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    Persistent hypertriglyceridemia in statin-treated patients with type 2 diabetes mellitus

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    Purpose: This paper reports the results of an audit that assessed the prevalence of residual hypertriglyceridemia and the potential need for intensified management among patients with statin-treated type 2 diabetes mellitus (T2DM) in primary care in the UK. Patients and methods: A cross-sectional, observational, systematic audit of patients with diagnosed diabetes from 40 primary care practices was undertaken. The audit collected basic demographic information and data on prescriptions issued during the preceding 4 months. T2DM patients were stratified according to the proportion that attained European Society of Cardiology treatment targets. Results: The audit collected data from 14,652 patients with diagnosed diabetes: 89.5% (n = 13,108) of the total cohort had T2DM. Of the people with T2DM, 22.2% (2916) were not currently receiving lipid-lowering therapy. Up to approximately 80% of these people showed evidence of dyslipidemia. Among the group that received lipid-lowering therapy, 94.7% (9647) were on statin monotherapy, which was usually simvastatin (69.5% of patients receiving statin monotherapy; 6707). The currently available statins were prescribed, with the most common dose being 40 mg simvastatin (44.2%; 4267). Irrespective of the statin used, around half of the patients receiving statin monotherapy did not attain the European Society of Cardiology treatment targets for triglycerides, low-density lipoprotein, high-density lipoprotein, and total cholesterol. Conclusion: T2DM patients managed in UK primary care commonly show persistent lipid abnormalities. Clinicians need to optimize compliance with lipid-lowering and other medications. Clinicians also need to consider intensifying statin regimens, prescribing additional lipid-modifying therapies, and specific treatments aimed at triglyceride lowering to improve dyslipidemia control in statin-treated patients with T2DM

    2019 ESC guidelines for the diagnosis and management of chronic coronary syndromes

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    Coronary artery disease (CAD) is a pathological process characterized by atherosclerotic plaque accumulation in the epicardial arteries, whether obstructive or non-obstructive. This process can be modified by lifestyle adjustments, pharmacological therapies, and invasive interventions designed to achieve disease stabilization or regression. The disease can have long, stable periods but can also become unstable at any time, typically due to an acute atherothrombotic event caused by plaque rupture or erosion. However, the disease is chronic, most often progressive, and hence serious, even in clinically apparently silent periods. The dynamic nature of the CAD process results in various clinical presentations, which can be conveniently categorized as either acute coronary syndromes (ACS) or chronic coronary syndromes (CCS). The Guidelines presented here refer to the management of patients with CCS. The natural history of CCS is illustrated in Figure 1

    Corrigendum to “2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk” (Atherosclerosis (2019) 290 (140–205), (S0021915019314595), (10.1016/j.atherosclerosis.2019.08.014))

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    In row 4 of Table 3, ‘should’ should read as ‘may’; In 4.2.1, paragraph 3, ‘should’ should read ‘may’ to read ‘Overall, CAC score assessment with CT may be considered in individuals … ’ Also in the second row of ‘Recommendations for cardiovascular imaging for risk assessment of atherosclerotic cardiovascular disease,’ the Class should read ‘llb’; In the second paragraph of 7.5.2, ‘5–10 mg of monacolin K’ should read ‘2.5–10 mg’; and in the Key messages section, number 4, ‘ApoB may be a better measure of an individual's exposure to atherosclerotic lipoproteins' should read ‘ApoB may be a better measure of an individual's exposure to pro atherogenic lipoproteins'

    Do ACE inhibitors improve the response to exercise training in functionally impaired older adults? A randomized controlled trial

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    <br>Background: Loss of muscle mass and strength with ageing is a major cause for falls, disability, and morbidity in older people. Previous studies have found that angiotensin-converting enzyme inhibitors (ACEi) may improve physical function in older people. It is unclear whether ACEi provide additional benefit when added to a standard exercise training program. We examined the effects of ACEi therapy on physical function in older people undergoing exercise training.</br> <b>Methods:</b> Community-dwelling people aged ≥65 years with functional impairment were recruited through general (family) practices. All participants received progressive exercise training. Participants were randomized to receive either 4 mg perindopril or matching placebo daily for 20 weeks. The primary outcome was between-group change in 6-minute walk distance from baseline to 20 weeks. Secondary outcomes included changes in Short Physical Performance Battery, handgrip and quadriceps strength, self-reported quality of life using the EQ-5D, and functional impairment measured using the Functional Limitations Profile.<p></p> <b>Results:</b> A total of 170 participants (n = 86 perindopril, n = 84 placebo) were randomized. Mean age was 75.7 (standard deviation [SD] 6.8) years. Baseline 6-minute walk distance was 306 m (SD 99). Both groups increased their walk distance (by 29.6 m perindopril, 36.4 m placebo group) at 20 weeks, but there was no statistically significant treatment effect between groups (−8.6m [95% confidence interval: −30.1, 12.9], p = .43). No statistically significant treatment effects were observed between groups for the secondary outcomes. Adverse events leading to withdrawal were few (n = 0 perindopril, n = 4 placebo).<p></p> <b>Interpretation:</b> ACE inhibitors did not enhance the effect of exercise training on physical function in functionally impaired older people.<p></p&gt

    Changes in plasma levels of B-type natriuretic peptide with acute exacerbations of chronic obstructive pulmonary disease.

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    Background: Elevated plasma B-type natriuretic peptide (BNP) levels and their association with heart failure have been reported in subjects with acute exacerbations of chronic obstructive pulmonary disease (AECOPD). Purpose: To examine and compare plasma BNP levels and diastolic and systolic dysfunction in subjects with AECOPD and s table chronic obstructive pulmonary disease (COPD). Methods: In all,87 unselected consecutive hospitalizations due to AECOPD in 61 subjects and a total of 190 consecutive subjects with stable COPD were recruited. Plasma BNP levels were compared cross-sectionally and longitudinally. Transthoracic echocardiographic examinations were also performed in the hospitalized subjects. Results: In the hospitalized subjects, the median plasma BNP level (interquartile range) was 55.4 (26.9–129.3) pg/mL and was higher than that of patients with stable COPD: 18.3 (10.0–45.3)for Global Initiative for Chronic Obstructive Lung Disease grade I; 25.8 (11.0–53.7) for grade II; 22.1 (9.1–52.6) for grade III; and 17.2 (9.6–22.9) pg/mL for grade IV, all P,0.001. In 15 subjects studied prospectively, the median plasma BNP level was 19.4 (9.8–32.2) pg/mL before AECOPD, 72.7 (27.7–146.3) pg/mL during AECOPD, and 14.6 (12.9–39.0) pg/mL after AECOPD (P,0.0033 and P,0.0013, respectively). Median plasma BNP levels during AECOPD were significantly higher in ten unsuccessfully discharged subjects 260.5 (59.4–555.0) than in 48 successfully discharged subjects 48.5(24.2–104.0) pg/mL (P=0.0066). Only 5.6% of AECOPD subjects were associated with systolic dysfunction defined as a left ventricular ejection fraction (LVEF),50%; a further 7.4% were considered to have impaired relaxation defined as an E/A wave velocity ratio,0.8 and a deceleration time of E.240 ms. BNP levels were weakly correlated with the E/peak early diastolic velocity of the mitral annulus (Ea) ratio (Spearman’s rank correlation coefficient =0.353,P =0.018), but they were not correlated with the LVEF (Spearman’s rank correlation coefficient =−0.221,P = 0.108). Conclusion: A modest elevation of plasma BNP is observed during AECOPD. It appears that AECOPD may have an impact on plasma BNP levels that is not attributable to heart failure
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