may be a combination of release of pro-thrombotic cytokines due to the thrombotic occlusion of the first coronary and low output state secondary to myocardial dysfunction leading to impaired flow in a severe stenotic coronary artery with subsequent thrombosis. [ABSTRACT FROM AUTHOR]

As the important factors in coronary artery thrombosis, endothelial injury and M1 macrophage polarization are closely related to the expression of miR-34a-5p. Exosomes in plasma are mainly derived from platelets and play an important role in thrombosis. Based on these facts, this study was conducted to investigate the acting mechanism of platelet-derived exosomes (PLT-exo) in the effects of endothelial injury and M1 macrophage polarization on coronary artery thrombosis. Firstly, rats were divided into the sham-operated group and the coronary microembolization (CME) group, and their plasma-derived exosomes were extracted to detect the expression of miR-34a-5p. Next, the PLT-exo were extracted from healthy volunteers and then co-cultured with ox-LDL-induced endothelial cells and LPS-induced macrophages, respectively. Subsequently, the expression of IL-1β, IL-6, TNF-α, and ICAM-1 in endothelial cells was measured, and the level of markers related to M1 macrophage polarization and Sirt1/NF-κB pathway was detected. Finally, the above indicators were examined again after PLT-exo combined with miR-34a-5p mimic were co-cultured with endothelial cells and macrophages, respectively. The results demonstrated that the expression of miR-34a-5p in the CME group was up-regulated compared with the sham-operated group. In cell experiments, PLT-exo modulated the Sirt1/NF-κB pathway by inhibiting the expression of intracellular miR-34a-5p and down-regulated the expression of IL-1β, IL-6, TNF-α, and ICAM-1 in endothelial cells and M1 macrophage polarization. After the transfection with miR-34a-5p mimic, endothelial cell inflammatory injury and M1 macrophage polarization increased to varying degrees. In conclusion, PLT-exo can alleviate coronary artery thrombosis by reducing endothelial cell inflammation and M1 macrophage polarization via inhibiting miR-34a-5p expression. In contrast, miR-34a-5p overexpression in PLT-exo may exacerbate these pathological injuries in coronary artery thrombosis. [ABSTRACT FROM AUTHOR]

BACKGROUND: Cardiovascular disease (CVD) is a global health challenge. Various studies have shown that genetic and environmental factors play roles in the development and progression of CVD. Small non-coding RNAs, namely microRNAs (miRs), regulate gene expression and have key roles in essential cellular processes such as apoptosis, cell cycle, differentiation, and proliferation. Currently, clinical studies highlight the critical role of platelets and miRs in coronary thrombosis, atherosclerosis, and CVD. METHODS: Using search engines such as PubMed and Scopus, articles studying platelet miRs and their effects on atherosclerosis and cardiovascular disease were reviewed. RESULTS: This article presents a comprehensive analysis of the association of platelet- related miRs as prognostic, diagnostic, and therapeutic biomarkers with the pathogenesis of atherosclerosis and cardiovascular disease. CONCLUSION: Taken together, data show that platelet-related miRs not only play important roles in the initial development of atherosclerosis and cardiovascular disease (CVD), but they are also considered prognostic and diagnostic biomarkers in CVD. [ABSTRACT FROM AUTHOR]

Background Myocardial infarction (MI) in a patient with immune thrombocytopenia is a rare scenario which is very challenging to manage. Case summary We present a rare case of a patient with immune thrombocytopenic purpura who developed double territory segment-elevation MI with cardiogenic shock. She had an extremely rare presentation with a fresh mobile thrombus in the aortic root which was trap-dooring the right coronary artery ostium and extending into the artery with an embolism into the distal left anterior descending artery. We managed this patient conservatively with excellent recovery owing to the dangerous location of the hanging thrombus, and severe thrombocytopenia. Conclusions Multidisciplinary approach is required for the management of MI in patients with pre-existing blood disorders, with therapy tailored to the patient's presentation and treatment requirements. [ABSTRACT FROM AUTHOR]

Background. Recombinant plasminogen activator (r-PA) consists of the Kringle-2 and protease domains of human tissue-type plasminogen. It is used clinically to treat coronary artery thrombosis and acute myocardial infarction. However, the expression and production of reteplase (r-PA) are limited due to its susceptibility to proteolysis during manufacturing processes. Therefore, efforts have been made to address this limitation. Materials and methods. To enhance the conformational stability of r-PA and increase its resistance to proteolysis, we used Gly 6 Ala substitutions in the Kringle-2 domain through in silico. We created an in silico mutant collection with eight structures, incorporating four designated mutations (R103S, G39A, G53A, and G55A). Using MODELLER software and homology modeling, we developed three-dimensional structures for two Kringle-2 and tissue plasminogen activator protease domains, including the wild noncleavable form (R103S) and mutants with all four designated mutations. We assessed protein stability using a dynamic cross-correlation matrix by extracting global properties such as Root Mean Square Deviation (RMSD) and Root Mean Square Fluctuation (RMSF) from trajectory files. Results. The findings revealed that a single glycine--alanine substitution (G39A) enhanced the conformational stability of r-PA, as evidenced by improvements in RMSD, RMSF, radius of gyration, surface accessibility, hydrogen bond formation, eigenvector projection, and density analysis. Conclusion. The conformational stability of r-PA conferred by glycine replacement with alanine may decrease the propensity for proteolysis in protease -- rich environments across various recombinant systems and potentially enhance its production and expression levels. [ABSTRACT FROM AUTHOR]

Cancer patients face a heightened risk for thromboembolic events, including arterial thromboembolism such as myocardial infarction (MI). Thrombosis is a major cause of mortality in these patients due to the hypercoagulable state induced by malignancy and its treatments. Pro-inflammatory cytokines and pro-coagulants secreted by tumor cells lead to endothelial damage and an increased risk of thrombus formation. Despite extensive research on venous thromboembolism in cancer, arterial thromboembolism remains less studied. This case report highlights an acute anterior wall MI in a patient with metastatic gallbladder cancer, who developed a sudden thrombotic event despite having a normal coronary angiogram shortly before. A 52-year-old female with metastatic gallbladder cancer presented to the emergency department with acute chest pain. Her cancer, diagnosed 6 months earlier, had been managed with cholecystectomy and subsequent chemotherapy. Fifteen days before her current admission, she had undergone a coronary angiogram due to atypical chest pain, which showed no significant coronary artery disease. At presentation, the patient reported, sudden chest pain radiating to the left arm. She was hemodynamically stable with normal blood pressure and heart rate. The physical examination was unremarkable. Electrocardiogram segment elevation (ST)-segment elevation in anterior leads (V2-V6) and limb leads (II, II, and augmented vector foot [aVF]), indicative of an acute anterior wall MI. Elevated cardiac biomarkers confirmed myocardial injury. A two-dimensional echocardiogram showed mild hypokinesia of the distal interventricular septum and the apex. A repeat coronary angiogram identified a thrombus in the left anterior descending artery, which was not present in the previous angiogram. The rapid appearance of the thrombus pointed to an acute thrombotic event. This case illustrates the aggressive nature of thrombotic events in cancer patients. Despite a normal angiogram 2 weeks prior, the patient developed a sudden coronary thrombus, reflecting the hypercoagulable state associated with malignancy. The management involved thrombus aspiration and tirofiban, which effectively resolved the acute event. This aligns with existing literature, emphasizing the need for vigilant monitoring and proactive management in cancer patients to address the risk of rapid-onset thrombotic events. Cancer patients can experience sudden and severe thrombotic events, even with recent normal coronary evaluations. This case highlights the importance of ongoing cardiovascular assessment and tailored therapeutic strategies in managing cancer-associated thrombosis, underscoring the need for a collaborative approach between oncologists and cardiologists. [ABSTRACT FROM AUTHOR]

Clopidogrel is the most widely used P2Y12 receptor inhibitor (P2Y12i) as a part of dual antiplatelet therapy along with aspirin. Clopidogrel is a pro‑drug and is metabolized to its active metabolite by the hepatic enzyme cytochrome P4502C19 (CYP2C19). This active metabolite is responsible for the antiplatelet action of clopidogrel. Recent studies have demonstrated that single nucleotide polymorphisms in the CYP2C19 gene, including CYP2C19*2,*3,*4, and *5 alleles, result in reduced production of the active metabolite of clopidogrel, and hence reduced inhibition of platelet aggregation. This in turn enhances the incidence of stent thrombosis and recurrent cardiovascular (CV) events. We report a case of coronary stent thrombosis due to clopidogrel resistance proven by CYP2C19 genotyping. We then review the literature on clopidogrel resistance and its impact on CV outcomes. Subsequently, we discuss the methods of diagnosis of resistance, evidence from clinical trials for tailoring clopidogrel therapy, the role of potent P2Y12 inhibitors, the current guidelines, and future directions. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases, among which includes coronary artery disease, represent one of the most important causes of mortality and morbidity worldwide. Research aimed at determining the risk factors involved recognizes a group of "traditional" risk factors, but also more recent studies identified over 100 "novel" ones which may have a role in the disease. Among the latter is the thrombophilia profile of a patient, a pathology well-established for its involvement in venous thromboembolism, but with less studied implications in arterial thrombosis. This paper reviews the literature, explaining the pathophysiology of the thrombophilia causes associated most with coronary thrombosis events. Results of several studies on the subject, including a meta-analysis with over 60,000 subjects, determined the significant involvement of factor V Leiden, prothrombin G20210A mutation, plasminogen activator inhibitor–1 and antiphospholipid syndrome in the development of coronary artery disease. The mechanisms involved are currently at different stages of research, with some already established and used as therapeutic targets. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to investigate the association between coronavirus disease-2019 (COVID-19) vaccination and stent thrombosis in patients with coronary stents. Material and Methods: This was a retrospective study conducted between January 2021 and December 2022. The study included patients with existing coronary stents who underwent coronary angiography for suspicion of stent thrombosis. A broad range of clinical data, including COVID-19 related data (disease history, number and brand of COVID-19 vaccinations), laboratory findings, follow-up time, and mortality data were obtained retrospectively. The endpoints of the study were coronary stent thrombosis and all-cause mortality. Results: A total of 969 patients were included in the study. Stent thrombosis was present in 538 patients (55.52%), who were significantly younger and had a higher proportion of males compared to those without stent thrombosis. Multivariable logistic regression revealed active smoking, hypertension, diabetes mellitus, and coronary artery bypass graft+stent history as being independently associated with higher risk for stent thrombosis. Whereas, anticoagulant use and receiving 4 or more vaccine doses were independently associated with lower likelihood of stent thrombosis. Diabetes mellitus, previous cerebrovascular disease, high urea, and stent thrombosis were independently associated with mortality; whereas hyperlipidemia and receiving the BioNTech vaccine were independently associated with lower risk for mortality. Conclusion: Receiving multiple COVID-19 vaccine doses (regardless of type) may reduce the likelihood of stent thrombosis, possibly by protecting against COVID-19. However, more research is needed to understand the potential pathophysiological links between COVID-19 vaccination and coronary stent thrombosis. [ABSTRACT FROM AUTHOR]

The present study investigated the relationship between pre-procedural radial intima-media thickness (rIMT) and radial artery thrombosis (RAO) in patients undergoing angiography using a transradial approach (TRA). Patients (n = 90) who underwent cerebral or peripheral arterial angiography using TRA were included in the study. Ultrasonographic evaluation was performed before and 12 h after the procedure. Preoperative rIMT measurement was performed at the distal radial artery. Presence of radial artery occlusion was evaluated by ultrasonography after radial catheterization and revealed occlusive thrombus in the radial artery in 13 patients. rIMT was found to be statistically significantly higher in patients with thrombus (P <.05). When it was evaluated whether there was a correlation between age and rIMT, a positive significant correlation was found (P <.01). Our study suggests that increase of rIMT may be a risk factor for RAO in the intervention area. Before the procedure, ultrasound (US) assessment of the radial artery may be useful in determining the risk of occlusion. Thus, RAO-related technical risk factors (procedure time, number of punctures, sheath thickness, etc.) can be managed more carefully in patients having radial angiography. [ABSTRACT FROM AUTHOR]

High-grade intracoronary thrombus (ICT) burden leads to greater myocardial injury following anterior myocardial infarction (MI). The modified Glasgow prohgnostic score (mGPS) is a novel immune-inflammatory index, calculated by using C-reactive protein (CRP) and albumin levels, was shown to have prognostic value in heart diseases. The present study investigated the role of mGPS in predicting high grade ICT in patients with acute anterior MI admitted between February 2017 and March 2020. Blood samples were obtained at admission and mGPS was calculated. The ICT burden was evaluated visually from angiographic images. Patients were divided into 2 groups according to the ICT burden as high and low. A total of 1132 patients were enrolled: a mean age 61 ± 12.4 years and 370 males (32.7%). Serum albumin was lower, whereas mGPS and CRP were higher in high grade ICT group. CRP (odds ratio (OR): 1.404 95% CI: 1.312–1.502; P <.001), albumin (OR:.486; 95% CI:.301–.782 P <.001), and mGPS (0 vs ≥ 1) (OR: 7.391; 95% CI: 3.910–13.972; P <.001) were independent predictors of high-grade ICT burden in the left anterior descending coronary artery. The mGPS is a novel predictor of high-grade ICT burden and may be useful for risk stratification in patients with acute anterior MI. [ABSTRACT FROM AUTHOR]

The complement is a crucial factor of the innate immune system. However, its activation can lead to various diseases, so it needs to be controlled. In mammals, surface-bound complement regulatory proteins safeguard cells from uncontrolled complement-mediated lysis. One of the human complement regulators is CD55, also known as the decay-accelerating factor (DAF), a single-chain, type I cell surface protein anchored to glycosylphosphatidylinositol (GPI). The genetic loss of the complement regulatory protein CD55 leads to a fatal illness known as CHAPLE disease. The complement and innate immunity become hyperactive in this disease, causing angiopathic thrombosis and protein-losing enteropathy. Patients with CHAPLE disease experience abdominal pain, nausea, vomiting, diarrhea, loss of appetite, weight loss, impaired growth, and swelling. This genetic condition has no known cure, and managing its symptoms can be challenging. Pozelimab, a human monoclonal immunoglobulin IgG4 antibody, is a drug that targets the terminal complement protein C5. The drug has a high affinity for both wild-type and variant human C5. Pozelimab has received designations such as fast track, orphan drug, and rare pediatric disease, making it a significant medical breakthrough. It is currently the only available treatment for this disease. In this review, we have summarized the preclinical and clinical data on pozelimab. [ABSTRACT FROM AUTHOR]

Background Kawasaki disease (KD) is a paediatric multi-system vasculitis. Mainly, the coronary arteries become affected due to acute inflammation and formation of coronary artery aneurysms (CAAs) may occur. As the size of the CAA increases, so does the risk of clinical complications and serious cardiac outcomes. These patients may experience life-threatening thrombotic coronary artery occlusion and myocardial ischaemia unless antiplatelet and anticoagulation therapy is not initiated in a timely manner. 1 Case summary This case report presents a 12-year-old patient with KD who developed CAAs in two coronary arteries despite initial administration of intravenous immunoglobulins and acetylsalicylic acid, followed by extensive thrombosis of both coronary arteries, although antithrombotic therapy was started after the diagnosis of CAAs. Discussion Our case is notable because of the severity of the clinical manifestation despite the administration of antiplatelet agents and anticoagulants. It could be speculated that the development of coronary thrombosis in this case might be strongly correlated with the late initiation of oral anticoagulation. The high-quality images of the affected coronary arteries in such a young patient could be of educational value. [ABSTRACT FROM AUTHOR]

Strenuous exercise may occasionally cause coronary thrombosis with myocardial infarction and sudden cardiac death. Patients with stable coronary artery disease (CAD) (n = 164) and healthy individuals (n = 25) performed strenuous exercise on a bicycle ergometer. Blood was drawn at baseline, immediately after exercise and 2 h later. Platelet aggregation was measured with Multiplate® Analyzer. Thrombin generation was determined using a thrombogram and by measuring prothrombin fragment 1 + 2 (F1 + 2). A clot lysis assay was used to investigate fibrinolysis. From baseline to immediately after exercise, thrombin receptor activating peptide (TRAP)-induced platelet aggregation increased in CAD patients (Δ77 AU × min, 95 % confidence interval (CI): 46;107) and in healthy individuals (Δ153 AU × min, 95%CI: 75;232). Endogenous thrombin potential (ETP) was unaffected by exercise, whilst F1 + 2 increased (Δ17%, 95%CI: 11;24) in CAD patients. Fibrin clot lysis time increased by 9 % (95%CI: 1–17) in CAD patients and by 26 % (95%CI: 8;45) in healthy individuals. When comparing baseline to 2 h post-exercise, TRAP-induced platelet aggregation remained slightly elevated in both CAD patients (Δ53 AU × min, 95%CI: 22;84) and healthy individuals (Δ140 AU × min, 95%CI: 62;219). In contrast, ETP and F1 + 2 decreased in CAD patients (Δ-6 %, 95%CI: −10;-1 and Δ-8 %, 95%CI: -14;-2). Moreover, clot lysis time decreased (Δ-19 %, 95%CI: −27;-11) in patients with CAD and returned to baseline in healthy individuals. All p -values were <0.05. Platelet aggregation and F1 + 2 were substantially elevated immediately after exercise in CAD patients, indicating a pro-thrombotic state. After 2 h of recovery, they exhibited a markedly increase in fibrinolysis. Similar results were observed in healthy individuals. • Acute strenuous exercise may occasionally induce coronary thrombosis. • Immediately after strenuous exercise, CAD patients were in a pro-thrombotic state. • Two hours after strenuous exercise, CAD patients were in a pro-fibrinolytic state. [ABSTRACT FROM AUTHOR]

Introduction: There is limited information regarding the clinical and angiographic characteristics and outcomes of patients with Coronavirus disease 2019 (COVID-19) presenting with ST segment elevation myocardial infarction (STEMI). The aim of this study was to describe the clinical and angiographic characteristics, as well as clinical outcomes, in COVID-19 positive patients with STEMI compared with COVID-19 negative STEMI patients. Methods: This was a single-center observational study conducted between May 2020 and May 2021. The study population consisted of 35 patients who were followed with active COVID-19 and diagnosed with STEMI, and 35 STEMI patients without COVID-19 infection. Results: Groups were similar in terms of gender, hypertension, obstructive airway disease, SYNTAX score, and localization of myocardial infarction (MI). Glucose levels, BUN, creatinine, and CRP levels were significantly higher in the COVID-19 group. LDL and hemoglobin levels were lower in the COVID-19 group (p<0.05). There was a positive correlation between in-hospital death and modified thrombus grade post-first device and a negative correlation between in-hospital death and post-procedural TIMI flow (p=0.001, r=0.480). Discussion and Conclusion: Our results demonstrate that patients presenting with STEMI and concurrent COVID-19 infection have a higher post-procedural thrombus burden and worse Thrombolysis in Myocardial Infarction (TIMI) flow. STEMI patients with COVID-19 face procedural challenges and are associated with poorer clinical outcomes. [ABSTRACT FROM AUTHOR]