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.

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.

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.

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.

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).

Air Pollution and Coronary Plaque Vulnerability and Instability: An Optical Coherence Tomography Study.

OBJECTIVES: We assessed the relationship between exposure to air pollutants and mechanisms of coronary instability evaluated by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS). BACKGROUND: Air pollution is an emerging key player in determining the residual risk of coronary events. However, pathophysiological mechanisms linking air pollution and coronary events have been not adequately investigated. METHODS: Patients with ACS undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT, and the presence of macrophage infiltrates (MØI) and thin-cap fibroatheroma (TCFA) at the culprit site was also assessed. Based on each case's home address, exposure to several pollutants was evaluated, including particulate matter 2.5 (PM2.5), PM10, and carbon monoxide (CO). Only patients with >2 years of available data on air pollution exposure prior to ACS were enrolled. RESULTS: We included 126 patients (median age: 67.0 years of age; IQR: 55.5-76.0; 97 male patients [77.0%]). Sixty-six patients (52.4%) had PR as the mechanism of plaque instability. Patients with PR were exposed to significantly higher PM2.5 levels than to IFC, and PM2.5 was independently associated with PR (odds ratio: 1.194; 95% CI: 1.036 to 1.377; P = 0.015). Moreover, exposure to higher levels of PM2.5 was independently associated with the presence of TCFA and of MØI at the culprit site. Interestingly, PM2.5, PM10, and Co levels were positively and significantly correlated with serum levels of C-reactive protein. CONCLUSIONS: We provide novel insights into the missing link between air pollution and increased risk of coronary events. In particular, exposure to higher concentrations of air pollutants is associated with the presence of vulnerable plaque features and with plaque rupture as a mechanism of coronary instability. An enhanced systemic and plaque inflammatory activation may explain these findings.

Dissecção espontânea da artéria coronária em gestação gemelar no terceiro trimestre: relato de caso / Spontaneous coronary artery dissection in a twin pregnancy in the third trimester: a case report

O infarto agudo do miocárdio no período gravídico-puerperal é uma condição rara em que a principal causa é a dissecção espontânea da artéria coronária. É um evento comumente subdiagnosticado, com pouca literatura disponível e elevado índice de morbimortalidade. Esse relato descreve o caso de uma gestante de 36 semanas de gravidez gemelar, monocoriônica-diamniótica, com infarto agudo do miocárdio secundário à dissecção espontânea da artéria coronária. As equipes de cirurgia cardíaca e obstetrícia optaram pela realização de parto cesariano e histerectomia subtotal, seguido da revascularização da artéria mamária descendente anterior. Discutem-se as orientações adotadas na dissecção espontânea da artéria coronária, bem como a abordagem terapêutica e a conduta obstétrica, quando essa condição ocorre durante a gravidez.(AU)

Acute myocardial infarction in the pregnancy-puerperal period is a rare condition the main cause of which is the spontaneous coronary artery dissection. A commonly underdiagnosed event with little available literature and a high rate of morbidity and mortality. This case reports a 36-week pregnant woman of mono-chorionic-diamniotic pregnancy who had a myocardial infarction secondary to a spontaneous coronary artery dissection. In a joint discussion between the team of cardiac surgery and obstetrics, it was decided to perform a cesarean delivery and subtotal hysterectomy followed by revascularization of the mammary anterior descendant. It discusses the conducts to be adopted in a case of spontaneous coronary artery dissection as well as therapeutic approaches and obstetric conducts to be taken in a case of dissection during pregnancy.(AU)

Risk factors for potential drug-drug interactions of statins in patients with acute coronary syndrome

Abstract The aim of our study was to assess risk factors for potential drug-drug interactions (pDDIs) of statins across different phases of treatment of acute coronary syndrome (ACS) patients: from the point of first medical contact to the coronary angiography (first phase), after coronary angiography to the last day of hospitalization (second phase) and at discharge from hospital (third phase). This was a post hoc analysis of the data collected during the retrospective observational cohort study conducted at the Clinic for Cardiology of the Clinical Centre Kragujevac, Serbia. Patients prescribed statins were identified from the original study population: 156, 240 and 236 patients for the first, second and third phases, respectively. At least one statin pDDI was present in 113 (72.4%), 161 (67.1%) and 139 (58.9%) patients in the first, second and third phases, respectively. Heart failure, arrhythmias after ACS, CRP, triglycerides, length of hospitalization, number of prescribed drugs, antiarrhythmic drugs, and clopidogrel seem to increase the risk of statin pDDIs in at least one treatment phase. Physicians should be vigilant to the possibility of statin pDDIs in ACS patients who have factors that may increase their rate.

Evaluation of the Prognostic Role of the Wall Motion Score Index and the SYNTAX Score II in Patients with Acute Coronary Syndrome Following Percutaneous Coronary Intervention by Evaluation of Major Adverse Cardiovascular Events at 12-Month Follow-Up.

BACKGROUND This study aimed to evaluate the wall motion score (WMS) index and the SYNTAX score II (SSII) in patients with acute coronary syndrome (ACS) following percutaneous coronary intervention (PCI) by evaluation of major adverse cardiovascular events (MACEs) at the 12-month follow-up at a single center. MATERIAL AND METHODS An observational study of 430 patients with ACS undergoing PCI at the Second Affiliated Hospital of Soochow University over a 1-year period was performed. Baseline data including WMS and SSII were recorded and compared with the rates of MACEs in the study group. WMS and SSII were stratified by the tercile from low to high. RESULTS Both WMS and SSII were associated with the rates of MACEs (P<0.001 and P=0.003, respectively). The incidence of MACEs was positively correlated with terciles of the WMS and SSII groups (3.7% vs 1.6% vs 7.0% [P<0.001] and 2.6% vs 5.8% vs 11.6% [P<0.001], lowest to highest, respectively). Logistic regression analyses identified combined predictors for 12-month outcome, including WMS and SSII. The use of a model combining both scores yielded a higher predictive value (area under the curve [AUC]=0.78; 95% confidence interval [CI], 0.733-0.835; P<0.001) than the use of either score alone. Using WMSs alone, the AUC was 0.73 (95% CI, 0.660-0.793; P<0.001). Using SSII alone, the AUC was 0.71 (95% CI, 0.649-0.769; P<0.001). CONCLUSIONS This study showed that the combined methods of the WMS index and the SSII were predictive factors of MACEs in patients with ACS following PCI at the 12-month follow-up.

Cost-effectiveness analysis of apixaban versus vitamin K antagonists for antithrombotic therapy in patients with atrial fibrillation after acute coronary syndrome or percutaneous coronary intervention in Spain.

BACKGROUND/OBJECTIVE: AUGUSTUS trial demonstrated that, for patients with atrial fibrillation (AF) having acute coronary syndrome (ACS) or undergoing percutaneous coronary intervention (PCI), an antithrombotic regimen with apixaban and P2Y12 resulted in less bleeding, fewer hospitalizations, and similar ischemic events than regimens including a vitamin K antagonist (VKA), aspirin, or both. This study objective was to evaluate long-term health and economic outcomes and the cost-effectiveness of apixaban over VKA, as a treatment option for patients with AF having ACS/PCI. METHODS: A lifetime Markov cohort model was developed comparing apixaban versus VKA across multiple treatment strategies (triple [with P2Y12 + aspirin] or dual [with P2Y12] therapy followed by monotherapy [apixaban or VKA]; triple followed by dual and then monotherapy; dual followed by monotherapy). The model adopted the Spanish healthcare perspective, with a 3-month cycle length and costs and health outcomes discounted at 3%. RESULTS: Treatment with apixaban resulted in total cost savings of €883 and higher life years (LYs) and quality-adjusted LYs (QALYs) per patient than VKA (net difference, LYs: 0.13; QALYs: 0.11). Bleeding and ischemic events (per 100 patients) were lower with apixaban than VKA (net difference, -13.9 and -1.8, respectively). Incremental net monetary benefit for apixaban was €3,041, using a willingness-to-pay threshold of €20,000 per QALY. In probabilistic sensitivity analysis, apixaban was dominant in the majority of simulations (92.6%), providing additional QALYs at lower costs than VKA. CONCLUSIONS: Apixaban was a dominant treatment strategy than VKA from both the Spanish payer's and societal perspectives, regardless of treatment strategy considered.