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Adherence to guideline-recommended, long-term secondary preventative therapies among patients with acute coronary syndrome (ACS) is fundamental to improving long-term outcomes. The purpose of this scoping review was to provide a broad synopsis of pertinent studies in a structured and comprehensive way regarding factors that influence patient adherence to medical therapy after ACS. Relevant articles focusing on adherence to medical therapy after ACS were retrieved from the EMBASE and MEDLINE databases (search date, September 7, 2021). Studies were independently screened, and relevant information was extracted. A total of 58 studies were identified by using the EMBASE and MEDLINE databases. Adherence to secondary prevention was moderate to low and steadily decreased over time. Nearly 30% of patients discontinued one or more medications within 90 days of their primary ACS, and adherence decreased to 50% to 60% at 1 year postdischarge. There were no major differences in adherence between drug classes. Factors influencing patient adherence can be broadly divided into 3 categories: patient related, health care system related, and disease related. Patients managed with percutaneous coronary interventions were more adherent to follow-up treatment than medically managed patients. Depression was reported as a major psychological factor that negatively affected adherence. Improved adherence was observed when higher levels of patient education and provider engagement were delivered during postdischarge follow-up, particularly when scheduled early. Notably, the incidence of major adverse cardiovascular events was lower in hospitals with high 90-day medication adherence than those with moderate or low adherence. Patient nonadherence to guideline-recommended long-term pharmacologic secondary preventative therapies after ACS is multifactorial. A comprehensive multifaceted approach should be implemented to improve adherence and clinical outcomes. This approach should include key interventions such as early follow-up visits, high medication adherence at 90 days, patient engagement and education, and development of novel interventions that support the 3 broad categories influencing patient adherence as discussed in this review.

Periprocedural myocardial necrosis, which can range from a low level elevation of cardiac biomarkers to a large myocardial infarction (MI), is a common complication after percutaneous coronary intervention (PCI). We hypothesized that insulin-like growth factor-1 (IGF-1) levels may play a protective role in myocardial injury after coronary stent placement and aimed to investigate the relationship between IGF-1 levels and plaque characteristics assessed by optical coherence tomography (OCT). Between May 2015 and December 2015 we prospectively enrolled 74 patients with stable angina pectoris in whom single de novo coronary artery stenosis was present. PCI was performed according to standard methods. OCT was applied to all patients. TnT was analyzed at admission, before PCI and at 6, 12, 24 and 48 h after PCI. Serum IGF-1 was measured prior to PCI. A total of 25 (33.7%) patients had periprocedural myocardial injury or type 4a myocardial infarction, and 49 (66.2%) patients had no events. IGF-1 level and reference intimal thickness, medial thickness, and plaque fibrous cap thickness in OCT had strong correlations ( = 0.88, 0.80 and 0.88 respectively, < 0.001). IGF-1 was an independent predictor of periprocedural myocardial injury or type 4a MI in univariate (OR = 0.929, 95% CI: 0.895-0.964, < 0.001) and multivariate regression analysis (OR = 0.757, 95% CI: 0.575-0.998, = 0.04). Based on ROC analysis, the best cut-off value of IGF-1 for predicting periprocedural myocardial injury or type 4a myocardial infarction was 144.5 ng/ml, with a maximum sensitivity of 88% and specificity of 77.6% (AUC = 0.80, 95% CI: 0.69-0.88, < 0.0001). The results from this study indicate that low IGF-1 levels are associated with plaque instability assessed by OCT. Low IGF-1 levels may identify patients who are at increased risk for periprocedural myocardial injury/infarction.

Carotid artery stenting is a method used in the treatment of extracranial carotid artery stenosis that is becoming increasingly more common. Acute carotid thrombosis following CAS is a very rare and devastating complication that can be lethal for the patient unless treated immediately. We report a case of acute carotid stent thrombosis occurring immediately after emergent revascularization, and that was treated with intraarterial tissue plasminogen activator and intravenous tirofiban infusion.

In current studies, vascular toxicity and throm- botic effects has been reported with some antineoplastic agents. [...]it is important for clinicians to be aware of infrequent and different, but potentially serious, adverse cardiac effects of these agents.

Coronary fractional flow reserve (FFR) is recommended as the gold standard method in evaluating intermediate coronary stenoses. However, there are significant debates concerning the agents and the timing of the measurement. To compare the contrast medium induced Pd/Pa ratio (CMR) with the FFR. We enrolled 28 consecutive patients with 34 intermediate lesions who underwent coronary FFR measurement by intracoronary (i.c.) adenosine. After baseline Pd/Pa was calculated, a single contrast medium (Iomeron) injection of 6 ml (3 ml/s) was performed manually. Within 10 s after the contrast medium injection, the CMR was calculated. Bolus injection of i.c. adenosine was performed to induce maximal hyperemia (from 60 µg to 600 µg), and when it was ≤ 0.80, the intermediate lesion was considered as significant. After bolus i.c. adenosine, 12 lesions of 34 (35.3%) were identified as significant. The CMR value was 0.86 ±0.06 (range: 0.71-0.97). There were no significant differences between FFR and CMR values (p = 0.108). A substantial positive correlation between adenosine and contrast values was detected (0.886 and p < 0.001). Good agreement in Bland-Altman analysis was revealed (mean bias was 0.027, 95% confidence interval 0.038-0.092). Receiver operating characteristics curve analysis showed 90.9% sensitivity and 91.7% specificity for a cut-off value of 0.85 for the CMR compared to FFR (≤ 0.80). Our study showed that measuring the CMR is a feasible method compared to FFR. The CMR may be used in situations where adenosine cannot be administered.

An elevated white blood cell (WBC) count is associated with an increased risk of ischemic events among acute coronary syndrome (ACS) patients, but the association between WBC count and bleeding in ACS patients is not well established. The aim of this analysis was to assess and compare the association between WBC count and the occurrence of short- and long-term bleeding and ischemic events. This was a post hoc analysis of the ATLAS ACS2-TIMI 51 trial. A subset of patients had a WBC count measurement at baseline (n = 14,231, 91.6%). Univariate and multivariable Cox proportional hazard models were constructed to determine if there is an association between WBC count at baseline and a composite outcome of Thrombolysis in Myocardial Infarction (TIMI) major and minor bleeds at 30 days and 1 year. Variables with a p <0.2 in the univariate analysis were included as potential parameters in the backward selection process A similar multivariable model was constructed to assess the association between WBC count and a composite ischemic endpoint of cardiovascular death, myocardial infarction and stroke. An increased risk of bleeding per a 1 × 109/L increase in WBC at baseline was observed at 30 days (Adjusted hazard ratio [HR] 1.08 95% confidence interval [CI] 1.01 to 1.17, p = 0.019) but not at 1 year (Adjusted HR 1.02 95% CI 0.97 to 1.08, p = 0.409). Additionally, an increased risk of ischemia per a 1 × 109/L increase in WBC at baseline was observed at 30 days (Adjusted HR 1.07, 95% CI: 1.03 to 1.12, p = 0.002) and at 1 year (Adjusted HR 1.05 95% CI 1.02 to 1.08, p = 0.001 at 1 year). In conclusion, a higher WBC count at baseline was associated with an increased risk of the composite bleeding endpoint by 30 days but not at 1 year. The association between WBC count and the risk of the composite ischemic endpoint was significant at 30 days and 1 year.

Background Despite low‐density lipoprotein cholesterol‐lowering therapies and other standard‐of‐care therapy, there remains a substantial residual atherosclerotic risk among patients with an acute coronary syndrome (ACS). This study aims to estimate the risk of early and late recurrent major adverse cardiovascular events (MACE) and address its implications on trial design. Methods A literature search was performed to collect phase III interventional trials on high‐risk ACS patients. Pooled event rates at 90 and 360 days were estimated by fitting random‐effects models using the DerSimonian–Laird method. Under the assumption of a total sample size of 10,000 and 1:1 allocation at a one‐sided alpha of 0.025 using the log‐rank test, the relationship between power and relative risk reduction (RRR) or absolute risk reduction (ARR) was explored for early versus late MACE endpoint. Results Seven trials representing 82,727 recent ACS patients were analyzed. The pooled rates of recurrent MACE were 4.1% and 8.3% at 90 and 360 days. Approximately 49% of events occurred within the first 90 days. Based on the estimated risks at 90 and 360 days, to attain 90% statistical power, a lower magnitude of RRR is required for late MACE than early MACE (22% vs. 30%), whereas a lower magnitude of ARR is required for early MACE than late MACE (1.2% vs. 1.8%). Conclusion The initial 90‐day window after ACS represents a vulnerable period for recurrent events. From a trial design perspective, determining a clinically important benefit by RRR versus ARR may influence the decision between early and late MACE as the study endpoint.

Purpose To assess the efficacy and safety of betrixaban for venous thromboembolism (VTE) prophylaxis among critically ill patients. Methods The APEX trial randomized 7513 acutely ill hospitalized patients to betrixaban for 35–42 days or enoxaparin for 10 ± 4 days. Among those, 703 critically ill patients admitted to the intensive care unit were included in the analysis, and 547 patients who had no severe renal insufficiency or P-glycoprotein inhibitor use were included in the full-dose stratum. The risk of VTE, bleeding, net clinical benefit (composite of VTE and major bleeding), and mortality was compared at 35–42 days and at 77 days. Results At 35–42 days, extended betrixaban reduced the risk of VTE (4.27% vs 7.95%, P  = 0.042) without causing excess major bleeding (1.14% vs 3.13%, P  = 0.07). Both VTE (3.32% vs 8.33%, P  = 0.013) and major bleeding (0.00% vs 3.26%, P  = 0.003) were decreased in the full-dose stratum. Patients who received betrixaban had more non-major bleeding than enoxaparin (overall population: 2.56% vs 0.28%, P  = 0.011; full-dose stratum: 3.32% vs 0.36%, P  = 0.010). Mortality was similar at the end of study (overall population: 13.39% vs 16.19%, P  = 0.30; full-dose stratum: 13.65% vs 16.30%, P  = 0.39). Conclusions Compared with shorter-duration enoxaparin, critically ill medical patients who received extended-duration betrixaban had fewer VTE without more major bleeding events. The benefit of betrixaban was driven by preventing asymptomatic thrombosis and offset by an elevated risk of non-major bleeding. The APEX trial did not stratify by intensive care unit admission and the present study included a highly selected population of critically ill patients. These hypothesis-generating findings need to be validated in future studies. Clinical trial registration http://www.clinicaltrials.gov . Unique identifier: NCT01583218.

Despite current standard of care treatment, the period shortly after acute myocardial infarction (AMI) is associated with particularly high residual cardiovascular (CV) risk, with high rates of recurrent AMI and CV death in the first 90 days following the index event. This represents an area of high unmet need which may be potentially addressed by the recent shift in focus away from raising levels of high-density lipoprotein cholesterol (HDL-C), to ones that optimize HDL function. Apolipoprotein A-I (apoA-I) is the major protein constituent of HDL and a key mediator of cholesterol efflux from macrophages within atherosclerotic plaque, a property which may convey therapeutic efficacy during the high-risk period. CSL112 is a novel formulation of human plasma-derived apolipoprotein A-I (apoA-I), reconstituted with phosphatidylcholine and stabilized with sucrose that is currently being evaluated in a phase 3 clinical trial (AEGIS-II) for the reduction of major adverse CV events (MACE) in the period of high-risk post AMI. Patients with diabetes mellitus are especially at high risk of recurrent MI, and are an enriched patient population in the AEGIS-II study. In this presentation, we provide an overview of the biological properties of CSL112 that contribute to its proposed mechanism of action for reducing rates of MACE post AMI. These properties include rapid and robust promotion of cholesterol efflux from cells abundant in atherosclerotic plaque, in addition to anti-inflammatory effects, which together, may have a stabilizing effect on atherosclerotic plaque. We provide a detailed overview of these mechanisms, in addition to information on the composition of CSL112 and how it is manufactured.