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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]

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]

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]

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]

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]

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: 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]

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 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]

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]

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]

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. 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]

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]

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]

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]

The emergence of SARS-CoV2 has presented itself as a significant global health crisis. The prevalence of thrombotic events is known to be high in these patients, affecting various organ systems, sometimes leading to cutaneous thrombosis, pulmonary embolism (PE), stroke, or coronary thrombosis. The available evidence suggests that thromboembolism, hypercoagulability, and the excessive production of proinflammatory cytokines play a significant role in the development of multiorgan failure. Methodology: This retrospective single-centre study was conducted at "Victor Babes" University of Medicine and Pharmacy from Timisoara, Romania, involving a total of 420 patients diagnosed with COVID-19. We separated them into a CONTROL group that included 319 patients, and an intervention group (PE) with 101 patients that, subsequent to infection with the virus, developed pulmonary embolism. The study included the reporting of demographic data, laboratory findings, and comorbidities. Results: Out of a total of 420 patients, 24% experienced pulmonary embolism, while 21.42% died. Arterial thrombotic events were found to be associated with factors such as age, cardiovascular disease, levels of white blood cells, D-dimers, and albumin in the blood. The findings of the study indicate that there is an independent association between pulmonary thrombosis and hypertension (odds ratio (OR): 1.1; 95% confidence interval (CI): 0.7 to 1.7; p = 0.6463), cancer (OR: 1.1; 95% CI: 0.6 to 2.3; p = 0.6014), and COPD (OR: 1.2; 95% CI: 0.6 to 2.3; p = 0.4927). On the other hand, there is a stronger correlation between PE and obesity (OR: 2.8; 95% CI: 1.7 to 4.6; p < 0.0001), diabetes (OR: 3.3; 95% CI: 2 to 5.3; p < 0.0001), and dyslipidemia (OR: 3.6; 95% CI: 2.3 to 5.8; p < 0.0001) in a multivariable regression logistic model. Conclusions: Patients diagnosed with severe forms of COVID-19 display a comparable incidence of arterial thrombotic events, which have been linked to poor survival rates. [ABSTRACT FROM AUTHOR]

Background: Most common cause of sudden cardiac death is coronary artery disease, which contributes to 75 to 90%. The present study is undertaken to describe the profile of autopsy cases of coronary artery disease. Methods: Descriptive cross-sectional study was conducted in all cases of sudden and unexpected death brought for autopsy a tertiary level centre in southern Kerala during a period of one year. Gross and microscopical examination of heart and coronary arteries were studied and in cases with coronary artery disease, associated factors like previous history of illness, personal habits, family history of illness, body mass index, abdominal circumference, horizontal earlobe crease were described in detail. Categorical variables were represented as frequency and percentage, continuous variables as mean and standard deviation and association was tested using Chi square test. Conclusions: Statistically significant association (p value = 0.001) was observed between the horizontal earlobe crease and occlusive coronary artery disease. No significant association was obtained between the obesity parameters like body mass index, waist to hip ratio and occlusive coronary artery disease. Majority of the cases with significant occlusion was observed in the left anterior descending artery. The most common site of thrombus was in the proximal third of left anterior descending artery. [ABSTRACT FROM AUTHOR]

The article presents a case report of a 55-year-old man who experienced cardiac arrest, cardiogenic shock, and hypoxemia. Topics include the patient's presentation after out-of-hospital cardiac arrest, initial management including defibrillation and intravenous medications, and subsequent complications such as acute respiratory failure and the need for mechanical ventilation and percutaneous left ventricular assist device (LVAD) support.

• Neutrophil extracellular traps (NET) formation in coronary thrombi did not correlate with markers of NETs in serum from patients with STEMI. • NET formation in coronary thrombi did not correlate with circulating inflammatory markers in patients with STEMI. • NET formation in coronary thrombosis could be a local phenomenon not detectable in the bloodstream. [ABSTRACT FROM AUTHOR]

Objectives: To evaluate the diagnostic utility of multiphase postmortem CT angiography (PMCTA) to detect plaque enhancement as a surrogate marker of inflammation, using fatal coronary plaques obtained from autopsies following sudden cardiac death. Methods: In this retrospective study, we included 35 cases (12 women, 34%; median [IQR] age, 52 [11] years), with autopsy-proven coronary thrombosis, histological examination, and multiphase PMCTA. Two radiologists blinded towards histological findings assessed PMCTA for plaque enhancement of the culprit lesion in consensus. Two forensic pathologists determined the culprit lesion and assessed histological samples in consensus. Cases with concomitant vasa vasorum density increase and intraplaque and periadventital inflammation were considered positive for plaque inflammation. Finally, we correlated radiology and pathology findings. Results: All 35 cases had histological evidence of atherosclerotic plaque disruption and thrombosis; 30 (85.7%) had plaque inflammation. Plaque enhancement at multiphase PMCTA was reported in 21 (60%) and resulted in a PPV of 95.2% (77.3–99.2%) and an NPV of 28.6% (17–43.9%). Median histological ratings indicated higher intraplaque inflammation (p =.024) and vasa vasorum density (p =.032) in plaques with enhancement. We found no evidence of a difference in adventitial inflammation between CT-negative and CT-positive plaques (p =.211). Conclusions: Plaque enhancement was found in 2/3 of fatal atherothrombotic occlusions at coronary postmortem CT angiography. Furthermore, plaque enhancement correlated with histopathological plaque inflammation and increased vasa vasorum density. Plaque enhancement on multiphase CT angiography could potentially serve as a noninvasive marker of inflammation in high-risk populations. Clinical relevance statement: Phenotyping coronary plaque more comprehensively is one of the principal challenges cardiac imaging is facing. Translating our ex vivo findings of CT-based plaque inflammation assessment into clinical studies might help pave the way in defining high-risk plaque better. Key Points: • Most thrombosed coronary plaques leading to fatality in our series had histological signs of inflammation. • Multiphase postmortem CT angiography can provide a noninvasive interrogation of plaque inflammation through contrast enhancement. • Atherosclerotic plaque enhancement at multiphase postmortem CT angiography correlated with histopathological signs of plaque inflammation and could potentially serve as an imaging biological marker of plaque vulnerability. [ABSTRACT FROM AUTHOR]

Objective. Primary percutaneous coronary intervention (PCI) is the best treatment for acute ST-elevation myocardial infarction (STEMI). Evidence is in favor of ticagrelor over clopidegrel in STEMI patients regarding the reduction of stent thrombosis risk during and after PCI. We compared initial thrombolysis in myocardial infarction (TIMI) flow in STEMI patients on ticagrelor vs. clopidogrel. Methods. This prospective cohort recruited 160 patients with acute STEMI, referred to the emergency department of Farshchian Heart Center, during March 2018–2019. Before angiography, the patients received clopidogrel (600 mg) or ticagrelor (180 mg) on top of aspirin. Initial TIMI flow was compared between the two groups as the primary outcome. A logistic regression was performed to calculate the predictors of initial TIMI flow. Analyses were performed using R, version 4.2.1. Results. In ticagrelor and clopidogrel groups, the mean ± standard deviation age of the patients was 59.46 ± 13.11 and 61.34 ± 11.08 years (p value = 0.33), respectively. In the ticagrelor and clopidogrel groups, initial TIMI flow grades were as follows: 0 : 50% and 71.2%, I: 26.2% and 16.2%, II: 12.5% and 10%, and III: 12.9% and 2.5%, respectively (p value = 0.005). Final TIMI flow grades were as follows: I: 26.2% and 16.2%, II: 7.5% and 13.8%, and III: 66.3% and 70%, respectively (p value = 0.41). Ticagrelor was associated with significantly higher initial TIMI flow grade compared to the clopidogrel group (adjusted odds ratio: 2.90 (95% CI: 1.51–5.72)). Conclusion. In STEMI patients who were candidates for primary PCI, ticagrelor administration led to a better initial TIMI flow grade compared to clopidogrel. [ABSTRACT FROM AUTHOR]

Aims Coronary microevaginations (CMEs) represent an outward bulge of coronary plaques and have been introduced as a sign of adverse vascular remodelling following coronary device implantation. However, their role in atherosclerosis and plaque destabilization in the absence of coronary intervention is unknown. This study aimed to investigate CME as a novel feature of plaque vulnerability and to characterize its associated inflammatory cell–vessel–wall interactions. Methods and results A total of 557 patients from the translational OPTICO-ACS study programme underwent optical coherence tomography imaging of the culprit vessel and simultaneous immunophenotyping of the culprit lesion (CL). Two hundred and fifty-eight CLs had a ruptured fibrous cap (RFC) and one hundred had intact fibrous cap (IFC) acute coronary syndrome (ACS) as an underlying pathophysiology. CMEs were significantly more frequent in CL when compared with non-CL (25 vs. 4%, P < 0.001) and were more frequently observed in lesions with IFC-ACS when compared with RFC-ACS (55.0 vs. 12.7%, P < 0.001). CMEs were particularly prevalent in IFC-ACS-causing CLs independent of a coronary bifurcation (IFC-ICB) when compared with IFC-ACS with an association to a coronary bifurcation (IFC-ACB, 65.4 vs. 43.7%, P = 0.030). CME emerged as the strongest independent predictor of IFC-ICB (relative risk 3.36, 95% confidence interval 1.67–6.76, P = 0.001) by multivariable regression analysis. IFC-ICB demonstrated an enrichment of monocytes in both culprit blood analysis (culprit ratio: 1.1 ± 0.2 vs. 0.9 ± 0.2, P = 0.048) and aspirated culprit thrombi (326 ± 162 vs. 96 ± 87 cells/mm2, P = 0.017), while IFC-ACB confirmed the accumulation of CD4+ T cells, as recently described. Conclusion This study provides novel evidence for a pathophysiological involvement of CME in the development of IFC-ACS and provides first evidence for a distinct pathophysiological pathway for IFC-ICB, driven by CME-derived flow disturbances and inflammatory activation involving the innate immune system. Trial registration Registration of the study at clinicalTrials.gov (NCT03129503). [ABSTRACT FROM AUTHOR]

Sudden Cardiac Death (SCD) may complicate diseases of the heart and great vessels. The cause is easily visible at the naked eye at autopsy in the presence of coronary thrombosis, aortic dissection, pulmonary thromboembolism, or at the microscope with histological anomalies (inflammation, necrosis, storage, fibrosis). However, there are cases of SCD in which the heart appears normal, both at gross and histological examination. They may present electrocardiogram (ECG) disorders of depolarization and repolarization of myocardial electrical activity (long and short QT, repolarization syndrome) or of electro-mechanical coupling (catecholaminergic ventricular tachycardia), due to alterations of Na+, K+ or Ca++ flows, known as channelopathies. They are genetic, hereditary morbid entities transmitted at the time of conception. Molecular studies of SCD at autopsy include both the detection of viral genomes in inflammatory cardiomyopathies and gene mutations in either structural or nonstructural genetically determined heart diseases. [ABSTRACT FROM AUTHOR]

The relationship between coronavirus disease 2019 (COVID-19) and myocardial injury was established at the onset of the COVID-19 pandemic. An increase in the incidence of out-of-hospital cardiac arrest was also observed. This case report aims to point to the prothrombotic and proinflammatory nature of coronavirus infection, leading to simultaneous coronary vessel thrombosis and subsequently to out-of-hospital cardiac arrest. During the COVID-19 pandemic, a 46-year-old male patient with no comorbidities suffered out-of-hospital cardiac arrest (OHCA) with ventricular fibrillation as the first recorded rhythm. The applied cardiopulmonary resuscitation (CPR) measures initiated by bystanders and continued by emergency medical service (EMS) resulted in the return of spontaneous circulation. The stabilized patient was transferred to the tertiary university center. Electrocardiogram (ECG) revealed "lambda-like" ST-segment elevation in DI and aVL leads, necessitating an immediate coronary angiography, which demonstrated simultaneous occlusion of the left anterior descending (LAD) and right coronary artery (RCA). Primary percutaneous coronary intervention (PCI) with the implantation of one drug-eluting stent (DES) in LAD and two DES in RCA was done. Due to the presence of cardiogenic shock (SCAI C), an intra-aortic balloon pump (IABP) was implanted during the procedure, and due to the comatose state and shockable cardiac arrest, targeted temperature management was initiated. The baseline chest X-ray revealed bilateral interstitial infiltrates, followed by increased proinflammatory markers and a positive polymerase chain reaction (PCR) test for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) demasking underlying COVID-19-related pneumonia. Within the following 48 h, the patient was hemodynamically stable, which enabled weaning from IABP and vasopressor discontinuation. However, due to the worsening of COVID-19 pneumonia, prolonged mechanical ventilation, together with antibiotics and other supportive measures, was needed. The applied therapy resulted in clinical improvement, and the patient was extubated and finally discharged on Day 26, with no neurological sequelae and with mildly reduced left ventricle ejection fraction. [ABSTRACT FROM AUTHOR]

Introduction: Functional echocardiography has been used to identify the etiologies of cardiac arrest and to evaluate the benefit of continued resuscitation after cardiac arrest. It gains more importance in the detection of treatable causes, especially in cardiopulmonary resuscitation of newborns with a diagnosed disease that may develop complications such as massive pericardial effusion and thrombosis. Case Report: Here, we present the findings and results of functional echocardiography performed during cardiopulmonary resuscitation of two newborns with neonatal lupus syndrome and congenital nephrotic syndrome. Conclusions: More studies are needed to clarify the usability of functional echocardiography in neonatal cardiopulmonary resuscitation. It is gaining more importance, especially in newborns with a possible diagnosis of complications. The most important situation here is that echocardiography should be performed without affecting the continuity of resuscitation. Accompanied by an experienced user, it will allow rapid identification of reversible causes of cardiac arrest. [ABSTRACT FROM AUTHOR]

Over the past four decades, percutaneous coronary intervention (PCI) safety and efficacy have significantly improved, particularly with the advent of the drug-eluting stent (DES). First-generation DESs reduced in-stent restenosis rates and targeted lesion revascularization; however, safety issues emerged, due to high incidences of stent thrombosis (ST) linked to death, myocardial infarction, and repeat revascularization. Second-generation DESs were developed to overcome these issues, reducing late-thrombotic-event risk while maintaining anti-restenosis efficacy. Nevertheless, ST still occurs with second-generation DES use. Stent thrombosis etiology is multifaceted, encompassing lesion-, patient-, procedural-, and stent-related factors. Overall, most early-stent-thrombosis cases are linked to procedural and patient-related aspects. Factors like premature discontinuation of dual antiplatelet therapy, resistance to clopidogrel, smoking, diabetes mellitus, malignancy, reduced ejection fraction or undertaking coronary angioplasty for an acute coronary syndrome can increase the risk of stent thrombosis. The aim of this study is to assess patient-related factors that potentially heighten the risk of stent thrombosis, with the objective of pinpointing and addressing modifiable contributors to this risk. By focusing on both patient- and procedure-related factors, a multifaceted approach to coronary revascularization can help minimize complications and maximize long-term benefits in managing ST. [ABSTRACT FROM AUTHOR]

Key Clinical Message: Our case demonstrated that thrombotic complications such as coronary thrombosis and left ventricular clot could occur even in coronavirus disease 2019 (COVID‐19) patients with nonspecific symptoms which indicates the mysterious face of COVID‐19. This complex process highlights the necessity of screening patients for COVID‐19 disease even with nonspecific cardiac symptoms. [ABSTRACT FROM AUTHOR]

Platypnoea–orthodeoxia is a rare clinical syndrome characterised by dyspnoea and oxygen desaturation in the upright position which improves when supine. It requires two components: a sufficiently sized anatomical vascular defect (typically intra‐cardiac or intra‐pulmonary) combined with a functional component that promotes positional right‐to‐left shunting. We describe the rare occurrence of a patient with platypnoea–orthodeoxia syndrome (POS) because of a paradoxical shunt through a patent foramen ovale caused by a large right atrial line‐associated thrombus in a male with metastatic oesophageal cancer undergoing chemotherapy. This case is a timely reminder to consider POS amongst differentials for hypoxia as it is often treatable if recognised. [ABSTRACT FROM AUTHOR]

This article discusses a case of a 28-year-old man who experienced unexpected coronary thrombosis (blood clot) after being infected with the delta variant of COVID-19. The man had no pre-existing health conditions or risk factors, and had previously contracted COVID-19 and received a vaccine. He presented with chest pain and further tests revealed the presence of a blood clot in one of his coronary arteries. Treatment was administered and the clot dissolved. The article highlights the importance of comprehensive coronary imaging in managing COVID-19 patients and emphasizes the thrombotic complications associated with the virus. [Extracted from the article]

Study objectives: While zolpidem is considered as an example of a gender effect on drug response, there is insufficient evidence to reach a consensus. This study aimed to investigate gender differences in adverse events (AEs) of zolpidem. Methods: We estimated the difference between the reporting odds ratios (RORs) calculated in gender subgroups for the AEs signals detected in data mining using 2015–2019 Korea voluntary adverse drug events reporting system (KAERS) data. Different reporting risk by gender was evaluated by using the log RORs being significantly different by gender at the 5% significance level and the 95% confidence intervals of the gender ROR. Results: A total of 94 AE signals were detected. Among these, 35 signals showed significant disparities by gender at the 5% level or were detected only in one gender. When categorized by similarity of AEs, parasomnia including somnambulism and paroniria, and cardiovascular disorders including coronary thrombosis had higher reporting risks in women. Men were more likely to report cognitive disorders such as delirium, insomnia related disorders, and movement disorders. Among all AEs with gender differences in reporting risk, the difference in somnambulism was the most consistent and substantial. Conclusion: For several AEs associated with zolpidem, gender-based reporting disparities were evident. Notably, women exhibited a higher susbeptibility to somnambulism, potentially serious adverse effects of zolpidem. This underscores the need for further investigation into the underlying factors influencing these gender-specific reporting patterns. [ABSTRACT FROM AUTHOR]

Key Clinical Message: Left coronary artery embolism from aortic valve leaflet tissue mass is a rare but potentially life‐threatening complication following transcatheter aortic valve replacement. It is important for interventional cardiologists to be aware of this rare complication for rapid identification and prompt treatment which is the key to a successful outcome. An 81‐year‐old female presented for elective transcatheter aortic valve replacement (TAVR) for severe low‐flow low‐gradient aortic stenosis. Immediately post‐procedure, she developed unexplained, persistent hypotension. There was no bleeding. There was no aortic injury. Activated clotting time was in therapeutic range. Coronary angiography revealed hazy filling defects in left anterior descending and left circumflex. Intravascular ultrasound showed heterogeneous, hypoechoic mass with mild calcification consistent with embolized valve leaflet tissue. This was treated with emergent percutaneous coronary intervention with excellent results. Left coronary artery embolism from aortic valve leaflet tissue is a rare, but potentially life‐threatening complication following TAVR. Prompt recognition is key to a successful outcome. [ABSTRACT FROM AUTHOR]

Cardiovascular disease is the leading cause of mortality and morbidity throughout the world, accounting for 16.7 million deaths each year. The underlying pathological process for the majority of cardiovascular diseases is atherosclerosis, a slowly progressing, multifocal, chronic, immune-inflammatory disease that involves the intima of large and medium-sized arteries. The process of atherosclerosis begins in childhood as fatty streaks—an accumulation of lipids, inflammatory cells, and smooth muscle cells in the arterial wall. Over time, a more complex lesion develops into an atheroma and characteristic fibrous plaques. Atherosclerosis alone is rarely fatal; it is the further changes that render fibrous plaques vulnerable to rupture; plaque rupture represents the most common cause of coronary thrombosis. The prevalence of atherosclerosis is increasing worldwide and more than 50% of people with circulatory disease die of it, mostly in modern societies. Epidemiological studies have revealed several environmental and genetic risk factors that are associated with the early formation of a pathogenic foundation for atherosclerosis, such as dyslipidemia, hypertension, diabetes mellitus, obesity, and smoking. The purpose of this review is to bring together the current information concerning the origin and progression of atherosclerosis in childhood as well as the identification of known risk factors for atherosclerotic cardiovascular disease in children. [ABSTRACT FROM AUTHOR]