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Background: Hyperkalaemia (HK) is a serious and potentially life-threatening condition. Both acute and chronic conditions may alter potassium homeostasis. Our aim is to describe HK incidence, clinical outcomes, and associated resource use within a large, integrated healthcare system. Methods: Adult patients seen at Intermountain Healthcare facilities with a serum potassium (sK) result between January 1, 2003 and December 31, 2018 were retrospectively studied. Descriptive assessment of a population with detected HK, defined by any sK > 5.0 mmol/L and HK frequency and severity to associated resource use and characteristics of HK predictors were made. Multivariable Cox hazard regression was used to evaluate HK to outcomes. Results: Of 1,208,815 patients included, 13% had HK. Compared to no-HK, HK patients were older (60 ± 18 vs 43 ± 18 years, P < 0.001), male (51% vs 41%, P < 0.001), and had greater disease burden (Charlson Comorbidity Index 3.5 ± 2.8 vs 1.7 ± 1.4, P < 0.001). At 3 years, more HK patients experienced major adverse cardiovascular events (MACEs) (19 vs 3%, P < 0.001), persisting post-adjustment (multivariable hazard ratio = 1.60, P < 0.001). They incurred higher costs for emergency department services ($552 ± 7,574 vs $207 ± 1,930, P < 0.001) and inpatient stays ($10,956 ± 93,026 vs $1,477 ± 21,423, P < 0.001). HyperK Risk Scores for the derivation and validation cohorts were: 44% low-risk, 45% moderate-risk, 11% high-risk. Strongest HK predictors were renal failure, dialysis, aldosterone blockers, diabetes, and smoking. Conclusion: Within this large system, HK was associated with a large clinical burden, affecting over 1 in 10 patients; HK was also associated with increased 3-year MACE risk and higher medical costs. Although risk worsened with more severe or persistently recurring HK, even mild or intermittent HK episodes were associated with significantly greater adverse clinical outcomes and medical costs. The HyperK Score predicted patients who may benefit from closer management to reduce HK risk and associated costs. It should be remembered that our assumptions are valid only for detected HK and not HK per se. [ABSTRACT FROM AUTHOR]

Aims Though statin therapy is known to slow coronary atherosclerosis progression and reduce cardiovascular (CV) events, significant CV risk still remains. In the REDUCE-IT study, icosapent ethyl (IPE) added to statin therapy reduced initial CV events by 25% and total CV events by 30%, but its effects on coronary atherosclerosis progression have not yet been fully investigated. Therefore, this study is to determine whether IPE 4 g/day will result in a greater change from baseline in plaque volume measured by serial multidetector computed tomography than placebo in statin-treated patients. Methods and results EVAPORATE is a randomized, double-blind, placebo-controlled trial. Patients had to have coronary atherosclerosis by coronary computed tomographic angiography (CCTA) (≥1 angiographic stenoses with ≥20% narrowing), on stable statin therapy with low-density lipoprotein cholesterol levels 40–115 mg/dL, and persistently high triglyceride levels (135–499 mg/dL). Patients underwent an interim scan at 9 months and were followed for an additional 9 months with CCTA at 0, 9, and 18 months. Here, we present the protocol-specified interim efficacy results. A total of 80 patients were enrolled, with 67 completing the 9-month visit and having interpretable CCTA at baseline and at 9 months (age = 57 ± 6 years, male = 36, 63%). At the 9-month interim analysis, there was no significant change in low attenuation plaque (LAP) between active and placebo groups (74% vs. 94%, P  = 0.469). However, there was slowing of total non-calcified plaque (sum of LAP, fibrofatty, and fibrous plaque) (35% vs. 43%, P  = 0.010), total plaque (non-calcified + calcified plaque) (15% vs. 26%, P  = 0.0004), fibrous plaque (17% vs. 40%, P  = 0.011), and calcified plaque (−1% vs. 9%, P  = 0.001), after adjustment by baseline plaque, age, sex, diabetes, baseline triglyceride levels, and statin use. Conclusion EVAPORATE is the first study using CCTA to evaluate the effects of IPE as an adjunct to statin therapy on atherosclerotic plaque characteristics in a high-risk CV population with persistently high triglyceride levels. It provides important mechanistic data in regards to the reduction in CV events in the REDUCE-IT clinical trial. ClinicalTrials. govIdentifier NCT029226027. [ABSTRACT FROM AUTHOR]

Introduction: The apolipoprotein A1 (apoA1) remnant ratio has been identified as an independent cardiovascular (CV) risk factor. Higher apoA1 remnant ratios may predict lower CV risk in some patients. This analysis aimed to evaluate the effects of evolocumab on the change from baseline in the apoA1 remnant ratio compared with placebo. Methods: This pooled post hoc analysis included 2464 patients with mixed dyslipidemia treated with evolocumab 140 mg every 2 weeks (Q2W) or 420 mg once monthly (QM) in three phase 3 evolocumab trials. The apoA1 remnant ratio was calculated by dividing apoA1 by the difference between non-high-density lipoprotein cholesterol (non-HDL-C) and low-density lipoprotein cholesterol (LDL-C). ApoA1 remnant ratio strata were generated using previously published tertile (< 4.7, 4.7–6.8, and > 6.8) and partitioning categories (< 3.6, 3.6–6.0, and > 6.0). Results: The baseline apoA1 remnant ratio in evolocumab and placebo treatment arms was 7.1 and 7.3, respectively. At week 12, evolocumab 140 mg Q2W and 420 mg QM increased the apoA1 remnant ratio by 25.0% and 33.6%, respectively, versus placebo (p < 0.0001 for both groups). When patients were categorized by week 12 apoA1 remnant ratio thresholds (< 3.6 vs. > 3.6, and < 4.7 vs. > 4.7), those with higher week 12 apoA1 remnant ratios were significantly more likely to have also achieved a target non-HDL-C level of < 100 mg/dl. In the subset of women > 50 years of age, the proportion of patients at apoA1 remnant ratio thresholds < 3.6, 3.6–6.0, and > 6.0 at baseline shifted toward or remained at higher thresholds at week 12. Conclusions: This post hoc analysis suggests that evolocumab increases the apoA1 remnant ratio. Funding: Amgen Inc. Plain Language Summary: Plain language summary available for this article. [ABSTRACT FROM AUTHOR]

Background The red cell distribution width (RDW) predicts mortality in numerous populations. The Intermountain Risk Scores (IMRS) predict patient outcomes using laboratory measurements including RDW. Whether the RDW or IMRS predicts in-hospital outcomes is unknown. Methods The predictive abilities of RDW and two IMRS formulations (the complete blood count [CBC] risk score [CBC-RS] or full IMRS using CBC plus the basic metabolic profile) were studied among percutaneous coronary intervention patients at Intermountain (males: N = 6007, females: N = 2165). Primary endpoints were a composite bleeding outcome and in-hospital mortality. Results IMRS predicted the composite bleeding endpoint (females: χ 2  = 47.1, odds ratio [OR] = 1.13 per +1 score, p < 0.001; males: χ 2  = 108.7, OR = 1.13 per +1 score, p < 0.001) more strongly than RDW (females: χ 2  = 1.6, OR = 1.04 per +1%, p = 0.20; males: χ 2  = 11.2, OR = 1.09 per +1%, p < 0.001). For in-hospital mortality, RDW was predictive in females (χ 2  = 4.3, OR = 1.13 per +1%, p = 0.037) and males (χ 2  = 4.4, OR = 1.11 per +1%, p = 0.037), but IMRS was profoundly more predictive (females: χ 2  = 35.5, OR = 1.36 per +1 score, p < 0.001; males: χ 2  = 72.9, OR = 1.40 per+1 score, p < 0.001). CBC-RS was more predictive than RDW but not as powerful as IMRS. Conclusions The IMRS, the CBC-RS, and RDW predict in-hospital outcomes. Risk score-directed personalization of in-hospital clinical care should be studied. [ABSTRACT FROM AUTHOR]

Background The red cell distribution width ( RDW) predicts mortality among many populations. RDW is calculated as the standard deviation ( SD) of the red blood cell ( RBC) volume divided by mean corpuscular volume ( MCV). Because higher MCV also predicts mortality, we hypothesized that the RDW numerator (one SD of RBC volume or 1 SD- RDW) predicts mortality more strongly than the RDW. Material and methods Adult subjects hospitalized during a contemporary clinical era (10/2005-1/2014, N = 135 963) and a historical era (1/1999-9/2005, N = 119 530) were studied. The RDW was obtained from the complete blood count ( CBC), while 1 SD- RDW was calculated ( RDW multiplied by MCV and divided by 100). Results In univariable Cox regression (2005-2014 cohort), 1 SD- RDW (quintile 5 vs. 1: hazard ratio [ HR] = 8·38, 95% confidence interval [ CI] = 7·94, 8·85; P < 0·001) was a superior predictor of mortality compared to RDW (quintile 5 vs. 1: HR = 4·78, CI = 4·57, 5·00; P < 0·001). This superiority remained after adjustment for age, sex, basic metabolic profile components and other CBC factors excluding MCV (1 SD- RDW: HR = 2·41, CI = 2·28, 2·55; RDW: HR = 2·01, CI = 1·92, 2·11). Further adjustment for MCV strengthened the RDW association ( HR = 2·14, CI = 2·04, 2·24; P < 0·001), becoming indistinct from 1 SD- RDW ( HR = 2·20, CI = 2·08, 2·33; P < 0·001). Findings were similar for the 1999-2005 cohort. Conclusions The 1 SD- RDW predicted mortality more strongly than RDW, suggesting that 1 SD- RDW is superior to RDW as an individual risk predictor. Further, these results indicate that the dispersion of RBC volume and its mean are independent risk markers. Further research is required to understand the clinical value and mechanistic basis of these associations. [ABSTRACT FROM AUTHOR]

Importance: Coronary artery disease (CAD) is a major cause of cardiovascular morbidity and mortality in patients with diabetes mellitus, yet CAD often is asymptomatic prior to myocardial infarction (MI) and coronary death.Objective: To assess whether routine screening for CAD by coronary computed tomography angiography (CCTA) in patients with type 1 or type 2 diabetes deemed to be at high cardiac risk followed by CCTA-directed therapy would reduce the risk of death and nonfatal coronary outcomes.Design, Setting, and Participants: The FACTOR-64 study was a randomized clinical trial in which 900 patients with type 1 or type 2 diabetes of at least 3 to 5 years' duration and without symptoms of CAD were recruited from 45 clinics and practices of a single health system (Intermountain Healthcare, Utah), enrolled at a single-site coordinating center, and randomly assigned to CAD screening with CCTA (n = 452) or to standard national guidelines-based optimal diabetes care (n = 448) (targets: glycated hemoglobin level <7.0%, low-density lipoprotein cholesterol level <100 mg/dL, systolic blood pressure <130 mm Hg). All CCTA imaging was performed at the coordinating center. Standard therapy or aggressive therapy (targets: glycated hemoglobin level <6.0%, low-density lipoprotein cholesterol level <70 mg/dL, high-density lipoprotein cholesterol level >50 mg/dL [women] or >40 mg/dL [men], triglycerides level <150 mg/dL, systolic blood pressure <120 mm Hg), or aggressive therapy with invasive coronary angiography, was recommended based on CCTA findings. Enrollment occurred between July 2007 and May 2013, and follow-up extended to August 2014.Main Outcomes and Measures: The primary outcome was a composite of all-cause mortality, nonfatal MI, or unstable angina requiring hospitalization; the secondary outcome was ischemic major adverse cardiovascular events (composite of CAD death, nonfatal MI, or unstable angina).Results: At a mean follow-up time of 4.0 (SD, 1.7) years, the primary outcome event rates were not significantly different between the CCTA and the control groups (6.2% [28 events] vs 7.6% [34 events]; hazard ratio, 0.80 [95% CI, 0.49-1.32]; P = .38). The incidence of the composite secondary end point of ischemic major adverse cardiovascular events also did not differ between groups (4.4% [20 events] vs 3.8% [17 events]; hazard ratio, 1.15 [95% CI, 0.60-2.19]; P = .68).Conclusions and Relevance: Among asymptomatic patients with type 1 or type 2 diabetes, use of CCTA to screen for CAD did not reduce the composite rate of all-cause mortality, nonfatal MI, or unstable angina requiring hospitalization at 4 years. These findings do not support CCTA screening in this population.Trial Registration: clinicaltrials.gov Identifier: NCT00488033. [ABSTRACT FROM AUTHOR]

IMPORTANCE Coronary artery disease (CAD) is a major cause of cardiovascular morbidity and mortality in patients with diabetes mellitus, yet CAD often is asymptomatic prior to myocardial infarction (MI) and coronary death. OBJECTIVE To assess whether routine screening for CAD by coronary computed tomography angiography (CCTA) in patients with type 1 or type 2 diabetes deemed to be at high cardiac risk followed by CCTA-directed therapy would reduce the risk of death and nonfatal coronary outcomes. DESIGN, SETTING, AND PARTICIPANTS The FACTOR-64 study was a randomized clinical trial in which 900 patients with type 1 or type 2 diabetes of at least 3 to 5 years' duration and without symptoms of CAD were recruited from45 clinics and practices of a single health system (Intermountain Healthcare, Utah), enrolled at a single-site coordinating center, and randomly assigned to CAD screening with CCTA (n = 452) or to standard national guidelines-based optimal diabetes care (n = 448) (targets: glycated hemoglobin level <7.0%, low-density lipoprotein cholesterol level <100mg/dL, systolic blood pressure <130mmHg). All CCTA imaging was performed at the coordinating center. Standard therapy or aggressive therapy (targets: glycated hemoglobin level <6.0%, low-density lipoprotein cholesterol level <70mg/dL, high-density lipoprotein cholesterol level >50mg/dL [women] or >40mg/dL [men], triglycerides level <150mg/dL, systolic blood pressure <120mmHg), or aggressive therapy with invasive coronary angiography, was recommended based on CCTA findings. Enrollment occurred between July 2007 and May 2013, and follow-up extended to August 2014. MAIN OUTCOMES ANDMEASURES The primary outcome was a composite of all-cause mortality, nonfatal MI, or unstable angina requiring hospitalization; the secondary outcome was ischemic major adverse cardiovascular events (composite of CAD death, nonfatal MI, or unstable angina). RESULTS At a mean follow-up time of 4.0 (SD, 1.7) years, the primary outcome event rates were not significantly different between the CCTA and the control groups (6.2% [28 events] vs 7.6% [34 events]; hazard ratio, 0.80 [95%CI, 0.49-1.32]; P = .38). The incidence of the composite secondary end point of ischemic major adverse cardiovascular events also did not differ between groups (4.4% [20 events] vs 3.8% [17 events]; hazard ratio, 1.15 [95%CI, 0.60-2.19]; P = .68). CONCLUSIONS AND RELEVANCE Among asymptomatic patients with type 1 or type 2 diabetes, use of CCTA to screen for CAD did not reduce the composite rate of all-causemortality, nonfatal MI, or unstable angina requiring hospitalization at 4 years. These findings do not support CCTA screening in this population. [ABSTRACT FROM AUTHOR]

Previously we discovered that routine periodic fasting was associated with a lower prevalence of coronary artery disease (CAD). Other studies have shown that fasting increases longevity in animals. A hypothesis-generating analysis suggested that fasting may also associate with diabetes. This study prospectively tested whether routine periodic fasting is associated with diabetes mellitus (DM). Patients (n = 200) undergoing coronary angiography were surveyed for routine fasting behavior before their procedure. DM diagnosis was based on physician reports of current and historical clinical and medication data. Secondary end points included CAD (physician reported for ≥1 lesion of ≥70% stenosis), glucose, and body mass index (BMI). Meta-analyses were performed by evaluation of these patients and 448 patients from a previous study. DM was present in 10.3% of patients who fasted routinely and 22.0% of those who do not fast (odds ratio [OR] 0.41, 95% confidence interval [CI] 0.17 to 0.99, p = 0.042). CAD was found in 63.2% of fasting and 75.0% of nonfasting patients (OR 0.42, CI 0.21 to 0.84, p = 0.014), and in nondiabetics this CAD association was similar (OR 0.38, CI 0.16 to 0.89, p = 0.025). Meta-analysis showed modest differences for fasters versus nonfasters in glucose concentrations (108 ± 36 vs 115 ± 46 mg/dl, p = 0.047) and BMI (27.9 ± 5.3 vs 29.0 ± 5.8 kg/m2, p = 0.044). In conclusion, prospective hypothesis testing showed that routine periodic fasting was associated with a lower prevalence of DM in patients undergoing coronary angiography. A reported fasting association with a lower CAD risk was also validated and fasting associations with lower glucose and BMI were found. [Copyright &y& Elsevier]

Plasma renin activity (PRA) is a measure of renin–angiotensin system activity and is associated with cardiovascular outcomes in patients with heart failure (HF). We conducted a prospective analysis to assess whether elevated baseline PRA is associated with cardiovascular outcomes in 1,165 patients with coronary artery disease (≥70% stenosis on the coronary angiogram) enrolled in the Intermountain Heart Collaborative Study. The exclusion criteria included previous myocardial infarction (MI) or HF, ejection fraction ≤45%, and a discharge diagnosis of MI/β-blocker treatment. Baseline PRA measurements were evaluated as risk categories (≤0.50, 0.51 to 2.30, and >2.30 ng/ml/h) and as tertiles (≤0.40, 0.41 to 1.90, and ≥1.90 ng/ml/h). Predefined cardiovascular outcomes were assessed for a minimum follow-up of 3 years (mean 6.4 ± 3.2, maximum 14.6) using Cox regression analysis to adjust for the baseline characteristics. The mean patient age was 64.4 years; most patients were men (73.1%) and hypertensive (63.2%). Elevated baseline PRA (high vs low category; >2.30 vs ≤0.50 ng/ml/h) was associated with a significantly increased risk of 3-year cardiac morbidity/mortality (hazard ratio 1.96; p = 0.004), MI (hazard ratio 2.41; p = 0.02), HF hospitalization (hazard ratio 4.39; p = 0.03), and all-cause death (hazard ratio 1.80; p = 0.01). Elevated baseline PRA was also associated with longer-term HF hospitalization (hazard ratio 2.12; p = 0.004) and all-cause death (hazard ratio 1.56; p = 0.002). Similar results were observed for the PRA tertiles. The association of PRA with outcomes was observed after correction for hypertension, hyperlipidemia, diabetes, a family history of cardiovascular events, smoking, renal failure, and the use of statins. In conclusion, elevated baseline PRA is associated with cardiac morbidity and mortality in patients with coronary artery disease but normal left ventricular function and no previous MI or HF. [Copyright &y& Elsevier]

Although increased cholesterol levels predict mortality in patients with coronary artery disease, it is unclear whether hypercholesterolemia is associated with adverse survival in patients with heart failure. A cohort of subjects derived from the Intermountain Heart Collaborative Study Registry (1993 to 2003) who had ejection fractions ≤40% or clinical diagnoses of heart failure and long-term follow-up for death were studied (n = 1,646). Total cholesterol (TC) was divided into quartiles: quartile 1, <141.3 mg/dl; quartile 2, 141.3 to 167.9 mg/dl; quartile 3, 168.0 to 201.0 mg/dl; and quartile 4, >201.0 mg/dl. Multivariate Cox regression models were used to evaluate the associations of cholesterol, statin therapy, and C-reactive protein to mortality. The mean age was 65.5 years; 65% of the subjects were men and 65% had coronary artery disease. Although 53% were using statins, statin use was not different across TC quartiles. Average time to death was 2.4 years (maximum 10). Mortality for quartile 4 versus quartile 1 was not different (hazard ratio [HR] 1.12, p = 0.52); mortality was reduced for quartile 3 versus quartile 1 (HR 0.66, p = 0.027) and tended to be reduced for quartile 2 versus quartile 1 (HR 0.77, p = 0.14). Subanalysis of patients not using statins (n = 737, death = 20.2%) found no association between TC and survival (for quartile 3 vs quartile 1, HR 0.97, p = 0.89), but for patients using statins (n=848, death = 16.3%), the effect was even greater for quartile 3 versus quartile 1 (HR 0.40, p = 0.002) than in the overall population. Nonsurvivors had higher levels of C-reactive protein than survivors. In conclusion, elevated TC appears to be associated with improved survival. The effect was stronger in patients receiving statin therapy, but the cause of this differential effect is uncertain. [Copyright &y& Elsevier]

Objectives: The primary objective was to determine the effect of statin-fibrate combination therapy on inflammatory biomarkers in patients with diabetes. Background: Atherosclerosis is a long-term, chronic inflammatory disease that is exacerbated in patients with diabetes. Methods: Patients (n = 300) with type II diabetes, mixed dyslipidemia (2 or more of low-density lipoprotein ≥100 mg/dl, triglycerides ≥200 mg/dl, or high-density lipoprotein <40 mg/dl), and no history of coronary heart disease were randomly assigned to receive simvastatin 20 mg, fenofibrate 160 mg, or a combination of simvastatin 20 mg and fenofibrate 160 mg daily. At 12 weeks after randomization, we measured levels of high-sensitivity C-reactive protein (hsCRP) and lipoprotein-associated phospholipase A2 (Lp-PLA2). Results: At 12 weeks, median hsCRP was significantly reduced (−14.6%, p = 0.004) from baseline, but the effect did not differ between treatments. The effect was greatest among patients with baseline hsCRP levels >2.0 mg/l (fenofibrate = −18.9%, p = 0.002 vs. baseline; simvastatin = −24.8%, p < 0.0001; combination = −27.3%, p = 0.002). Likewise, median Lp-PLA2 levels in the overall study population were significantly reduced (−16.8%, p < 0.0001), and the effect did not differ among treatments. This effect also was greatest among patients with increased baseline levels of Lp-PLA2 greater than the median of 320.9 ng/ml (fenofibrate = −41.3%, p < 0.0001; simvastatin = −47.5%, p < 0.0001; combination = −46.8%, p < 0.0001). Conclusions: Simvastatin, fenofibrate, and combination therapy each lowered hsCRP and Lp-PLA2. These anti-inflammatory effects were most pronounced among patients with increased baseline levels. Combination therapy was no more effective than either form of monotherapy. (The DIACOR Study; http://www.clinicaltrials.gov/ct/show/NCT00309712?order=1) [Copyright &y& Elsevier]

Beta-blocker therapy has been shown to benefit patients who have coronary artery disease and present with acute myocardial infarction (AMI) and/or congestive heart failure (HF). However, whether β-blocker therapy provides a similar benefit in patients who have coronary artery disease but not AMI or HF is unknown. A population of 4,304 patients who did not have HF but did have angiographically confirmed coronary artery disease (≥1 stenosis of ≥70%) without AMI at hospital presentation was evaluated. Baseline demographics, cardiac risk factors, clinical presentation, therapeutic procedures, and discharge medications were recorded. Patients were followed for a mean of 3.0 ± 1.9 years (range 1 month to 6.9 years) for outcomes of all-cause death or AMI. Patients'' average age was 65 ± 11 years and 77% were men. Overall, 10% died and 5% had a nonfatal AMI. Discharge β-blocker prescription was associated with an increased event-free AMI survival rate for all-cause death (no β blocker 88.3%, β blocker 94.5%, p &#60;0.001) and death/AMI (no β blocker 83.4%, β blocker 89.2%, p &#60;0.001) but not non-fatal AMI (no β blocker 93.6%, β blocker 94.1%, p = 0.60). After adjustment for 16 covariates, including statin prescription, angiotensin-converting enzyme inhibitor prescription, and type of baseline therapy, the effect of β blockers on the combination end point of death/AMI was eliminated. However, the effect of β blockers on death remained (hazard ratio 0.66, 95% confidence interval 0.47 to 0.93, p = 0.02). Thus, β blockers are clearly indicated for most patients who have HF or AMI, and our results suggest that patients who have coronary artery disease without these conditions have approximately the same protective benefit against death. No effect was observed on longitudinal incidence of AMI or the combination of death/nonfatal MI. [Copyright &y& Elsevier]

Acute coronary syndromes (ACS), such as myocardial infarction and unstable angina, are leading causes of death in developed countries. The risk of recurrent adverse events, rehospitalization, and death remain high in the weeks to months following ACS. Large secondary prevention trials have shown that the initiation of statin therapy within 3–6 months after hospitalization for ACS decreases the risk of recurrent cardiovascular events and death. Although the precise mechanisms behind these clinical benefits are unknown, data from human and animal studies have implicated statins in inflammatory response modulation, plaque stability, thrombus formation, and endothelial function. Several observational studies have demonstrated cardiovascular mortality and morbidity benefits in patients with ACS who were placed on statins within hours to days of their event. Three recent prospective controlled trials confirmed these benefits and demonstrated that moderate doses of statins are safe when used in patients with ACS. We recommend the initiation of statin therapy in all ACS patients prior to hospital discharge.(J Interven Cardiol 2005;18:55–63) [ABSTRACT FROM AUTHOR]

Statins improve survival in patients with coronary artery disease, especially those with elevated C-reactive protein (CRP). Although some randomized studies have shown a delay in statin-related survival advantage of up to 2 years, recent studies demonstrated early (<2 months) survival benefit in certain patient groups. We hypothesized that this early benefit relates to baseline CRP concentration. Patients (n = 2,924) with significant, angiographically defined coronary artery disease (≥70% stenosis in ≥1 coronary artery) were followed for an average of 2.4 years after discharged on a statin prescription. CRP was divided into tertiles (<1.2, 1.2 to 1.7, >1.7 mg/dl), and Kaplan-Meier methods were used to determine timing of statin benefit in both the overall population and a propensity score-matched subgroup. Cox regressions (multivariable and propensity score approaches) were used to predict mortality. Statins were prescribed for 28.4% of patients. In the first CRP tertile, no early statin benefit was observed (adjusted hazard ratio 0.69, 95% confidence interval [CI] 0.30 to 1.6, p = 0.39), and survival curves separated after >2 years. However, in the second and the third tertiles, statin survival curves separated much earlier (∼3 months and 1 week, respectively) and statins predicted improved survival (second tertile: hazard ratio 0.63, 95% CI 0.32 to 1.2, p = 0.17; third tertile: hazard ratio 0.35, 95% CI 0.18 to 0.67, p = 0.002). Propensity score analysis confirmed both statin benefit and early timing. Thus, statin use in patients with high CRP provides not only a larger but also a significantly earlier absolute survival benefit than statin use in patients with lower CRP. This provides further evidence of an anti-inflammatory effect of statins. [Copyright &y& Elsevier]

Abstract: Objective: : Cytomegalovirus (CMV) has been epidemiologically associated with multiple disease processes including coronary, carotid and cardiac graft atherosclerosis. An early initiating event in atherogenesis is the uptake by macrophages of oxidized low-density lipoproteins (OxLDL) via the scavenger receptor, CD36. Because CMV can activate host-cell gene transcription, we hypothesized that CMV may upregulate CD36 expression. Methods and results: : THP-1 monocyte/macrophage cells were treated with Davis strain CMV and cell surface CD36 expression measured by flow cytometry. Virus challenge increased the percentage of cells expressing CD36 from 21.8 ± 1.7 to 48.2 ± 4.0% (mean ± S.D. for three experiments, P = 0.0005); CD36 mRNA accumulation was increased by CMV treatment as determined by reverse transcription-polymerase chain reaction. Viral challenge also upregulated the mitogen-activated protein kinase p38; further, the specific p38 inhibitor, SB203580, reversed the CMV-induced CD36 cell surface expression from 57.2% of cells to baseline levels (29.0 and 30.1% for SB203580 treated and control cells, respectively; P = 0.001). Treatment with virus also stimulated uptake of OxLDL: microscopically, virus-treated cells had a mean of 32 ± 4.0 lipid vacuoles compared with 20 ± 1.3 for control cells (P = 0.01). Conclusions: : These findings suggest that CMV-induced CD36 expression is one mechanism through which CMV may promote atherosclerosis. Other CMV-associated atherogenic mechanisms may exist; additional investigation is necessary. [Copyright &y& Elsevier]

To determine whether sex and age affect serum C-reactive protein level and its prognostic value in patients with coronary artery disease.In a consecutive series of 2254 patients with angiographically defined coronary artery disease, baseline C-reactive protein and predictive value for incident death or nonfatal myocardial infarction by sex and age (<55 and ≥55 years) were compared. C-reactive protein levels were measured by fluorescence polarization immunoassay with use of a medium-sensitivity method. Patients were followed for a mean (±SD) of 3.1 ± 2.2 years. Comparisons used ln-transformed C-reactive protein and linear and time-to-event regression analyses, adjusting for confounders.Overall, women had higher geometric mean C-reactive protein levels than did men (1.47 vs. 1.30 mg/dL, P <0.001), even after adjustment for age, hyperlipidemia, diabetes, prior myocardial infarction, body mass index, and heart failure (P = 0.002). High C-reactive protein levels were associated with increased mortality or myocardial infarction among men (adjusted hazard ratio [HR] = 1.9; 95% confidence interval [CI]: 1.5 to 2.3) but not among women (HR = 1.0; 95% CI: 0.69 to 1.4). Among patients aged <55 years, C-reactive protein level was similarly predictive in men and women (HR = 2.2 vs. 2.7), whereas in patients ≥55 years of age, it remained predictive for men (HR = 1.8; 95% CI: 1.5 to 2.3) but not women (HR = 0.93; 95% CI: 0.63 to 1.4).We found that the prognostic value of C-reactive protein in coronary artery disease patients varied by sex and age. This sex-age interaction may have important implications for C-reactive protein–based secondary risk assessment and requires further investigation. [Copyright &y& Elsevier]

Background: Despite recent advances in the treatment and prevention of cardiovascular disease, a treatment gap for secondary prevention medications still exists. Objective: To develop and implement a program ensuring appropriate prescription of aspirin, statins, β-blockers, angiotensin-converting enzyme inhibitors, and warlarin at hospital discharge. Design: A nonrandomized before-after study comparing patients hospitalized before (1996-1998) and after (1999-2002) implementation of a discharge medication program (DMP). Patients were followed for up to 1 year. Setting: The 10 largest hospitals in the Utah-based Intermountam Health Care system. Patients: In the pre-DMP and DMP time periods, 26 000 and 31 465 patients, respectively, were admitted to cardiovascular services (n = 57465). Measurements: Prescription of indicated medications at hospital discharge; post discharge death or readmission. Results: By 1 year, the rate of prescription of each medication increased significantly to more than 90% (P< 0.001); this rate was sustained. At 1 year, unadjusted absolute event rates for readmission and death, respectively, were 210 per 1000 person-years and 96 per 1000 person-years before OMP implementation and 191 per 1000 person-years and 70 per 1000 person-years afterward. Relative risk for death and readmission at 30 days decreased after OMP implementation; hazard ratios (HRs) for death and readmission were 0.81 (95% CI, 0.73 to 0.89) and 0.92 (CI, 0.87 to 0.99) (P < 0.001 and P = 0.017, respectively). At I year, risk for death continued to decrease (hazard ratio, 0.79 [CI, 0.75 to 0.84]; P < 0.001) while risk for readmission stabilized (hazard ratio, 0.94 [CI, 0.90 to 0.98]; P= 0.002), probably because survivors had more opportunities to be readmitted. Limitations: The study design was observational and nonrandomized, and the authors could not control for potential confounders or determine the extent to which secular trends accounted for the observed improvements. Conclusions: A relatively simple quality improvement program aimed at enhancing the prescription of appropriate discharge medications among cardiovascular patients is feasible and can be sustained within an integrated multihospital system. Such a program may be associated with improvements in cardiovascular readmission rates and mortality. [ABSTRACT FROM AUTHOR]

The possibility has been raised in recent years that infection might contribute as an inflammatory stimulus to chronic "noninfectious" degenerative diseases. Within the past decade, serious attention has been given to the possibility of bacterial vectors as causal factors of atherosclerosis. To date, the greatest amount of information has related to the intracellular organism Chlamydia pneumoniae. This interest has been stimulated by the frequent finding of bacterial antigens and, occasionally, recoverable organisms, within human atherosclerotic plaque. Indirect evidence for and against the benefit of anti-Chlamydia antibiotic agents comes from epidemiologic studies. Given the potential for confounding in observational studies, prospective, randomized intervention trials are required. These antibiotic trials have generated enthusiastic expectations for proving (or disproving)the infectious-disease hypothesis of atherosclerosis and establishing new therapies. However, these expectations have been tempered by important limitations and uncertainties. Negative outcomes can be explained not only by an incorrect hypothesis but also by inadequate study size or design or by an ineffective antibiotic regimen. In contrast, if studies are positive, the hypothesis still is not entirely proved, because a nonspecific anti-inflammatory effect or an anti-infective action against other organisms might be operative. The clinical trial data to date have not provided adequate support for the clinical use of antibiotics in primary or secondary prevention of coronary heart disease. New and innovative experimental approaches, in addition to traditionally designed antibiotic trials, should be welcome in our attempts to gain adequate insight into the role of infection in atherosclerosis and its therapy. [ABSTRACT FROM AUTHOR]

: PurposeLow socioeconomic status (SES) predicts coronary artery disease (CAD) onset, but its value among patients with CAD is uncertain. Geographic measures (e.g., residential neighborhood) may predict risk, but this requires further evaluation.: MethodsA cohort of 3410 patients with significant, angiographically-defined CAD (≥1 lesion of ≥70% stenosis) joined a registry during the period between 1993 and 2000 and was followed for 6.7 years (median 3.7 years). A geographic SES measure—residential economic status (RES)—and insurance type were examined for association with mortality or myocardial infarction (MI).: ResultsIn Cox regression adjusting for 17 covariates, lower RES quartile was associated with increased death/MI (p-trend<0.001), death (p-trend = 0.001), and MI (p-trend = 0.07). First RES quartile (vs. fourth) predicted death/MI (hazard ratio [HR] = 1.32, 95% confidence interval [CI] = 1.07–1.62, p = 0.01) and death (HR = 1.46, CI = 1.12–1.91, p = 0.006), but not MI (HR = 1.18, p = 0.31). Compared with private insurance, self-pay (HR = 1.88, p = 0.053), charity care (HR = 1.71, p<0.001), and Medicaid (HR = 1.43, p = 0.24), but not Medicare (HR = 0.95, p = 0.68), were associated with death/MI.: ConclusionsBoth geographic (RES) and economic (insurance) measures of SES independently predicted risk of death/MI in a large population with angiographically-defined CAD. This suggests that SES remains a significant predictor of health outcomes after CAD has developed, and that geographic measures of SES deserve further evaluation. [Copyright &y& Elsevier]

: ObjectivesThis study evaluated the effect of statin therapy on mortality in individuals with significant coronary artery disease (CAD) stratified by age.: BackgroundHydroxymethylglutaryl coenzyme A reductase inhibitors (statins) significantly reduce morbidity and mortality in individuals with CAD. Unfortunately, the large statin trials excluded individuals over 80 years old, and it is therefore unknown whether very elderly individuals benefit from statins as do younger individuals.: MethodsA cohort of 7,220 individuals with angiographically defined significant CAD (≥70%) was included. Statin prescription was determined at hospital discharge. Patients were followed up for 3.3 ± 1.8 years (maximum 6.8). Patients were grouped by age (<65, 65 to 79, and ≥80 years) to determine whether statin therapy reduced mortality in an age-dependent manner.: ResultsAverage age was 65 ± 12 years; 74% were male; and 31% had a postmyocardial infarction status. Overall mortality was 16%. Elderly patients were significantly less likely to receive statins than younger patients (≥80 years: 19.8%; 65 to 79 years: 21.1%; <65 years: 28.0%; p < 0.001). Mortality was decreased among statin recipients in all age groups: ≥80 years: 29.5% among patients not taking a statin versus 8.5% of those taking a statin (adjusted hazard ratio [HR] 0.50, p = 0.036); 65 to 79 years: 18.7% vs. 6.0% (HR 0.56, p < 0.001); and <65 years: 8.9% vs. 3.1% (HR 0.70, p = 0.097).: ConclusionsStatin therapy is associated with reduced mortality in all age groups of individuals with significant CAD, including very elderly individuals. Although older patients were less likely to receive statin therapy, they received a greater absolute risk reduction than younger individuals. More aggressive statin use after CAD diagnosis may be indicated, even in older patients. [Copyright &y& Elsevier]

Objectives: The objective of this study was to determine the prognostic value of C-reactive protein (CRP) independent of coronary angiographic findings.Background: High sensitivity CRP, a marker of inflammation, predicts risk of cardiovascular events. However, it is uncertain whether it remains predictive once angiographic findings are considered.Methods: A total of 2,554 patients with angina but without acute myocardial infarction (MI) were studied angiographically; 1,848 patients had coronary artery disease (CAD) and 706 patients did not. Coronary artery disease was quantified in five ways and combined for a CAD score. C-reactive protein was measured and patients were followed for up to five years for death or MI.Results: C-reactive protein correlated with the extent of CAD, but correlation coefficients were low (0.02 to 0.08). Of angiographic measures, the CAD score best predicted future events (hazard ratio [HR] = 1.8 [1.2 to 2.6], p = 0.004, for CAD score > 4). C-reactive protein > or = 1.0 mg/dl was predictive in both patients without CAD (HR = 2.3 [0.9 to 5.5], p = 0.07) and with CAD (HR = 2.1 [1.5 to 3.1], p = 0.0001). Multivariate adjustment resulted in little change in HR. C-reactive protein retained predictive value within each quintile of CAD score. C-reactive protein and CAD independently and additively contributed to the risk prediction: low CRP and lowest CAD score was associated with lowest risk, and high CRP and highest CAD score was associated with the highest risk, with a 10-fold difference between extremes (2.5% vs. 24%).Conclusions: C-reactive protein correlates with extent of CAD, but the degree of correlation is low. Severity/extent of CAD and CRP are independent and additive predictors of risk. Therapy should target CRP-associated risk as well as angiographically evident stenosis. [ABSTRACT FROM AUTHOR]

: ObjectivesThe objective of this study was to determine the prognostic value of C-reactive protein (CRP) independent of coronary angiographic findings.: BackgroundHigh sensitivity CRP, a marker of inflammation, predicts risk of cardiovascular events. However, it is uncertain whether it remains predictive once angiographic findings are considered.: MethodsA total of 2,554 patients with angina but without acute myocardial infarction (MI) were studied angiographically; 1,848 patients had coronary artery disease (CAD) and 706 patients did not. Coronary artery disease was quantified in five ways and combined for a CAD score. C-reactive protein was measured and patients were followed for up to five years for death or MI.: ResultsC-reactive protein correlated with the extent of CAD, but correlation coefficients were low (0.02 to 0.08). Of angiographic measures, the CAD score best predicted future events (hazard ratio [HR] = 1.8 [1.2 to 2.6], p = 0.004, for CAD score >4). C-reactive protein ≥1.0 mg/dl was predictive in both patients without CAD (HR = 2.3 [0.9 to 5.5], p = 0.07) and with CAD (HR = 2.1 [1.5 to 3.1], p = 0.0001). Multivariate adjustment resulted in little change in HR. C-reactive protein retained predictive value within each quintile of CAD score. C-reactive protein and CAD independently and additively contributed to the risk prediction: low CRP and lowest CAD score was associated with lowest risk, and high CRP and highest CAD score was associated with the highest risk, with a 10-fold difference between extremes (2.5% vs. 24%).: ConclusionsC-reactive protein correlates with extent of CAD, but the degree of correlation is low. Severity/extent of CAD and CRP are independent and additive predictors of risk. Therapy should target CRP-associated risk as well as angiographically evident stenosis. [Copyright &y& Elsevier]

Despite well-documented clinical benefit of the use of statins in patients with coronary artery disease (CAD) and even mild lipid elevations, studies have documented the presence of a significant "treatment gap" between those patients in whom treatment is indicated and those patients who actually receive it. It has been proposed that a prescription for statin therapy given to indicated patients at the time of initial angiographic diagnosis of CAD has the potential to improve long-term medication compliance, but this requires further evaluation. We prospectively followed 600 patients with angiographically demonstrated CAD (diameter stenosis > or = 70%) who met the National Cholesterol Education Project (NCEP) guidelines for statin therapy for an average of 3.0 years (range 2.0 to 4.6). Patients were an average of 65 years of age, 78% were men, 77% presented initially with acute ischemic syndrome, and 64 (10.7%) died during follow-up. Overall, 105 patients (18%) were discharged from the initial hospitalization with a statin prescription. At long-term follow-up, the number of patients taking statins had increased to 47%. However, long-term statin compliance was significantly higher among patients initially discharged with a statin prescription than those who were not (77% vs 40%; p < 0.0001). Additionally, those patients discharged with a statin prescription had significantly reduced mortality rate at long-term follow-up (5.7% vs 11.7%; p = 0.05). Cox hazard regression analysis, controlling for all known clinical baseline variables, confirmed the absence of a prehospital discharge statin prescription to be an independent predictor of increased mortality (hazard ratio 2.4) with a statistical trend (p = 0.06). Thus, this study demonstrates that after angiographic diagnosis of CAD, prescription of appropriate statin therapy at the time of hospital discharge improves long-term statin compliance and may significantly enhance survival. [ABSTRACT FROM AUTHOR]

The article reports on the use of hyperlipidemia drugs in reducing inflammatory biomakers in patients with diabetes. It is stated that with its effect on lipid parameters and effect on inflammatory markers, combination therapy with statin and fibrate may be the treatment of choice on patients with dyslipidemia and type 2 diabetes. Further, the effectivity of combination therapy in reducing cardiovascular risk is being assessed in the Action to Control Cardiovascular Risk in Diabetes trial.

A recent European case-control study suggested that statins increase the risk for polyneuropathy, a rare but serious neurologic condition. This risk was assessed in 272 patients with idiopathic polyneuropathy and 1,360 matched controls in the Intermountain Health Care electronic database. It was found that statin use before diagnosis was not significantly greater in patients than controls (odds ratio 1.30, 95% confidence interval 0.3 to 2.1, p = 0.27), nor were doses different between patients and controls. [Copyright &y& Elsevier]

Evaluates the need for additional clinical antibiotic trials of a primary or secondary nature for the treatment of atherosclerotic heart disease and to suggest possible designs for future trials. Status of ongoing and already completed clinical trials; Limitations of the trials; Points to consider in planning for further clinical trials.

Tests the effects of three months of azithromycin treatment or placebo in patients with chronic coronary heart disease seropositive to Chlamydia pneumoniae at three to six months. Clinical cardiovascular events between the drug and placebo groups; Reduction of infection and toleration of the drug; Effect of azithromycin in markers of inflammation.

Presents a rabbit model with arterial intimal thickening induced by direct intravascular and intranasal inoculation with Chlamydia pneumoniae. Aim of establishing a causative relationship between C. pneumoniae and atherosclerosis; Role of C. pneumoniae infection in inducing acceleration of atherosclerosis in a mildly hyperlipidemic rabbit model.

Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines are being administered on an unprecedented scale. Assessing the risks of side effects is needed to aid clinicians in early detection and treatment. This study examined the risk of inflammatory heart disease, including pericarditis and myocarditis, after SARS-CoV-2 vaccination. Methods Intermountain Healthcare patients with inflammatory heart disease from December 15, 2020 to June 15, 2021, and with or without preceding SARS-CoV-2 vaccinations, were studied. Relative rates of inflammatory heart disease were examined for vaccinated patients compared to unvaccinated patients. Results Of 67 patients identified with inflammatory heart disease, 21 (31.3%) had a SARS-Cov-2 vaccination within the previous 60 days. Overall, 914 611 Intermountain Healthcare patients received a SARS-CoV-2 vaccine, resulting in an inflammatory heart disease rate of 2.30 per 100 000 vaccinated patients. The relative risk of inflammatory heart disease for the vaccinated patients compared to the unvaccinated patients was 2.05 times higher rate within the 30-day window (P  = .01) and had a trend toward increase in the 60-day window (relative rate = 1.63; P  = .07). All vaccinated patients with inflammatory heart disease were treated successfully with 1 death related to a pre-existing condition. Conclusions Although rare, the rate of inflammatory heart disease was greater in a SARS-CoV-2-vaccinated population than the unvaccinated population. This risk is eclipsed by the risk of contracting coronavirus disease 2019 and its associated, commonly severe outcomes. Nevertheless, clinicians and patients should be informed of this risk to facilitate earlier recognition and treatment. [ABSTRACT FROM AUTHOR]

Background: Patient outcomes after percutaneous coronary intervention (PCI) have improved over the last 30 years due to better techniques, therapies, and care processes. This study evaluated contemporary predictors of post-PCI major adverse cardiovascular events (MACE) and summarized risk in a parsimonious risk prediction model. Methods: The Cardiovascular Patient-Level Analytical Platform (CLiPPeR) is an observational dataset of baseline variables and longitudinal outcomes from the American College of Cardiology's CathPCI Registry® and national claims data. Cox regression was used to evaluate 2–6 years of patient follow-up (mean: 2.56 years), ending in December 2017, after index PCI between 2012 and 2015 (N = 1,450,787), to examine clinical and procedural predictors of MACE (first myocardial infarction, stroke, repeat PCI, coronary artery bypass grafting, and mortality). Cox analyses of post-PCI MACE were landmarked 28 days after index PCI. Results: Overall, 12.4% (n = 179,849) experienced MACE. All variables predicted MACE, with cardiogenic shock, cardiac arrest, four diseased coronary vessels, and chronic kidney disease having hazard ratios (HRs) ≥ 1.50. Other major predictors of MACE were in-hospital stroke, three-vessel disease, anemia, heart failure, and STEMI presentation. The index revascularization and discharge prescription of aspirin, P2Y12 inhibitor, and lipid-lowering medication had HR ≤ 0.67. The primary Cox model had c-statistic c = 0.761 for MACE versus c = 0.701 for the parsimonious model and c = 0.752 for the parsimonious model plus treatment variables. Conclusions: In a nationally representative US sample of post-PCI patients, predictors of longitudinal MACE risk were identified, and a parsimonious model efficiently encapsulated them. These findings may aid in assessing care processes to further improve care post-PCI outcomes. [ABSTRACT FROM AUTHOR]

Background: Atherosclerotic disease (ASCVD) is the leading cause of mortality and healthcare expenditures. Annual indirect and direct costs of ASCVD are estimated to be $330 billion. Although many patients are diagnosed with ASCVD, it is usually only a small percentage of them that are responsible for most of the costs. If it were possible to predict which patients are expected to cost the most, targeted approaches to best manage them could be developed. Methods: A total 62,070 Intermountain Healthcare patients ≥18 years of age with a first encounter for ASCVD (CAD, CVD, and PAD) between January 1, 1999 and December 31, 2013 who survived the index ASCVD event were studied. Patients were stratified into high-cost (>$4,500) and lower-cost (≤$4,500) categories by their average annual costs (calculated by summing the average outpatient, emergency, and inpatient costs per month for each year divided by the number of years contributed). Multivariable analysis was used to determined baseline independent predictors of highest cost. Results: Overall, 2,805 (4.5%) patients fell into the high-cost group (mean = $14,541 [median = $8,018] vs. mean = $526 [median = $223] in the lower-cost group). Total cost over long-term follow-up was $150,932 vs. $34,788. The strongest multivariable predictors of high-cost included age, a PAD diagnosis, diabetes, renal failure, heart failure, COPD, and malignancy (Table). A high-cost risk model was developed and shown to be highly predictive of a high-cost patient (AUC=0.738 [0.729, 0.748], p<0.0001). Conclusion: A small (<5%) population of patients diagnosed with ASCVD have more than 27 times as much average annual per-month cost, and more than 4 times as much over long-term follow-up, than the remaining 95%. Many of the expected high-risk baseline clinical characteristics account for this large disparity in cost. However, by quantitatively integrating these into a multivariable risk model, high-cost patients can best be pre-identified, so they may be selected to receive special attention. [ABSTRACT FROM AUTHOR]

Background: Medical management (MM), percutaneous coronary intervention (PCI) and coronary artery bypass surgery (CABG) are the three main management strategies for patients with symptomatic coronary artery disease (CAD). Over time, improvements in all three strategies have occurred, and the relative frequencies of their use has changed. However, exactly what these changes are, and how they have affected long-term clinical outcomes, is unknown. Methods: All patients (n=43,046) within Intermountain Healthcare ≥18 years of age and enrolled in the IMPRES Registry with a first encounter for a CAD diagnosis from January 1, 1999 to December 31, 2013 who survived the index event were studied. Baseline characteristics were collected, and patients were stratified according to their index management strategies into three time-periods (T1 = 1999-2003, [n=16,289]; T2 = 2004-2008 [n=14,889]; T3 = 2009-2013, [n=11,868]) and followed for five years for the future outcomes of PCI, CABG, myocardial infarction (MI), cerebrovascular accident (CVA), and death according to time periods of enrollment. Multivariable Cox hazard regression analysis was used to determine hazard ratios. Results: Baseline characteristics included age = 65.5±12.4, males = 70.6%, diabetes = 28.7%, smoking = 35.2%, and heart failure = 16.7%. See Table for further results. Conclusions: Over the past 15 years, PCI has become the major initial management strategy for patients diagnosed with CAD. Among those receiving initial PCI, the need for repeat PCI/CABG at 1 year, and at 2-5 years, has dropped by 52% and 38% respectively. The adjusted risk of death/MI/CVA for those initially treated with medical management has improved steadily, but it has remained stable in those initially treated with PCI or CABG. Even with these significant advances in treatment of CAD, 27% of patients diagnosed with CAD in the five years between 2009 and 2013 experienced a major adverse cardiovascular event. These findings emphasize that although major improvements in the secondary management of CAD have occurred, more remains to be accomplished. Additionally, a real need for improved primary prevention of CAD has become evident. [ABSTRACT FROM AUTHOR]

Background: Patients with STEMI who receive rapid diagnosis and reperfusion therapy have improved clinical outcomes. The rate-limiting step in STEMI diagnosis is often the availability of a 12-lead electrocardiogram (ECG) and its interpretation. Recent technology has provided a means of obtaining an ECG recording through smartphones equipped with a 2-wire attachment and software that can potentially produce the equivalent of a standard 12-lead ECG. The ST LEUIS study tested whether a smartphone ECG (AliveCor Inc., Mountain View, CA) can accurately diagnose STEMI in patients presenting with chest pain compared to a standard 12-lead ECG. Methods: Consenting subjects presenting with chest pain or STEMI protocol activation had simultaneous recordings performed with a standard 12-lead and a smartphone '12-lead equivalent' ECG. Matched smartphone and standard ECGs were evaluated separately, both quantitatively and qualitatively, by a panel of blinded, experienced readers and were classified as STEMI/LBBB, not-STEMI, or not interpretable. Interpretable ECG pairs also were subjectively graded as showing good, fair, or poor correlation. Results: A total of 204 subjects (age = 60 years, males = 57%, STEMI activation = 45%) were enrolled from 5 international sites (See Table). For all interpretable smartphone ECGs, versus standard ECGs, the sensitivity, specificity, positive, and negative predictive value for STEMI/LBBB were 0.89, 0.84, 0.70 and 0.95, respectively. Qualitative, interpretable paired ECG evaluations showed 152 (79.2%), 32 (16.7%) and 8 (4.2%) pairs with good, fair and poor correlation, respectively. Conclusion: This first-of-its-kind multicenter, international comparison study demonstrates that a 12-lead equivalent ECG obtained using a smartphone, coupled with a software app and an inexpensive 2-wire attachment, can identify STEMI vs not-STEMI with good correlation and high sensitivity compared to a traditional 12-lead ECG. This technology, including further technical refinements, may provide more rapid ECG access to patients presenting in less urban or remote areas, third world nations, or at home (by family members) before first medical contact, thus potentially improving early STEMI diagnosis and care throughout the world. [ABSTRACT FROM AUTHOR]

Background: Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of mortality and healthcare expenditures. Annual indirect and direct costs of ASCVD are estimated to be $330 billion in the US. The Intermountain Mortality Risk Scores (IMRS) are practical parsimonious models that are highly predictive of death and other major adverse events. It is unknown if IMRS tools predict healthcare utilization and cost. Methods: Patients ≥18 years of age with a first encounter for ASCVD (CAD/MI, CVD, and PAD) between Jan 1, 1999 and Dec 31, 2013, and who survived index ASCVD event were studied. Sex-specific weightings of the comprehensive metabolic panel and complete blood count components were applied to calculate IMRS and patients were stratified into low, moderate, and high risk categories based on previously published thresholds. Results: nAmong females (n=9,150), age averaged 69±15 years, 53.6% had CAD, and 61.4%, 29.6%, and 9.0% were in the low, moderate, and high risk categories, respectively. Males (n=14,176) averaged 66±13 years, 71.1% had CAD, and 56.2%, 35.8%, and 8.0% were in the low moderate, and high risk categories, respectively. IMRS was highly predictive of gradients in 1 year death across low, moderate, and high risk categories (females: 4.8%, 16.8%, 32.6%, p<0.0001; males: 2.0%, 8.9%, and 25.9%, p<0.0001). The higher-risk categories were also associated with more PCIs and angiograms among both genders in the year after the index ASCVD event. Risk strata of IMRS predicted cost among those who did not die by 1 year, but not among those who died before 1 year (Figure). Conclusion: A practical parsimonious clinical decision tool, IMRS predicted higher utilization of angiograms and PCIs at 1 year, greater risk of death at 1 year, and higher costs among those who survived the first year. IMRS identified the higher-risk patients as to risk of death and healthcare utilization and cost. IMRS may be a useful new tool to predict and manage increasing costs. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to a comment to the article "Effect of Screening for Coronary Artery Disease Using CT Angiography on Mortality and Cardiac Events in High-Risk Patients with Diabetes," published in a 2014 issue of "Journal of the American Medical Association" (JAMA).

• ICHRON predicted a 3-year chronic disease among an Australian validation cohort. • ICHRON is valuable for primary care patients in distinct locales. • ICHRON was found to be more predictive among Aboriginal and Torres Islanders. • ICHRON can be calculated within the EHR using standardized laboratory parameters. The Intermountain Chronic Disease Risk Score (ICHRON) is a primary prevention risk prediction tool that uses commonly ordered blood tests and is designed to be calculated by the electronic health record. ICHRON was highly predictive of 3-year chronic disease (ChrD) diagnosis in an internal validation; however, external validation is needed. ICHRON was calculated among patients from a region of Australia using sex-specific weightings of age and components of the comprehensive metabolic panel and the complete blood count. Original ICHRON weightings and risk stratification thresholds from the US-based derivation at Intermountain Healthcare were used. ICHRON was evaluated as a predictor of an incident 3-year ChrD diagnosis (coronary artery disease, myocardial infarction, heart failure, atrial fibrillation, stroke, dementia, diabetes, renal failure, chronic obstructive pulmonary disease, and peripheral vascular disease). A total 5,512 females (49.6 ± 19.2) and 3,461 males (53.0 ± 18.6) were studied. Among females, 50.3%, 33.7% and 16.0% were low, moderate, and high-risk, respectively; and for males, 39.6%, 35.0%, and 25.4%. Frequency of a 3-year ChrD diagnosis among females was 2.2%, 8.5%, and 15.9% for low, moderate, and high-risk groups, respectively, and 4.7%, 9.7%, and 20.0% among males. C-statistics were 0.726 (0.700, 0.752) for females and 0.694 (0.665, 0.724) for males. ICHRON predicted ChrD diagnosis at 3-years among an external, geographically distant validation cohort. These findings show the value of ICHRON for primary care patients in distinct locales. Additionally, electronic calculation of ICHRON empowers the clinical use of this tool to identify and differentially manage and treat high-risk patients. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Prognostic value of fasting versus nonfasting low-density lipoprotein cholesterol levels on long-term mortality: insight from the National Health and Nutrition Examination Survey III (NHANES-III)," by B. Doran and colleagues in the 2014 issue.

Background: Coronary artery disease (CAD) is the major cause of mortality and morbidity in pts with diabetes mellitus (DM). It is proposed that 64-slice coronary CT angiography (CCTA) may provide early CAD information on both myocardial ischemia and plaque burden, which could guide preventative therapy and reduce future cardiovascular events in high-risk otherwise asymptomatic DM patients. Methods: A total of 900 participants with high risk DM (males ≥50 yrs / females ≥55 yrs with DM ≥3 years on DM medication ≥1 yr, or males ≥40 yrs / females ≥45 yrs with DM ≥5 yrs on medication ≥1 yr) and no symptoms of CAD were randomly assigned to be assessed by CCTA or not. Pts randomized to CCTA (n=452) were managed by their physicians according to pre-specified trial recommendations based on the results of CCTA screening. Those randomized to the control arm (n=448) received standard medical therapy. Participants were monitored for procedures performed and changes in medical therapy accomplished at one year, and prospectively followed up for 4.0±1.7 years for the combined primary clinical endpoint of death, Ml and unstable angina. Results: Major baseline characteristics included age = 61±8 years, males = 52%, DM duration = 13±10 years, Type I DM = 12%, Insulin requiring = 43%, systolic BP = 130±12 mm Hg, HgA1C = 7.5±1.4% and LDL cholesterol = 87±32 mg/dL. Of those randomized to the screening arm 285(63%) had at least some degree of atherosclerosis and 21 (4.7%) had severe (>70% stenosis) proximal vessel CAD. This resulted in 26 (5.8%) protocol coronary revascularization procedures, more use of statin therapy (83.1% versus 75.7%; p=0.008) and a significant reduction in blood pressure and LDL levels at one year compared to those randomized to control. The primary event rate was 7.6% and 6.2% for non-screened and screened groups respectively (Hazard ratio (HR) = 0.80, p=0.38). Conclusions: In this contemporary study population of patients with high risk, but well medically managed, asymptomatic diabetes, randomization to screening with CCTA resulted in a modest number of protocol recommended coronary revascularization procedures and a significant increase in the use of statin therapy. However, it did not result in a significant reduction in the primary clinical endpoint by 4.0 years. [ABSTRACT FROM AUTHOR]