Time Trends in Lifestyle, Risk Factor Control, and Use of Evidence-Based Medications in Patients With Coronary Heart Disease in Europe: Results From 3 EUROASPIRE Surveys, 1999-2013.

BACKGROUND: The EUROASPIRE (European Action on Secondary and Primary Prevention by Intervention to Reduce Events) cross-sectional surveys describe time trends in lifestyle and risk factor control among coronary patients between 1999 and 2013 in Belgium, Czech Republic, Finland, France, Ireland, the Netherlands, Poland, Slovenia, and the United Kingdom as part of the EuroObservational Research Programme under the auspices of European Society of Cardiology. OBJECTIVES: This study sought to describe time trends in lifestyle, risk factor control, and the use of evidence-based medication in coronary patients across Europe. METHODS: The EUROASPIRE II (1999 to 2000), III (2006 to 2007), and IV (2012 to 13) surveys were conducted in the same geographical areas and selected hospitals in each country. Consecutive patients (≤70 years) after coronary artery bypass graft, percutaneous coronary intervention, or an acute coronary syndrome identified from hospital records were interviewed and examined ≥6 months later with standardized methods. RESULTS: Of 12,775 identified coronary patients, 8,456 (66.2%) were interviewed. Proportion of current smokers was similar across the 3 surveys. Prevalence of obesity increased by 7%. The prevalence of raised blood pressure (≥140/90 mm Hg or ≥140/80 mm Hg with diabetes) dropped by 8% from EUROASPIRE III to IV, and therapeutic control of blood pressure improved with 55% of patients below target in IV. The prevalence of low-density lipoprotein cholesterol ≥2.5 mmol/l decreased by 44%. In EUROASPIRE IV, 75% were above the target low-density lipoprotein cholesterol <1.8 mmol/l. The prevalence of self-reported diabetes increased by 9%. The use of evidence-based medications increased between the EUROASPIRE II and III surveys, but did not change between the III and IV surveys. CONCLUSIONS: Lifestyle habits have deteriorated over time with increases in obesity, central obesity, and diabetes and stagnating rates of persistent smoking. Although blood pressure and lipid management improved, they are still not optimally controlled and the use of evidence-based medications appears to have stalled apart from the increased use of high-intensity statins. These results underline the importance of offering coronary patients access to modern preventive cardiology programs.

Extended-release niacin/laropiprant improves endothelial function in patients after myocardial infarction.

Raising high-density lipoprotein cholesterol (HDL-C) is an important strategy for reducing residual cardiovascular risk. In the present study, we sought to assess the effect of extended-release niacin/laropiprant on endothelial function in patients after a myocardial infarction with target low-density lipoprotein cholesterol (LDL-C). In this double-blind, placebo-controlled trial, 63 men (35-60 years of age) after a myocardial infarction were randomized to either niacin/laropiprant (1000/20 mg daily for 4 weeks and 2000/40 mg daily thereafter) or placebo. Flow-mediated dilation (FMD) and nitroglycerin-induced (GTN) dilation of the brachial artery, total cholesterol (TC), LDL-C, HDL-C, triglycerides (TG), lipoprotein(a) [Lp(a)], and apolipoprotein (Apo) A1/B were measured at baseline and after 12 weeks of intervention. FMD significantly increased (from 3.9 ± 5.1 to 9.8 ± 4.4%, p < 0.001) in the niacin/laropiprant group, but not in the placebo group (4.6 ± 4.4 to 6.1 ± 4.4%, p = 0.16) (p = 0.02 for comparison of interventions). GTN dilation also increased in the niacin/laropiprant group (from 12.5 ± 6.1 to 16.7 ± 4.8%, p = 0.02), but not in the placebo group (13.4 ± 5.0 to 15.1 ± 5.2%, p = 0.18), (p = 0.60 for comparison of interventions). Niacin/laropiprant reduced TC and LDL-C (p = 0.05 for both) and increased HDL-C (p < 0.001) without influencing TG, with no changes in the placebo group. Lp(a) (p = 0.026) and ApoB (p = 0.014) were significantly lower in the niacin/laropiprant group, with no difference in the placebo group. ApoA1 did not change in either of the groups (p = 0.13; p = 0.26). FMD and GTN dilation improvements did not correlate with changes in the lipid profile. Niacin/laropiprant improves endothelium-dependent and endothelium-independent dilation of the brachial artery. This improvement does not correlate with changes in lipid parameters.

Endothelial nitric oxide synthase T(-786)C polymorphism in children and adolescents with type 1 diabetes and impaired endothelium-dependent dilatation.

BACKGROUND/AIMS: This study aimed to investigate the association of endothelial nitric oxide synthase (eNOS) polymorphisms with impaired endothelium-dependent dilatation (EDD) in a cohort of children and adolescents with type 1 diabetes. METHODS: Ninety-seven children and adolescents with type 1 diabetes underwent ultrasound assessment of EDD. The association of various factors with EDD was analyzed with multivariate linear regression analysis. Genotypes were determined for the eNOS T(-786)C and 4ab polymorphisms, and their association with EDD was tested with logistic regression analysis. RESULTS: Thirty-three percent of children had impaired EDD. EDD was independently associated with A1c (p = 0.0005) and inversely correlated with A1c (p = 0.0037, OR = 2.14) using logistic regression analysis. The presence of any C allele at eNOS (-786) was significantly more frequent in patients with impaired EDD (OR = 2.97, 95% CI = 1.08-8.87, p = 0.03). Logistic regression analysis revealed OR of 3.09 for impaired EDD for patients with any C allele as compared to TT patients when controlling for all other covariates (p = 0.048). CONCLUSION: A third of children and adolescents with type 1 diabetes had impaired EDD independently associated with A1c. The presence of any C at (-786) of the eNOS gene conveyed a significantly increased independent risk for impaired EDD.

Atrial fibrillation is an independent determinant of increased NT-proBNP levels in outpatients with signs and symptoms of heart failure.

BACKGROUND: N-terminal pro-B-type natriuretic peptide (NT-proBNP) is increasingly used in the diagnosis and prognostic assessment of heart failure; however, the possible influence of atrial fibrillation on BNP is still a matter of controversy. We assessed the influence of atrial fibrillation on NT-proBNP levels in outpatients with signs and symptoms of heart failure. METHODS: Consecutive outpatients (n = 306) referred to a university hospital heart-failure clinic for evaluation of signs and symptoms of heart failure underwent clinical and echocardiographic assessment and had their NT-proBNP levels determined in a sandwich chemiluminescent immunoassay with two antibodies on an Elecsys analyzer. The influence of atrial fibrillation on NT-proBNP levels was assessed using a non-parsimonious linear regression model with propensity score adjustments to balance for possible confounders. RESULTS: Atrial fibrillation was associated with increased NT-proBNP levels in patients with (median concentration 1944 vs. 1390 pg/ml) and without (1093 vs. 172 pg/ml) underlying structural disease (P < 0.001). In a linear regression model with a propensity score, atrial fibrillation emerged as an independent determinant of NT-proBNP levels (P = 0.023), even after allowing for possible confounders (left ventricular ejection fraction and end-diastolic diameter, left atrial diameter, mitral insufficiency, age, sex, NYHA class or heart rate). CONCLUSIONS: Atrial fibrillation is an independent determinant of increased NT-proBNP levels. This association should be taken into account when NT-proBNP levels are used in the diagnosis of heart failure in patients with atrial fibrillation.

Procoagulant state in heart failure with preserved left ventricular ejection fraction.

The impact of heart failure with preserved left ventricular ejection fraction (LVEF) on activated hemostasis is still unclear. We sought to compare the activation of hemostasis in patients with heart failure with preserved LVEF, with impaired LVEF, and in healthy controls. Biomarkers of coagulation and fibrinolysis (D-dimer, tPA and PAI-1) were determined in outpatients with chronic stable (NYHA I-III), optimally managed heart failure with preserved LVEF (n = 46) and with impaired LVEF (n = 52), and in healthy age- and gender-matched controls (n = 14). In comparison to healthy controls, patients with heart failure and preserved LVEF had increased median D-dimer levels (606 [330-1222] microg/L versus 174 [86-249] microg/L; P < 0.001), and median PAI-1 (20 [15.3-33.1] microg versus 6.2[3.4-8.9] microg/L; P < 0.001) and tPA antigen concentrations (9.6 [8.1-13.3] versus 3.6 [2.2-5.0] microg/L; P < 0.001). However, unlike tPA and PAI antigens, D-dimer levels in preserved LVEF did not reach values as high as in impaired LVEF (917 [454-1185] microg/L; P = 0.013). Moreover, in patients with impaired LVEF, but not in those with preserved LVEF, age and NT-proBNP emerged as independent predictors of log-transformed D-dimer levels. Heart failure with preserved LVEF is associated with a procoagulant state as determined by increased levels of D-dimer, tPA and PAI-1 antigens. D-dimer levels are significantly higher in patients with impaired LVEF, while tPA and PAI-1 levels are increased regardless of LVEF.

Prognostic impact of haemostatic derangements in chronic heart failure.

Heart failure is characterised by activation of haemostasis. We sought to explore the prognostic impact of deranged haemostasis in chronic heart failure. In stable, optimally managed outpatients with chronic heart failure, baseline levels of prothrombin fragment F1+2, D-dimer, and tPA and PAI-1 antigens were determined. Clinical follow-up was obtained and the rate of events (heart failure related deaths or hospitalisations) was recorded. We included 195 patients [32.3% female, NYHA class II (66.2%) or III (33.8%), mean age 71 years]. During a median follow up of 693 (interquartile range [IQR] 574-788) days, 63 (30.9%) patients experienced an event; those with an event had higher levels of tPA antigen (median 11.8 [IQR 8.7-14.0] vs. 9.4 [7.9-12.1] microg/l; p = 0.033) and D-dimer (938 [485-1269] vs. 620 [37-1076] microg/l; p = 0.018). However, on Cox multivariate analysis, only tPA levels above optimal cut-off value of 10.2 microg/l (but not D-dimer) emerged as an independent predictor of prognosis (HR(adjusted) 2.695, 95% confidence interval 1.233-5.363; p = 0.017). Our findings suggest that elevated tPA antigen levels are an independent prognostic predictor in patients with chronic stable heart failure.

Interleukin-6 is a stronger prognostic predictor than high-sensitive C-reactive protein in patients with chronic stable heart failure.

Heart failure is characterized by activation of the immune system which is strongly associated with disease severity and outcome. We sought to compare the prognostic impact of two established inflammatory markers - interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hsCRP) - in patients with chronic heart failure. In stable, optimally managed outpatients with chronic heart failure, baseline levels of hsCRP and IL-6 were determined. Clinical follow-up was obtained and the rate of events (heart failure related deaths or hospitalizations) were recorded. We included 201 patients (32.7% female, NYHA class II [66.2%] or III [33.8%], mean age 70 years). During a median follow up of 614 (367-761) days, 64 (30.9%) patients experienced an event; those with an event had higher levels of hsCRP (median 2.93 [interquartile range 2.36-8.92] vs 2.23 [1.32-5.77] mmol/l) and IL-6 (7.8 [4.7-10.3] vs 4.3 [2.6-7.9] pg/ml). However, on Cox multivariate analysis, IL-6 but not hsCRP emerged as an independent predictor of prognosis (hazard ratio HR(adjusted) 2.74, 95% confidence interval 1.17-6.43; P = 0.020). Our findings suggest that IL-6 is a better prognostic predictor than hsCRP in patients with chronic stable heart failure.

Improvement of endothelial function with metformin and rosiglitazone treatment in women with polycystic ovary syndrome.

OBJECTIVE: There is evidence of preclinical cardiovascular disease even in young women with polycystic ovary syndrome (PCOS). The aim of our study was to assess and compare the effects of metformin (MET) and rosiglitazone (ROSI) on endothelial function in PCOS patients. METHODS: For 6 months, 26 women with PCOS received either MET or ROSI. Blood samples for assessment of androgens, lipids, and high-sensitive C-reactive protein were taken at baseline and at endpoint. Endothelium-dependent flow-mediated dilation (FMD) and glyceryl trinitrate-induced endothelium-independent dilation of brachial artery were studied before and after treatment. Homeostasis model assessment (HOMA(IR)) calculation was applied as a measure of insulin resistance (IR). RESULTS: With treatment, FMD of brachial artery improved significantly from 4.2+/-6.6 to 10.2+/-5.9% in MET group (P=0.036) and from 2.9+/-3.2 to 7.6+/-4.9% in ROSI group (P=0.026), MET being as effective as ROSI (P=0.70). The endothelium-independent dilation did not change. Additionally, administration of MET was associated with a significant decrease in HOMA(IR) (P=0.003), serum total and serum-free testosterone (P=0.045 and P=0.008 respectively) and significantly higher frequencies of menstrual bleeding (P=0.006). CONCLUSIONS: A 6-month therapy with insulin sensitizers, MET and ROSI, resulted in marked improvement of endothelial function in young PCOS patients without clinically evident atherosclerosis who were not severely insulin resistant. Neither drug was superior to the other. We conclude that therapeutic intervention with either insulin sensitizer may reverse the atherosclerotic process in PCOS patients at its early stage.

Return to work after acute myocardial infarction--listen to your doctor!

Predictors of return to work after an acute myocardial infarction (AMI) are not fully established. In multivariate analysis adjusted for sex, age and type of intervention, only doctor's advice remained associated with return to work (HR 47.6, 95% CI 4.7-500). This suggests that doctor's advice is a comprehensive integration of patient interview, clinical examination, evidence based medicine and clinical experience, and thus the key predictor of return to work after AMI.

Recall of lifestyle advice in patients recently hospitalised with heart failure: a EuroHeart Failure Survey analysis.

BACKGROUND: There are limited data on recall and implementation of lifestyle advice in patients with heart failure (HF). AIM: To investigate what advice patients with HF recall being given, and whether they report following the advice they remember. METHODS AND RESULTS: 3261 patients with suspected HF participating in the EuroHeart Failure Survey were interviewed by a health professional 12 weeks after hospital discharge. Patients recalled receiving 46% of pre-specified items of advice and 67% reported that they followed these completely. Both recall (53%) and implementation (71%) was best in patients with left ventricular systolic dysfunction (LVSD). In multivariate analysis, younger age, male sex, patient awareness of the condition and patients reporting that they received a clear explanation of the diagnosis by a health professional, all factors associated with having LVSD, were the strongest predictors of recall. CONCLUSIONS: Recall of and adherence to advice by patients with HF in this large European cross-sectional survey was disappointing. Responsibility for patient education lies with health professionals who should ensure that patients receive and understand advice, and are able to recall and follow it. A greater awareness of the issues surrounding lifestyle advice and more evidence supporting its value could improve patient care.

Nonpharmacologic measures and drug compliance in patients with heart failure: data from the EuroHeart Failure Survey.

Advice on lifestyle, diet, vaccination, and therapy are part of the standard management of heart failure (HF). However, there is little information on whether patients with HF recall receiving such recommendations and, if so, whether they report following them. We obtained information on the recall of and adherence to nonpharmacologic advice from patients enrolled in the EuroHeart Failure Survey. This article focuses on 2,331 patients who had a clinical diagnosis of HF during the index admission and attended an interview 12 weeks after discharge. Their mean age was 67 +/- 12 years and 38% were women. Patients recalled receiving 4.1 +/- 2.7 items of advice with higher rates in Central Europe and the Mediterranean region. Recall of dietary advice (cholesterol or fat intake, 63%; dietary salt, 60%) was higher than for some other interventions (influenza vaccination, 36%; avoidance of nonsteroidal anti-inflammatory drugs, 17%). Among those who recalled the advice, a substantial proportion indicated that they did not follow advice completely (cholesterol and fat intake, 61%; dietary salt, 63%; influenza vaccination, 75%; avoidance of nonsteroidal anti-inflammatory drugs, 80%), although few patients indicated they ignored the advice completely. Patients who recalled >4 items versus < or =4 items of advice were younger and more often received angiotensin-converting enzyme inhibitors (71% vs 62%), beta-blockers (51% vs 38%), and spironolactone (25% vs 21%). In conclusion, after hospitalization for HF, many patients do not recall nonpharmacologic advice. In addition, a substantial proportion of those who recall the advice follow it incompletely. Younger age and prescription of appropriate pharmacologic treatment are associated with higher rates of recall and implementation.

Interleukin-6 correlates with endothelial dysfunction in young post-myocardial infarction patients.

BACKGROUND: The estimation of coronary risk based on consideration of classical risk factors is insufficient in young patients with myocardial infarction who have low expressions of classical risk factors. Endothelial dysfunction (ED) and markers of vascular inflammation may be more appropriate for risk estimation. The relations among ED and inflammation markers in such patients have not yet been explored. PATIENTS AND METHODS: Twenty-one patients (on average 44 years old) in the stable phase after myocardial infarction, with low expressions of risk factors, were included in the study. The control group consisted of 25 healthy age-matched males. ED was estimated by ultrasound measurement of the endothelium-dependent dilatation of the brachial artery. The following inflammation markers were measured: hsCRP, interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), ICAM-1, VCAM-1, selectin-P and selectin-E. RESULTS: Patients had a significantly reduced level of endothelium-dependent vasodilatation (5.6 +/- 3.5 vs. 8.8 +/- 6.5%, p < 0.05), and an increased level of IL-6 (3.2 [1.5-8.4] vs. 1.4 [0.9-2.3] ng/ml; p < 0.01). All other inflammation markers were comparable to controls. We found a significant negative correlation between ED and the levels of IL-6 (r = -0.54, p = 0.012). CONCLUSION: It appears that IL-6 is the most valuable circulating marker of ED, and consequently a useful marker of coronary risk.

Role of endothelial function and inflammation in patients with cardiovascular risk factors, with and without a history of myocardial infarction.

BACKGROUND: Endothelial dysfunction and inflammation, in particular their lack of improvement after risk reduction, might better reflect advanced atherosclerosis than just the presence of risk factors. The aim of this study was to compare endothelial function and inflammatory parameters in high-risk patients who had no history of myocardial infarction and in patients in a stable phase after myocardial infarction. METHODS: We compared endothelial function of the brachial artery, measured using high-resolution ultrasound, in 45 patients with hyperlipidaemia (Group 1), and in 45 patients in a stable period after myocardial infarction (Group 2). Forty-five healthy individuals served as a control group (Group 3). RESULTS: Compared to patients with treated hyperlipidaemia, patients after myocardial infarction had lower values of total and LDL cholesterol (p = 0.015; 0.005) and homocysteine (p < 0.005), but marginally higher IL-6 levels (p = 0.1). Other measurements were comparable. However, flow-mediated dilation of the brachial artery was significantly diminished in patients after myocardial infarction (10.6 +/- 3.0; 5.9 +/- 4.0; 14.0 +/- 1.9% for Groups 1-3; ANOVA p = 0.0001; respectively). CONCLUSIONS: We found that patients with previous myocardial infarction have substantially lower endothelial function and increased some inflammatory parameters than patients with a similar level of atherosclerotic risk profile but without clinically evident coronary artery disease.

Clopidogrel is associated with a lesser increase in NT-proBNP when compared to aspirin in patients with ischemic heart failure.

BACKGROUND: Aspirin has been associated with adverse heart failure outcomes, probably because of a blunting interaction with angiotensin-converting enzyme (ACE) inhibitors. Therefore, we hypothesized that clopidogrel when compared with aspirin would be associated with a slower progression of heart failure as determined by levels of amino-terminal pro-brain natriuretic peptide (NT-proBNP). METHODS AND RESULTS: In an open-label, randomized, 2-treatment, 2-period crossover study, 18 patients with ischemic heart failure (14 post-myocardial infarction, left ventricular ejection fraction 0.32 +/- 0.08), median age 73, New York Heart Association class II (11 patients) or III (7 patients), all taking ACE inhibitors were included. Patients were randomized to 8 weeks of aspirin 100 mg/day followed by 8 weeks of clopidogrel 75 mg/day, or the reversed sequence. Blood levels of NT-proBNP were measured using sandwich immunoassay. Patients on aspirin experienced an 8-times greater increase in log-transformed values of NT-proBNP compared with patients on clopidogrel (average change 4.757% versus 0.597%; P = .0395 for intervention, P = .4453 for period, P = .4046 for sequence). We observed no change in functional class, 6-minute walking test, creatinine levels, or electrolytes. CONCLUSION: Aspirin is associated with a greater increase in natriuretic peptides (log-transformed NT-proBNP levels), implying that aspirin therapy is associated with a more progressive course of heart failure.

The effect of various menopausal hormone therapies on markers of inflammation, coagulation, fibrinolysis, lipids, and lipoproteins in healthy postmenopausal women.

OBJECTIVE: Androgenic progestins such as norethisterone acetate (NETA) may influence the effect of estradiol (E(2)) therapy. We compared the influence of oral E(2), with and without NETA, and transdermal E(2) on markers of coagulation, fibrinolysis, and inflammation and on lipids and lipoproteins in healthy postmenopausal women. DESIGN: A total of 112 healthy postmenopausal women were randomized to receive treatment with either oral E(2), with or without NETA, transdermal E(2), or placebo. At baseline and after 28 weeks, levels of serum lipids and lipoproteins and markers of coagulation, fibrinolysis, and inflammation were determined. RESULTS: Of the fibrinolytic parameters, oral E(2) (P < 0.05) and E(2) with NETA (P < 0.01) shortened euglobulin clot lysis time. Oral E(2) decreased plasminogen activator inhibitor-1 activity (P < 0.05). Oral E(2) with NETA reduced plasminogen activator inhibitor-1 antigen levels (P < 0.01) and increased D-dimer antigen levels (P < 0.001). All three modes of menopausal hormone therapy reduced tissue type plasminogen activator antigen. Of the coagulation parameters, both routes of E(2) therapy decreased fibrinogen levels (P = 0.002 for oral and P = 0.007 for transdermal E(2)), whereas E(2) with NETA showed no effect. The decrease of fibrinogen was larger after oral E(2) (P = 0.02). Oral E(2) with NETA reduced antithrombin III (P < 0.001) and protein C (P < 0.001) activity. Oral E(2) (P = 0.04) and E(2) with NETA (P < 0.01) increased C-reactive protein (CRP). Transdermal E(2) showed no influence on CRP. The addition of NETA influenced the change in CRP, as the increase in CRP was more pronounced after E(2) without NETA (P = 0.005). The levels of serum amyloid A, interleukin-6, and tumor necrosis factor-alpha did not change significantly after any of the modes of hormone therapy. Of the lipids and lipoproteins, oral E2 decreased low-density lipoprotein cholesterol (P < 0.01), lipoprotein (a) (P < 0.05), and increased high-density lipoprotein cholesterol (P < 0.05). Transdermal E(2) decreased triglycerides (P < 0.02) and increased high-density lipoprotein cholesterol (P < 0.03). Oral E(2) with NETA decreased total cholesterol (P < 0.01) and high-density lipoprotein cholesterol (P < 0.005). CONCLUSIONS: Oral E(2), with or without NETA, produced no net activation of coagulation but improved fibrinolysis. Both modes of oral menopausal hormone therapy have a greater impact on markers of inflammation, coagulation, fibrinolysis, lipids, and lipoproteins than transdermal E(2). NETA attenuates some E(2) effects. Further studies are needed to elucidate the impact of these effects on clinical endpoints.

Heart failure clinic in a community hospital improves outcome in heart failure patients.

PRINCIPLES: Heart failure is associated with a grim prognosis. Disease management programmes can improve prognosis in heart failure patients but the applicability to the general population remains limited. We aimed to compare the outcome, pharmacological therapy, and quality of life in unselected heart failure patients from a community hospital area who were managed either in the heart failure clinic or who received the usual care. METHODS AND RESULTS: We followed 115 patients receiving care in the heart failure clinic (n = 50) or the usual care (n = 65) for at least twelve months. During the follow-up of 561 (463, 701) days significantly less patients from the heart failure clinic were rehospitalized due to heart failure or died (42% vs 65%). Assignment to the heart failure clinic (Hazard ratio [HR] 0.39, 95% Confidence interval [CI] 0.20-0.75), New York Heart Association class (HR 2.32, 95% CI 1.22-4.41), and systolic blood pressure (HR 0.98, 95% CI 0.96-0.99) independently predicted occurrence of heart failure rehospitalisations or death. At the end of the follow-up patients from the heart failure clinic received more optimal pharmacological therapy and reported better quality of life. CONCLUSIONS: Patient management in the community hospital heart failure clinic reduced the incidence of heart failure rehospitalisation or death with further benefits in terms of pharmacological therapy and quality of life.

Inflammation markers in young post-myocardial patients exhibiting various expressions of classic coronary risk factors.

OBJECTIVE: We investigated inflammation markers in young post-myocardial infarction patients exhibiting various expressions of classical risk factors. METHODS: Forty-one male patients with high (n=20) and low (n=21) expression of classical risk factors (risk of coronary events calculated by the prospective cardiovascular Munster study program high or low, respectively), on average 44 years old, who were in the stable phase after myocardial infarction (on average 20.5 months after myocardial infarction) were included in the study. The control group consisted of 25 healthy, age-matched men. The following inflammation markers were measured: leukocyte count, high-sensitive C-reactive protein, interleukin-6, tumor necrosis factor-alpha, intracellular adhesion molecule-1, vascular cellular adhesion molecule-1, selectin-P and selectin-E. RESULTS: No differences in the levels of leukocytes, high-sensitive C-reactive protein, tumor necrosis factor-alpha, intracellular adhesion molecule-1, vascular cellular adhesion molecule-1, selectin-P and selectin-E were found between the group of patients and the controls. In contrast, interleukin-6 was significantly (P<0.01) elevated in the group of patients with high [2.5 (1.9-5.3) ng/ml] and low [3.2 (1.5-8.4) ng/ml] expression of risk factors compared with the controls [1.4 (0.9-2.3) ng/ml]. Significantly, there was no difference in interleukin-6 between the two groups of patients. CONCLUSIONS: We did not find differences in inflammation markers between young post-myocardial infarction patients with or without classical risk factors. Thus, it seems that the presence of (treated) risk factors or their absence does not affect the levels of inflammation markers in the stable period after myocardial infarction. Importantly, we found similarly elevated interleukin-6 in both groups of patients, most probably indicating slight local vascular inflammation. Interleukin-6 appears to be the most suitable marker of vascular inflammation in post-myocardial infarction patients who are aggressively treated pharmacologically.

Patients' knowledge and beta blocker treatment improve prognosis of patients from a heart failure clinic.

BACKGROUND: Several studies have shown improvement of prognosis in patients managed in heart failure (HF) clinics. However, the value of the individual management components is not well established. AIM: To assess the prognostic value of pharmacological treatment and patient's knowledge in patients receiving care in a HF clinic. METHODS AND RESULTS: In our prospective cohort study we followed 115 patients (50 from an HF clinic and 65 receiving usual care) for at least 12 months. Knowledge was assessed using a Patient Knowledge Questionnaire (PKQ). During a median follow-up of 561 days, fewer patients from the HF clinic died or were rehospitalized due to HF than those receiving usual care (42% vs. 65%, p = 0.016). The prescription rates of ACE inhibitors (94% to 98%) and beta blockers (40% to 94%) increased in the patients from the HF clinic. In these patients the PKQ score also increased from 4.8 (1.5) to 7.9 (1.3), p<0.001. In the Cox proportional hazard model, treatment with beta blockers at > or = 50% of the target daily dose (Hazard Ratio [HR] 0.3, 95% Confidence Interval [CI] 0.10-0.95) and a PKQ score <7 (HR 3.92, 95% CI 1.39-11.03) predicted prognosis in the patients from the HF clinic. CONCLUSIONS: Patient management in the HF clinic reduced the incidence of death or of HF rehospitalization. Poor prognosis of patients receiving care in the HF clinic was predicted by poor patient knowledge and underdosing with beta blockers.

Body composition changes in patients with systolic heart failure treated with beta blockers: a pilot study.

BACKGROUND: Cachexia is an independent risk factor for mortality in chronic heart failure (CHF). Beta blockers can reduce body energy expenditure and improve efficiency of substrate utilization. AIM: To assess the changes in body composition in non-cachectic patients with CHF treated with beta blockers. METHODS: We prospectively followed 41 non-cachectic ambulatory CHF patients (mean age 67 +/- 10 years, ejection fraction 37 +/- 4%) treated with beta blockers for at least 6 months. Body composition was measured by bioimpedance. RESULTS: At baseline 16/41 patients were treated with beta blockers while at the end of follow-up all patients received beta blockers (31/41 at full recommended dose). During follow up of 263 +/- 106 days body weight (83.1 +/- 16.7 vs. 83.0 +/- 16.9 kg), body mass index (29.3 +/- 5.5 vs. 29.3 +/- 5.6) and total body water did not change (51.2 +/- 6.4% vs. 51.0 +/- 6.4%), while total body fat mass (27.4 +/- 9.6 to 28.3 +/- 10.2 kg, median change +0.89 kg, p = 0.01) and percent of total body fat increased (32.3 +/- 7.4% to 33.4 +/- 7.5%, median change +0.7%, p < 0.001). New York Heart Association class and Minnesota Living with Heart Failure Questionnaire improved from 2.9 +/- 0.4 and 48 +/- 15 to 2.3 +/- 0.6 and 32 +/- 16, respectively (p < 0.001 for both). CONCLUSION: In patients with CHF, treatment with beta blockers can increase total body fat mass and total body fat content.