Platelet Function, Platelet Size and Content of Reticulated Platelets: Interactions in Patients Receiving Dual Antiplatelet Therapy.

Increased platelet activity is a risk factor of thrombotic events in cardiovascular patients. We studied the relationship between platelet function, platelet size, and the content of reticulated platelets (RP) in patients with coronary heart disease (CHD, n = 55) and acute coronary syndrome (ACS, n = 95) receiving acetylsalicylic acid + clopidogrel or ticagrelor, respectively. The control group consisted of patients with risk factors for CHD, but with no CHD/ACS and free of antiplatelet drugs (n = 66). Platelet function was evaluated by the exposure of activated glycoprotein (GP) IIb-IIIa and P-selectin. In the control group, platelets were activated by TRAP (Thrombin Receptor Activating Peptide) 10 µM, and ADP 20, 5, 2.5 µM, and in the CHD/ACS groups, by TRAP 10 µM, and ADP 20 5 µM (±epinephrine 20 µM). Platelet size was assessed by the mean volume, % large forms, and forward scattering. RP were stained by thiazole orange. In the control group, activated GP IIb-IIIa and P-selectin correlated with platelet size and RP content after platelet activation by all agonists. Despite the decrease in platelet activity by antiplatelet drugs, most correlations (primarily for activated GP IIb-IIIa) were preserved in the CHD/ACS patients. In conclusion, increased platelet size and RP content are associated with increased platelet activity and the reduced efficacy of antiplatelet therapy.

Dendritic cell-derived lncRNAs in patients with acute coronary syndrome.

Long non-coding RNAs (lncRNAs) and dendritic cells (DC) play crucial roles in the development of acute coronary syndrome (ACS); however, the mechanisms remain unclear. To investigate this, we analysed the differentially expressed lncRNAs in monocyte-derived DCs (moDCs) from patients with ACS. Peripheral blood mononuclear cells were transformed into moDCs. Cellular morphology and expression levels of moDC-specific markers (CD80, CD86, CD11c, CD14 and HLA-DR) were analysed using electron microscopy (EM) and flow cytometry (FCM), respectively. Differentially expressed lncRNAs and their functions were predicted using gene sequencing, gene ontology and the Kyoto Encyclopedia of Genes and Genomes. The expression levels of markers, signalling pathway molecules (p-PI3K and p-AKT), inflammatory cytokines (IL-6 and IL-12p70) and target gene (C-C motif chemokine ligand (CCL) 15 and CCL14) were analysed by overexpression or silencing of candidate lncRNAs. EM revealed the cells to be suspended in dendritic pseudopodia. CD11c and HLA-DR were upregulated, while CD80 and CD86 were downregulated. Comparison between the UA versus ST group showed the highest number of differentially expressed lncRNAs (n = 113), followed by UA versus NST (n = 115), CON versus NST (n = 49) and CON versus ST (n = 35); however, the number was low for CON versus UA and ST versus NST groups. moDC-specific marker expression, signalling pathway molecules, inflammatory cytokines and CCL14 were upregulated following lentiviral overexpression of smart silencer-CCL15-CCL14; however, expression levels decreased following transfection with siRNA. The morphology, function and lncRNA expression of moDCs differ depending on the type of ACS. The differentially expressed lncRNAs, particularly CCL15-CCL14, regulate the function of moDCs. Thus, our study provides new insights regarding the role of lncRNAs in ACS and indicates the potential use of CCL15-CCL14 as a novel diagnostic marker and therapeutic target.

Tissue characteristics of residual lesion in patients with acute coronary syndrome caused by plaque rupture versus plaque erosion: a single-center, retrospective, observational study.

Patients with acute coronary syndrome (ACS), frequently caused by plaque rupture (PR), often have vulnerable plaques in residual lesions as well as in culprit lesions. However, whether this occurs in patients with plaque erosion (PE) as well is unknown. We retrospectively analyzed the data of 88 patients with ACS who underwent both optimal coherence tomography (OCT) and intravascular ultrasound (IVUS). Based on plaque morphology of the culprit lesions identified using OCT, patients were classified into PE (n=23) and PR (n=35) groups. The tissue characteristics of residual lesions evaluated using integrated backscatter IVUS were compared between both groups after percutaneous coronary intervention. The PE group had a significantly lower percent lipid volume and a higher percent fibrous volume than the PR group (35.0±17.8% vs 49.2±13.4%, p<0.001; 63.2±17.1% vs 50.3±13.1%, p=0.002, respectively). Receiver operating characteristic curve analysis revealed that percent lipid volume in the residual lesions was a significant discriminant factor in estimating the plaque morphology of the culprit lesion (optimal cut-off value, <43.5%; sensitivity and specificity values were 73.9% and 68.6%, respectively). In conclusion, patients with PE had a significantly lower percent lipid volume and a significantly higher percent fibrous volume in the residual lesions than those with PR, suggesting that the nature of coronary plaques in patients with PE is different from that of those with PR.

Dynamic natural components and morphological changes in nonculprit subclinical atherosclerosis in patients with acute coronary syndrome and mild chronic kidney disease at the 1-year follow-up and clinical significance at the 5-year follow-up.

INTRODUCTION: The natural outcome of coronary plaque in acute coronary syndrome (ACS) patients with chronic kidney disease (CKD) is unique, which can be analyzed quantitatively by optical flow ratio (OFR) software. METHODS: A total of 184 ACS patients with at least one nonculprit subclinical atherosclerosis (NSA) detected by optical coherence tomography (OCT) at baseline and 1-year follow-up were divided into non-CKD group (n = 106, estimated glomerular filtration rate (eGFR)> 90 mL/(min×1.73 m2)) and mild CKD group (n = 78, 60≤eGFR<90 mL/(min×1.73 m2)). Changes of normalized total atheroma volume (TAVn) of NSA was the primary endpoint at the 1-year follow-up. RESULTS: Patients with mild CKD showed more TAVn progression of NSA than non-CKD (p = 0.019) from baseline to the 1-year follow-up, which was mainly due to an increase in calcium TAVn (p<0.001). The morphological change in the maximal calcification thickness (p = 0.026) was higher and the change in the distance from the calcified surface to the contralateral coronary media membrane (ΔC-to-M) at the maximal cross-sectional calcium area was lower (p<0.001) in mild CKD group than in non-CKD group. Mild CKD had more NSA related MACEs at the 5-year follow-up than non-CKD (30.8% vs. 5.8%, p = 0.045). CONCLUSIONS: Mild CKD patients had more plaque progression of NSA which showed the increase of calcium component with more protrusion into the lumen morphologically at the 1-year follow-up and a higher corresponding incidence of NSA-related MACEs at the 5-year follow-up. TRIAL REGISTRATION: Clinical Trial registration ClinicalTrials.gov. NCT02140801. https://classic.clinicaltrials.gov/ct2/show/NCT02140801.

High-risk coronary plaque of sudden cardiac death victims: postmortem CT angiographic features and histopathologic findings.

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.

Coronary Plaque Characteristics and Underlying Mechanism of Acute Coronary Syndromes in Different Age Groups of Patients With Diabetes.

BACKGROUND: High cardiovascular mortality has been reported in young patients with diabetes. However, the underlying pathology in different age groups of patients with diabetes has not been studied. METHODS AND RESULTS: The aim of this study was to investigate the plaque characteristics and underlying pathology of acute coronary syndrome in different age groups of patients with or without diabetes in a large cohort. Patients who presented with acute coronary syndrome and underwent preintervention optical coherence tomography imaging were included. Culprit plaque was classified as plaque rupture, plaque erosion, or calcified plaque and stratified into 5 age groups. Plaque characteristics including features of vulnerability were examined by optical coherence tomography. Among 1394 patients, 482 (34.6%) had diabetes. Patients with diabetes, compared with patients without diabetes, had a higher prevalence of lipid-rich plaque (71.2% versus 64.8%, P=0.016), macrophage (72.0% versus 62.6%, P<0.001), and cholesterol crystal (27.6% versus 19.7%, P<0.001). Both diabetes and nondiabetes groups showed a decreasing trend in plaque erosion with age (patients with diabetes, P=0.020; patients without diabetes, P<0.001). Patients without diabetes showed an increasing trend with age in plaque rupture (P=0.004) and lipid-rich plaque (P=0.018), whereas patients with diabetes had a high prevalence of these vulnerable features at an early age that remained high across age groups. CONCLUSIONS: Patients without diabetes showed an increasing trend with age in plaque rupture and lipid-rich plaque, whereas patients with diabetes had a high prevalence of these vulnerable features at an early age. These results suggest that atherosclerotic vascular changes with increased vulnerability start at a younger age in patients with diabetes. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifiers: NCT04523194, NCT03479723. URL: https://www.umin.ac.jp/ctr/. Unique identifier: UMIN000041692.

Culprit lesion plaque characteristics and angiopoietin like 4 in acute coronary syndrome: A virtual histology-intravascular ultrasound analysis.

BACKGROUND: Thin-cap fibroatheroma is a rupture-prone vulnerable plaque that leads to acute coronary syndrome (ACS). However, its underlying mechanisms are not fully understood. Several studies have investigated the clinical association between angiopoietin-like protein 4 (ANGPTL4) and coronary artery disease. Therefore, this study aimed to investigate the correlation of plasma ANGPTL4 in culprit lesion of ACS patients using intravascular ultrasound (IVUS) and virtual-histology IVUS (VH-IVUS). METHODS: Fifty patients newly diagnosed with ACS between March to September 2021 were selected. Blood samples for baseline laboratory tests, including ANGPTL4, were collected before percutaneous coronary intervention (PCI), and all pre- and post-PCI IVUS examinations were performed of the culprit lesions. RESULTS: Linear regression analysis between plasma ANGPTL4 and grayscale IVUS/VH-IVUS parameters revealed that plasma ANGPTL4 was strongly correlated with the necrotic core (NC) of the minimal lumen site (r = -0.666, p = 0.003) and largest NC site (r = -0.687, p < 0.001), and patients with lower plasma ANGPTL4 levels showed a significantly higher proportion of TFCA. CONCLUSION: The present study further demonstrated the protective role of ANGPTL4 in the spectrum of atherosclerotic development in patients with ACS by culprit lesion morphology analysis using IVUS and VH-IVUS.

Assessment of vasa vasorum on coronary plaques in patients with acute coronary syndromes using intravascular ultrasound and iMap analysis: A retrospective cohort study.

Studies have revealed that vasa vasorum (VV) neovascularization is vital for the progression and vulnerability of coronary atherosclerotic plaques. The correlation between VV, plaque constituents, and the no-reflow phenomenon (NRP) in percutaneous coronary intervention (PCI) remains elusive. We explored plaque constituents in iMap-intravascular ultrasound (iMap-IVUS) and NRP during PCI for VV lesions. We studied 166 coronary lesions in 166 patients with acute coronary syndromes (ACS) (118 lesions with VV) undergoing pre-intervention intravascular ultrasound (IVUS). We evaluated the diversity in plaque morphological status and post-PCI results based on the presence or absence of VV. The lesions with VV group had significantly higher high-sensitivity C-reactive protein (hs-CRP) levels than the lesions without VV group (8.41 ± 4.98 vs 4.19 ± 3.69 mg/L, P < .001). The frequency of after-stent deployment thrombolysis in myocardial infarction (TIMI) flow grades 0, 1, and 2 was remarkably greater in lesions with VV than in those without VV (22.9% vs 10.4%, P < .001). Plaques at the minimum lumen, necrotic core (1.26 ± 0.64 vs 0.92 ± 0.61 mm2, P < .001; 20.95 ± 7.19 vs 13.34% ± 6.54%, P < .001), and fibrous areas (4.23 ± 1.32 vs 3.92 ± 1.01 mm2, P = .006; 61.01 ± 9.41 vs 56.92% ± 11.42%, P = .001) were considerably larger in the lesions with VV than in those without VV. In addition, densely calcified plaques (0.41 ± 0.26 vs 0.81 ± 0.59 mm2, P < .001; 3.63 ± 2.19 vs 7.18% ± 2.01%, P < .001) were considerably smaller in the lesions with VV than in those without VV. Multivariate analyses revealed that VV and plaque volume were independent predictors of NRP after stent deployment (odds ratio [OR]: 5.13, 95% confidence interval [CI]: 1.19-15.32, P = .002; OR: 4.79, 95% CI: 1.08-9.01, P = .005). Lesions with VV exhibited considerable plaque vulnerability in patients with ACS, and they displayed more NRP during PCI. VV and plaque volume were independent predictors of NRP after stent deployment.

Layered plaque and plaque volume in patients with acute coronary syndromes.

BACKGROUND: Layered plaque is a signature of previous subclinical plaque destabilization and healing. Following plaque disruption, thrombus becomes organized, resulting in creation of a new layer, which might contribute to rapid step-wise progression of the plaque. However, the relationship between layered plaque and plaque volume has not been fully elucidated. METHODS: Patients who presented with acute coronary syndromes (ACS) and underwent pre-intervention optical coherence tomography (OCT) and intravascular ultrasound (IVUS) imaging of the culprit lesion were included. Layered plaque was identified by OCT, and plaque volume around the culprit lesion was measured by IVUS. RESULTS: Among 150 patients (52 with layered plaque; 98 non-layered plaque), total atheroma volume (183.3 mm3[114.2 mm3 to 275.0 mm3] vs. 119.3 mm3[68.9 mm3 to 185.5 mm3], p = 0.004), percent atheroma volume (PAV) (60.1%[54.7-60.1%] vs. 53.7%[46.8-60.6%], p = 0.001), and plaque burden (86.5%[81.7-85.7%] vs. 82.6%[77.9-85.4%], p = 0.001) were significantly greater in patients with layered plaques than in those with non-layered plaques. When layered plaques were divided into multi-layered or single-layered plaques, PAV was significantly greater in patients with multi-layered plaques than in those with single-layered plaques (62.1%[56.8-67.8%] vs. 57.5%[48.9-60.1%], p = 0.017). Layered plaques, compared to those with non-layered pattern, had larger lipid index (1958.0[420.9 to 2502.9] vs. 597.2[169.1 to 1624.7], p = 0.014). CONCLUSION: Layered plaques, compared to non-layered plaques, had significantly greater plaque volume and lipid index. These results indicate that plaque disruption and the subsequent healing process significantly contribute to plaque progression at the culprit lesion in patients with ACS. CLINICAL TRIAL REGISTRATION: http://www. CLINICALTRIALS: gov , NCT01110538, NCT03479723, UMIN000041692.

Application of optical coherence tomography in decision-making of post-thrombectomy adjunctive treatments.

An adult patient with acute basilar artery occlusion underwent mechanical thrombectomy. After complete reperfusion, a 70% residual stenosis of the proximal basilar artery was observed. Intravascular optical coherence tomography (OCT) identified lipid plaques with an intact fibrous cap and thrombus in the culprit lesion, indicating plaque erosion was the mechanism of in situ thrombosis. Adjunctive antiplatelet therapy rather than rescue interventions was pursued for its beneficial effects in acute coronary syndrome caused by plaque erosion. The patient had a 90-day modified Rankin Scale score of 0. OCT enables precise evaluation of vessel characteristics following thrombectomy, so may improve outcomes through subsequent tailored treatments.

Unusual echocardiographic finding as cause of acute coronary syndrome with ST- segment elevation.

Biventricular metastatic heart tumors from gynecological malignancies presented as an acute coronary syndrome with ST segment elevation are an unusual finding. We present a case of stage-4 vulvar carcinoma that metastasized in both the left and right ventricle. The particularity of the case is the echocardiographic aspect in the emergency room: multiple, large, hyperechogenic masses disseminated in the myocardium, with pericardial extension, in context of acute coronary syndrome with ST segment elevation.

Impact of early intervention with alogliptin on coronary plaque regression and stabilization in patients with acute coronary syndromes.

BACKGROUND AND AIMS: Anti-atherosclerotic effects of early intervention with dipeptidyl peptidase-4 inhibitors remain poorly defined. METHODS: In a prospective, single-center, randomized trial, 66 patients with acute coronary syndrome (ACS) and mild dysglycemia (HbA1c 6.0 (5.7, 6.3)%, 58% of impaired glucose tolerance) were randomly assigned to receive alogliptin (n = 33) or placebo (n = 33) in addition to standard treatments. Serial intravascular ultrasound (IVUS) was performed at baseline and 10 months to evaluate changes in coronary percent plaque volumes (%PV) and plaque tissue components of non-culprit lesions (NCLs). RESULTS: Baseline clinical and IVUS characteristics, as well as decreases in HbA1c and lipid variables during 10 months, did not differ significantly between the 2 groups. In contrast, with respect to vascular responses, the alogliptin group showed significantly greater decreases in plaque volumes (-0.3 ± 0.6 vs. -0.04 ± 0.7 mm3/mm, p = 0.03) and %PV (-0.9 ± 2.8 vs. 1.2 ± 3.6%, p = 0.01), with a tendency toward smaller lumen loss (-0.1 ± 0.7 vs. -0.4 ± 0.8 mm3/mm, p = 0.07) compared with the placebo group. Significantly decreased percent necrotic volumes (%NV) (-1.9 ± 3.8 vs. 0.3 ± 3.7%, p = 0.03) and increased fibrotic volumes (2.5 ± 5.0 vs. -0.3 ± 5.3%, p = 0.05) were or tended to be seen in alogliptin versus placebo groups at 10 months. In multiple regression analysis, alogliptin use was a statistically significant determinant of changes in %PV (ß = -0.33, p = 0.004) and %NV (ß = -0.28, p = 0.03) at 10 months. CONCLUSIONS: Alogliptin treatment, independently of glycemic and lipid status, resulted in significant plaque regression and stabilization in NCLs in patients with ACS and mild dysglycemia, suggesting the potential utility of early intervention with incretin-based treatments for this patients' subset.

Assessment of radial artery atherosclerosis in acute coronary syndrome patients: an in vivo study using optical coherence tomography.

BACKGROUND: Radial artery (RA) atherosclerosis in acute coronary syndrome (ACS) patients has not been systematically observed in vivo. The study aims to characterize plaque morphology and intimal hyperplasia of the RA in patients with ACS, using optical coherence tomography (OCT). METHODS: In this retrospective study involving 239 ACS patients underwent RA OCT without guidewire shadow, 3 groups were divided according to the following criteria: radial artery plaque (RAP) group included patients with fibrous, lipid or calcified plaque; patients without RAP were further classified into radial intimal hyperplasia (RIH) group (intima media thickness ratio [IMR] ≥ 1) or normal group (IMR < 1). The presence and characteristics of RAP and its related risk factors were identified. RESULTS: The RAP, RIH and normal groups included 76 (31.8%), 69 (28.9%) and 94 (39.3%) patients, respectively. Patients in RAP group were the oldest, compared with those in the RIH and normal groups (p < 0.001), and more frequently had triple vessel disease (p = 0.004). The percentage of plaque rupture (72.4% vs. 56.4%, p = 0.018) and calcification (42.1% vs. 27.6%, p = 0.026) at culprit lesion were significantly higher in patients with RAP than those without RAP. A total of 148 RAP were revealed by OCT, including fibrous (72, 48.6%), lipid (50, 33.8%) and calcified plaques (26, 17.6%). The microvessels were also frequently observed in the RAP group than that in RIH and normal groups (59.2% vs. 8.7% vs. 9.6%, p < 0.001). Multivariate logistic regression analysis showed that age, diabetes, and smoking history (all p < 0.05) were independent risk factors for RAP. CONCLUSIONS: In terms of insights gained from OCT, RA atherosclerosis is not uncommon in ACS patients by OCT, sharing several morphological characters with early coronary atherosclerosis. Aging, diabetes, and smoking are risk factors for RAP.

Acute coronary syndromes in diabetic patients, outcome, revascularization, and antithrombotic therapy.

Diabetes exacerbates the progression of atherosclerosis and is associated with increased risk of developing acute coronary syndrome (ACS). Approximatively 25-30% of patients admitted for ACS have diabetes. ACS occurs earlier in diabetics and is associated with increased mortality and a higher risk of recurrent ischemic events. An increased proinflammatory and prothrombotic state is involved in the poorer outcomes of diabetic patients. In the past decade advancement in both percutaneous coronary intervention (PCI) and coronary artery by-pass graft (CABG) techniques and more potent antiplatelet drugs like prasugrel and ticagrelor improved outcomes of diabetic patients with ACS, but this population still experiences worse outcomes compared to non-diabetic patients. While in ST elevation myocardial infarction urgent PCI is the method of choice for revascularization, in patients with non-ST elevation ACS an early invasive approach is suggested by the guidelines, but in the setting of multivessel (MV) or complex coronary artery disease (CAD) the revascularization strategy is less clear. This review describes the accumulating evidence regarding factors involved in promoting increased incidence and poor prognosis of ACS in patients with diabetes, the evolution over time of prognosis and outcomes, revascularization strategies and antithrombotic therapy studied until now.

Pericoronary Fat Attenuation Index Is Associated With Vulnerable Plaque Components and Local Immune-Inflammatory Activation in Patients With Non-ST Elevation Acute Coronary Syndrome.

Background The pericoronary fat attenuation index (FAI) is assessed using standard coronary computed tomography angiography, and it has emerged as a novel imaging biomarker of coronary inflammation. The present study assessed whether increased pericoronary FAI values on coronary computed tomography angiography were associated with vulnerable plaque components and their intracellular cytokine levels in patients with non-ST elevation acute coronary syndrome. Methods and Results A total of 195 lesions in 130 patients with non-ST elevation acute coronary syndrome were prospectively included. Lesion-specific pericoronary FAI, plaque components and other plaque features were evaluated by coronary computed tomography angiography. Local T cell subsets and their intracellular cytokine levels were detected by flow cytometry. Lesions with pericoronary FAI values >-70.1 Hounsfield units exhibited spotty calcification (43.1% versus 25.0%, P=0.015) and low-attenuation plaques (17.6% versus 4.2%, P=0.016) more frequently than lesions with lower pericoronary FAI values. Further quantitative plaque compositional analysis showed that increased necrotic core volume (Pearson's r=0.324, P<0.001) and fibrofatty volume (Pearson's r=0.270, P<0.001) were positively associated with the pericoronary FAI, and fibrous volume (Pearson's r=-0.333, P<0.001) showed a negative association. An increasing proinflammatory intracellular cytokine profile was found in lesions with higher pericoronary FAI values. Conclusions The pericoronary FAI may be a reliable indicator of local immune-inflammatory response activation, which is closely related to plaque vulnerability. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT04792047.

Predictive Value of CHA2DS2 -VASc-HSF Score for Severity of Acute Coronary Syndrome.

CHADS2 and CHA2DS2-VASc scores have been used to assess the prognostic risk of thromboembolism in non-valvular atrial fibrillation patients. Recent studies have shown the utility of CHADS2 and CHA2DS2-VASc scores for evaluating the severity of coronary artery disease (CAD). The newly defined CHA2DS2-VASc-HSF score evaluates atherosclerosis and is associated with CAD severity. This study investigated the association between the CHA2DS2-VASc-HSF score and acute coronary syndrome (ACS) severity as assessed by the Gensini score and the number of vessels. Furthermore, this study also compared the diagnostic value of the CHADS2, CHA2 DS2-VASc, and CHA2DS2-VASc-HSF score for ACS. A total of 2367 eligible inpatients (ACS group [n = 2030]; non-CAD group [n = 337]) were consecutively enrolled in this study. Receiver operating characteristic curve diagnostic tests and logistic regression models were used to analyze the risk factors for ACS. The CHADS2, CHA2DS2-VASc, and CHA2DS2-VASc-HSF scores were significantly higher in the ACS group than those in the control group. After adjusting for numerous traditional CAD risk factors, an increased CHA2DS2-VASc-HSF score was found to be an independent risk factor for patients with ACS (odds ratio 1.401, 95% confidence interval 1.044, -1.879; P < 0.05). A newly diagnosed CHA2DS2-VASc-HSF score predicts the severity of ACS.

Involvement of enhanced expression of classical complement C1q in atherosclerosis progression and plaque instability: C1q as an indicator of clinical outcome.

Activation of the classical complement pathway plays a major role in regulating atherosclerosis progression, and it is believed to have both proatherogenic and atheroprotective effects. This study focused on C1q, the first protein in the classical pathway, and examined its potentialities of plaque progression and instability and its relationship with clinical outcomes. To assess the localization and quantity of C1q expression in various stages of atherosclerosis, immunohistochemistry, western blotting, and real-time polymerase chain reaction (PCR) were performed using abdominal aortas from eight autopsy cases. C1q immunoreactivity in relation to plaque instability and clinical outcomes was also examined using directional coronary atherectomy (DCA) samples from 19 patients with acute coronary syndromes (ACS) and 18 patients with stable angina pectoris (SAP) and coronary aspirated specimens from 38 patients with acute myocardial infarction. C1q immunoreactivity was localized in the extracellular matrix, necrotic cores, macrophages and smooth muscle cells in atherosclerotic lesions. Western blotting and real-time PCR illustrated that C1q protein and mRNA expression was significantly higher in advanced lesions than in early lesions. Immunohistochemical analysis using DCA specimens revealed that C1q expression was significantly higher in ACS plaques than in SAP plaques. Finally, immunohistochemical analysis using thrombus aspiration specimens demonstrated that histopathological C1q in aspirated coronary materials could be an indicator of poor medical condition. Our results indicated that C1q is significantly involved in atherosclerosis progression and plaque instability, and it could be considered as one of the indicators of cardiovascular outcomes.

Plaque erosion masquerading as spontaneous coronary artery dissection: A case of sudden coronary death.

The three most common mechanisms of thrombosis in acute coronary syndrome (ACS) are plaque rupture, plaque erosion and calcified nodule. Plaque erosion occurs over an intact fibrous cap, commonly over pathological intimal thickening (PIT) rather than thin cap fibroatheroma (TCFA), and is more common among younger and female patients.1 A very rare mechanism of ACS is spontaneous coronary artery dissection (SCAD), resulting from the formation of an intramural hematoma and/or intimal disruption.2 We present a case of sudden coronary death with the appearance of SCAD on coronary computed tomography angiography (CCTA).