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• Remnant lipoprotein-cholesterol is associated with CVD independent of inflammation. • A joint association was found between increased RLP-C and hsCRP with CVD risk. • There was a strong correlation between NMR-derived RLP-C and calculated RLP-C. • Combined with hsCRP, calculated and measured RLP-C yielded a similar association. Elevated remnant-lipoprotein (RLP)-cholesterol (RLP-C) and high-sensitivity C-reactive protein (hsCRP) are each individually associated with atherosclerotic cardiovascular disease (ASCVD). To evaluate the interplay of nuclear magnetic resonance (NMR)-derived RLP-C and hsCRP and their association with ASCVD in the Multi-Ethnic Study of Atherosclerosis (MESA). Lipoprotein particles were measured using NMR spectroscopic analysis at baseline. RLP-C includes very-low-density lipoprotein cholesterol and intermediate-density lipoprotein cholesterol. Four groups were created as follows: Group 1: RLP-C ≤ median (≤29.14 mg/dL) and hsCRP < 2 mg/L; Group 2: RLP-C ≤ median and hsCRP≥ 2 mg/L; Group 3: RLP-C > median and hsCRP level < 2 mg/L; and Group 4: RLP-C > median and hsCRP level ≥ 2 mg/L. Kaplan-Meier survival curves and multivariable-adjusted Cox proportional hazard models were used to examine the relationship between RLP-C and hsCRP with incident ASCVD. A total of 6,720 MESA participants (mean age 62.2 y, 53% female) with a median follow-up of 15.6 years were included. In the fully adjusted model, compared to those in the reference group (Group 1), participants in Group 2, Group 3, and Group 4 demonstrated a 20% (95% CI, -2%-48%), 18% (-4%-44%), and 43% (18%-76%) increased risk of incident ASCVD events, respectively (p < 0.01). An additive and multiplicative interaction between RLP-C and hsCRP was not statistically significant. NMR-derived RLP-C and hsCRP showed a similar independent association with incident ASCVD. Notably, the combination of increased RLP-C and hsCRP was associated with an increased risk of future ASCVD events. [ABSTRACT FROM AUTHOR]

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• FH ACS patients present at young age with fewer comorbidities. • FH ACS patients are likely to present with STEMI. • FH ACS patients commonly experience high in-hospital complications. • FH ACS patients are more likely to be readmitted with recurrent ACS. Individuals with Familial Hypercholesterolemia (FH) are at high risk for atherosclerotic cardiovascular disease (ASCVD) events. The purpose of this study was to evaluate the incidence, predictors, and outcomes of admissions for acute coronary syndromes (ACS) in this high-risk group. Utilizing the National Readmission Databases, we identified individuals with or without FH admitted to participating hospitals for ACS. The primary outcome was admission for recurrent ACS at 11 month follow-up. There were a total of 1,697,513 ACS admissions from 10/2016 to 12/2017 (non-FH=1,696,979 and FH=534). Individuals with FH admitted for ACS were younger (median age 57 vs 69 y), had fewer comorbidities (hypertension 74.7% vs 79.6%; diabetes mellitus 30.5% vs 39.0%;p<0.01), were more likely to present with ST-elevation-myocardial infarction (32.8% vs 22.6%;p<0.01) and more likely to undergo multivessel percutaneous coronary intervention (11.4% vs 7.6%;p<0.01) than patients without FH. After propensity-score matching, FH patients more commonly experienced in-hospital VT arrest (11.8% vs 8.0%;p<0.01) and required more mechanical circulatory support (8.6% vs 3.3%; p<0.01). The 30-day readmission in those with FH was more frequently for cardiovascular disease (81.5% vs 46.5%; =p<0.01). At 11-month follow-up, FH patients were more likely to be readmitted with recurrent ACS compared to those without FH (hazard ratio=2.34; 95% confidence interval=1.30-4.23; p<0.01). Individuals with FH admitted for ACS are younger, have fewer comorbidities, and more frequently present with STEMIs compared to those without FH. FH patients were more likely to suffer in-hospital cardiac complications and have a higher incidence of recurrent ACS. [ABSTRACT FROM AUTHOR]

A clinician has a large number of guidelines to follow. Searching the words "cardiovascular" and "guideline" on the website, www.guideline.gov yielded 502 cardiovascular guidelines, 40 alone in 2015. 1 [National Guideline Clearinghouse: Agency for Healthcare Research and 19 Quality (n.d.)] Similarly, searching the words "cholesterol" and "guideline" yielded 107 results, 6 alone in 2015. This information overload can decrease providers' self-efficacy in using guidelines, particularly if they have inconsistent messages. Moreover, a busy provider can easily be lost if the emphasis is on highlighting differences rather than similarities on the same topic. There are several guidelines for management of blood cholesterol and lipids. Despite being more similar than different, their similarities have not received as much attention as the differences between them. Unfortunately, there are still major gaps in current clinical practice even across these common themes. In this review, we will provide a brief overview of various cholesterol/lipid guidelines followed by a discussion of the differences but more importantly, similarities between them. [ABSTRACT FROM AUTHOR]

Objective Prior studies have shown provider-level knowledge gaps regarding the 2013 American College of Cardiology/American Heart Association guideline on the treatment of cholesterol and concerns about 10-year atherosclerotic cardiovascular disease (ASCVD) risk estimation. The effect of an educational intervention to mitigate knowledge gaps is unknown. Methods We developed a questionnaire and administered it to providers before (pre-training) and after (post-training) a case-based educational intervention across 6 sites in Texas. The intervention highlighted the key recommendations of the 2013 guideline and the differences from the prior guideline mainly using clinical-vignettes. Several practice pertinent items were also discussed. Results Most participants were providers-in-training (78%) in internal medicine (68%). Compared to pre-training, the post-training metrics were: 43% vs. 82% for providers' ability to identify 4 statin benefit groups; 47% vs. 97% for their awareness of the ASCVD risk threshold of ≥7.5% to initiate discussion about risks/benefits of statin therapy; 9% vs. 40% for awareness of differences between the Framingham and the ASCVD risk estimator; 26% vs. 78% for awareness of the definition of statin intensity; 35% vs. 62% for using a repeat lipid panel to document treatment response and adherence; and 46% vs. 81% for confidence in using the ASCVD risk estimator, respectively. Conclusions A case-based educational intervention was associated with significant increase in providers' knowledge towards the 2013 cholesterol guideline, which could be related to the engaging nature of our intervention, using practice pertinent information and clinical vignettes. Such interventions could be useful in effective dissemination of the cholesterol guideline. [ABSTRACT FROM AUTHOR]

Objective Lipoprotein-associated phospholipase A 2 (LpPLA 2 ) activity was associated with higher CHD risk in a meta-analysis, which was partly dependent on circulating lipid levels. Apolipoprotein C3 loss-of-function (ApoC3 LOF) mutations were related with reduced postprandial lipemia and CHD risk. However, the association of LpPLA 2 activity with ApoC3 LOF is not known. Methods We examined the association of LpPLA 2 activity and ApoC3 LOF mutations and incident cardiovascular disease (CVD) (defined as coronary heart disease [CHD] plus ischemic stroke) and all-cause mortality in the biracial longitudinal Atherosclerosis Risk In Communities (ARIC) study. Results The mean LpPLA 2 activity was 229.3 nmol/min/mL and was higher in men and whites. LpPLA 2 activity correlated positively with atherogenic dyslipidemia. ApoC3 LOF carriers had lower LpPLA 2 activity levels compared to non-carriers, and there was inverse association between LpPLA 2 activity and ApoC3 LOF mutations in whites. In a fully adjusted model, greater LpPLA 2 activity was independently associated with incident CVD (HR 1.35, 1.09–1.68 for highest vs. lowest quintile), which was mainly explained by its association with CHD, and was also associated with all-cause mortality (HR 1.65, 1.38–1.98). Conclusions Greater LpPLA 2 activity was associated with increased CHD and all-cause mortality in both whites and African–Americans in the ARIC study. The inverse relation between LpPLA 2 activity and ApoC3 LOF mutations suggests that delayed lipoprotein clearance may at least in part explain the observed association of LpPLA 2 activity with increased CVD risk. [ABSTRACT FROM AUTHOR]

Retired National Football League (NFL) linemen have an increased prevalence of risk factors for atherosclerosis and have an increased risk of cardiovascular death compared with non-linemen and the general population. We evaluated whether playing in lineman position is independently associated with an increased risk of the presence and severity of subclinical atherosclerosis. Players were categorized as linemen if they reported playing on the offensive or defensive line during their careers. Subclinical atherosclerosis was assessed using coronary artery calcium (CAC) scores in 931 retired NFL players (310 linemen, 621 nonlinemen). CAC scores were evaluated for absence of subclinical atherosclerosis (CAC = 0), presence of mild subclinical atherosclerosis (CAC 1 to 100), and moderate to severe subclinical atherosclerosis (CAC ≥100). We performed multivariate logistic regression to determine whether the lineman position is independently associated with the presence and severity of subclinical athero-sclerosis. Linemen were noted to have a lesser likelihood of absence of subclinical athero-sclerosis (CAC = 0, 33.8% vs 41.7%, p = 0.02), a similar likelihood of mild subclinical atherosclerosis (CAC 1 to 100,33.2% vs 31.8%, p = 0.7), and a greater likelihood of moderate to severe subclinical atherosclerosis (CAC >100, 32.9% vs 26.4%, p = 0.04) compared with nonlinemen. Adjusting for demographic and metabolic covariates, lineman status remained independently associated with mild subclinical atherosclerosis (CAC 1 to 100, odds ratio [OR] 1.41, 95% confidence interval [CI] 1.05 to 2.2, p = 0.04) and moderate to severe subclinical atherosclerosis (CAC ≥100, OR 1.67,95% CI 1.05 to 2.2). The association was attenuated after adjustment for race (CAC 1 to 100, OR 1.24, 95% CI 0.82 to 1.8; CAC >100, OR 1.59, 95% CI 1.01 to 2.49). In conclusion, lineman status in retired NFL players is associated with presence and severity of subclinical atherosclerosis, which is partly explained by race. [ABSTRACT FROM AUTHOR]

Objectives Retired National Football League (NFL) players were reported to have high prevalence of cardiovascular risk factors. Lipoprotein Associated Phospholipase A 2 (LpPLA 2 ) has shown to be associated with cardiovascular disease in the general population, but it is unknown whether such an association exists in retired NFL players. Our objective was to assess whether LpPLA 2 mass was associated with coronary artery calcium (CAC) and carotid artery plaque (CAP) in retired NFL players. Methods LpPLA 2 mass was assessed using a dual monoclonal antibody immunoassay. CAC presence was defined as CAC score>0. CAP was defined as focal thickening ≥50% than that of the surrounding vessel wall with a minimal thickness of 1.2 mm on carotid ultrasound. Results In 832 NFL players, the median (IQR) age and LpPLA 2 levels were 54 (45–63) years and 142 (109–181) ng/mL respectively. LpPLA 2 mass was positively correlated with low-density lipoprotein (LDL) cholesterol and high-density lipoprotein cholesterol; negatively correlated with LDL particle concentration and body mass index; and not correlated with high-sensitivity C-reactive protein. CAC was present in 659 (79%) and CAP in 544 (65%) players. In a fully adjusted model, LpPLA 2 was not associated with CAC (OR per 1-SD increase, 0.85; 95% CI 0.71–1.02) or CAP (0.90, 0.75–1.08). LpPLA 2 was also not associated with CAC burden in those with CAC>0. Results were similar when highest and lowest LpPLA 2 tertiles were compared, and also in various subgroups. Conclusion LpPLA 2 mass was not associated with coronary or carotid subclinical atherosclerosis in retired NFL players. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to evaluate the frequency and predictors of stent thrombosis (ST) after stenting for ST-segment elevation myocardial infarction (STEMI). Background: Stent thrombosis remains a major concern with STEMI patients treated with primary percutaneous coronary intervention. Methods: Consecutive patients (N = 1,640) undergoing stenting for STEMI were prospectively enrolled in our database and followed for 1 to 15 years. Bare-metal stents were implanted from 1995 to 2002, and drug-eluting and bare-metal stents were implanted from 2003 to 2009. Stent thrombosis was defined as definite or probable. Results: Our population had a high risk profile, including a high incidence of Killip class III to IV (11.5%) and STEMI due to ST (10.2%). Stent thrombosis occurred in 124 patients, including 42 with early ST (0 to 30 days), 35 with late ST (31 days to 1 year), and 47 with very late ST (>1 year). The frequency of ST was 2.7% at 30 days, 5.2% at 1 year, and 8.3% at 5 years. Independent predictors of early or late ST were STEMI due to ST (hazard ratio [HR]: 4.38, 95% confidence interval [CI]: 2.27 to 8.45), small stent size (HR: 2.44, 95% CI: 1.49 to 4.00), Killip class III to IV (HR: 2.39, 95% CI: 1.30 to 4.40), and reperfusion time ≤2 h (HR: 2.09, 95% CI: 1.03 to 4.24). Drug-eluting stent was the only independent predictor of very late ST (HR: 3.73, 95% CI: 1.81 to 7.88). Conclusions: Stent thrombosis after primary percutaneous coronary intervention is relatively frequent and continues to increase out to 5 years. New strategies are needed to prevent ST in STEMI patients, and targeted therapies are needed in patients identified at highest risk. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to assess the frequency of very late stent thrombosis (VLST) after stenting with bare-metal stents (BMS) and drug-eluting stents (DES) for ST-segment elevation myocardial infarction (STEMI). Background: Stent thrombosis occurs more frequently after stenting for STEMI than after elective stenting, but there are little data regarding VLST. Methods: Consecutive patients (n = 1,463) who underwent stenting for STEMI were prospectively enrolled in our database. BMS were implanted exclusively from 1995 to 2002, and DES and BMS were implanted from 2003 to 2009. Follow-up was obtained at 1 to 15 years. Results: BMS patients (n = 1,095) were older and had more shock, whereas DES patients (n = 368) had more diabetes and smaller vessels. Stent thrombosis occurred in 107 patients, of which 42 were VLST (>1 year). Stent thrombosis continued to increase to at least 11 years with BMS and to at least 4.5 years with DES. Stent thrombosis rates with BMS versus DES were similar at 1 year (5.1% and 4.0%, respectively) but increased more with DES after the first year (1.9%/year vs. 0.6%/year, respectively). Landmark analysis (>1 year) found DES had a higher frequency of VLST (p < 0.001) and reinfarction (p = 0.003). DES was the only significant independent predictor of VLST (hazard ratio: 3.79, 95% confidence interval: 1.64 to 8.79, p = 0.002). Conclusions: VLST after primary PCI for STEMI occurs with relatively high frequency to at least 11 years with BMS and to at least 4.5 years with DES. Very late stent thrombosis and reinfarction (>1 year) were more frequent with DES. New strategies are needed to manage this problem. [ABSTRACT FROM AUTHOR]

Background Studies of incident coronary heart disease risk within low-density lipoprotein (LDL) subclass (small, dense vs large, buoyant) have shown mixed results. No prospective cohort study has examined the association of small, dense, or large, buoyant LDL with mortality after myocardial infarction (MI). Objective The objective of the study was to examine association of LDL pattern after MI and death. Methods In 2476 patients hospitalized for MI, LDL pattern (A [large, buoyant], A/B [mixed], and B [small, dense]) was established by ultracentrifugation using Vertical Auto Profile. Using time-to-event analysis, we examined the association with 5-year mortality within LDL patterns, after adjusting for important patient and treatment characteristics. We additionally adjusted for LDL cholesterol (LDL-C) and triglyceride levels and used directly measured LDL-C and non-high-density lipoprotein cholesterol as exposures. Results Patterns A, A/B, and B were present in 39%, 28%, and 33% of patients, respectively, with incident rates (per 1000 patient-years) of 50, 34, and 24 for all-cause and 24, 19, and 10 for CV mortality. The hazard ratios (95% confidence interval) with LDL patterns A/B and B compared with pattern A were 0.77 (0.61, 0.99) and 0.67 (0.51, 0.88) for all-cause, 0.94 (0.67, 1.33) and 0.69 (0.46, 1.03) for cardiovascular, and 0.64 (0.45, 0.91) and 0.65 (0.45, 0.93) for noncardiovascular mortalities, respectively. Results were similar when further adjusted for LDL-C and triglycerides, or with LDL-C and non-high-density lipoprotein cholesterol as exposures. Conclusion Compared with LDL pattern A, pattern B was significantly associated with reduced all-cause and non-CV mortalities with a trend for lower CV mortality after MI, independent of LDL-C and triglycerides. [ABSTRACT FROM AUTHOR]

Background Providers' understanding of the 2013 American College of Cardiology (ACC)/American Heart Association (AHA) cholesterol guideline in clinical practice is not known. Methods We designed a questionnaire, which was administered to internal medicine, family practice, cardiology, and endocrinology providers at 21 venues across the United States. We compared responses between providers in training or practice and between specialists (cardiology and endocrinology) and nonspecialists (internal medicine and family practice). Results Response rate was 72.1% (543 of 725). About 43% of the providers in training and 48% of those in practice indicated having read the guideline. Almost 50% in each group were unable to identify the 4 statin benefit groups and a large proportion (41% in training and 49% in practice) were not aware of the ≥7.5% 10-year risk threshold for discussion regarding statin therapy. Most (∼85%) were unaware of the 4 outcomes assessed by the 10-year ASCVD risk equation. About 36% of the providers in training and 48% in practice could identify a patient with familial hypercholesterolemia and start a discussion regarding statin therapy. Only 27.6% of the providers in training and 40.4% in practice recommended repeating a lipid panel 6–8 weeks after starting statins in a patient with recent myocardial infarction. Similar gaps were noted when comparing specialists to nonspecialists. Conclusion Most providers do not completely understand the 2013 ACC/AHA cholesterol guideline. As an unintended consequence, providers are moving away from lipid testing to document response and adherence to statin therapy. Efforts are needed to address these gaps. [ABSTRACT FROM AUTHOR]