In-hospital, six - and eighteen month's results of Ephesos coronary stent implantation in patients with unstable or stable angina

This is an open non-randomized study designed to evaluate clinical and angiographic short-and long-term results of the EPHESOS stent implantation in 457 patients (M/F=348/109) with unstable angina (UA) or stable angina (SA) and native lesions. In SA group 268 stents were implanted in 231 patients. In UA group 271 stents were implanted in 226 patients. 46% of lesions were complex. The length of stenosis was 12.9±6.7 mm in SA group, and 14.1±7.4 mm in UA group. The rate of long stenosis was 30%. Coronary Stenting success rate appeared to be 99% of cases free from acute thrombosis. 1.3% of patients in UA group suffered a non-fatal myocardial infarction (MI) during the in-hospital period. Major adverse cardiac events (MACE) rate including mortality rate and the occurrence of recurrent angina, MI and restenosis as well as repeat revascularization during 6-month follow-up, was 15.6% in SA group and 18.1% in UA group. Angiographic 6-month control revealed the loss index of 0.22±0.20 in SA group and 0.30±0.27 in UA group. 18-month follow-up did not reveal any significant differences in MACE rate between the groups (21.6% for SA and 22.6% for UA group). These results indicate the efficacy and safety of EPHESOS stent with reasonable rates of stent thrombosis and restenosis in SA and UA patients undergone high risk endovascular interventions

Quality of life and adherence to therapy in patients with chronic heart failure who were remotely monitored by chatbot compared to the standard follow-up group for 3 months

BACKGROUND: Chronic heart failure (CHF) is one of the leading causes of death. Telemedicine and remote monitoring (RM) are a way to increase life expectancy and quality of life in patients with CHF. Methods based on messengers familiar to patients promote adherence and do not require additional training. AIM: To compare quality of life and adherence to therapy in patients with CHF who were on RM using a chatbot compared to the standard follow-up (SFU) group for 3 months. METHODS: Patients with CHF on optimal drug therapy discharged from the hospital were included in the study. Comparison groups were formed according to the method of observation, particularly, RM and SFU. A chatbot was set up for patients in the RM group. Monitoring was done using a seven-question survey sent daily. The signs of decompensation (red flags [RF]) were increased edema, dyspnea, body weight 2 kg per week, and changes in individual parameters of heart rate and blood pressure. If a RF was detected, telephone contact was made, and the therapy was corrected if necessary. Quality of life was assessed according to the Minnesota Quality of Life Questionnaire for patients with CHF (highest, 0 points; lowest, 105 points), and adherence was assessed using the Adherence Scale of the National Society for Evidence-based Pharmacotherapy. RESULTS: A total of 60 patients were included in the study; 37 patients completed a 3-month follow-up. The RM group (n=17, 13 men, 76.5%; median age 61 [51; 62]) and comparison group (n=20, 14 men, 70%; mean age 64.98.9) were comparable according to the functional class (New York Heart Association), but differed in ejection fraction (42.813% versus 53.210.4% [p 0.05]). Adherence to the chat-bot was 67.2%. Adherence to therapy was not significantly different between the RM and SFU groups accounting for (17 [100%]) and (18 [90%], respectively, (p=0.62). In the RM group, RF was detected in 7 (41%) patients. Only one patient required correction of therapy. Patients in the RM group required no referral to a medical facility, whereas 2 patients in the SFU group required medical care. Quality of life was statistically significantly higher in the RM group, reaching 28.713.9 points compared to 37.717.9 points in the SFU group (p=0.04). CONCLUSIONS: After 3 months, patients in the RM group were committed to the chatbot, with adherence to therapy comparable to the SFU group. Quality of life was statistically significantly higher in the RM group. Patients in the RM group did not go to medical facilities, in contrast to the SFU group. The limitations of the study were the small sample size and short follow-up period. The results require further research to obtain additional data

Target Metabolome Profiling-Based Machine Learning as a Diagnostic Approach for Cardiovascular Diseases in Adults

Metabolomics is a promising technology for the application of translational medicine to cardiovascular risk. Here, we applied a liquid chromatography/tandem mass spectrometry approach to explore the associations between plasma concentrations of amino acids, methylarginines, acylcarnitines, and tryptophan catabolism metabolites and cardiometabolic risk factors in patients diagnosed with arterial hypertension (HTA) (n = 61), coronary artery disease (CAD) (n = 48), and non-cardiovascular disease (CVD) individuals (n = 27). In total, almost all significantly different acylcarnitines, amino acids, methylarginines, and intermediates of the kynurenic and indolic tryptophan conversion pathways presented increased (p< 0.05) in concentration levels during the progression of CVD, indicating an association of inflammation, mitochondrial imbalance, and oxidative stress with early stages of CVD. Additionally, the random forest algorithm was found to have the highest prediction power in multiclass and binary classification patients with CAD, HTA, and non-CVD individuals and globally between CVD and non-CVD individuals (accuracy equal to 0.80 and 0.91, respectively). Thus, the present study provided a complex approach for the risk stratification of patients with CAD, patients with HTA, and non-CVD individuals using targeted metabolomics profiling

Pre-discharge and early post-discharge management of patients hospitalized for acute heart failure: a scientific statement by the Heart Failure Association (HFA) of the ESC

Acute heart failure is a major cause of urgent hospitalizations. These are followed by marked increases in death and rehospitalization rates, which then decline exponentially though they remain higher than in patients without a recent hospitalization. Therefore, optimal management of patients with acute heart failure before discharge and in the early post-discharge phase is critical. First, it may prevent rehospitalizations through the early detection and effective treatment of residual or recurrent congestion, the main manifestation of decompensation. Second, initiation at pre-discharge and titration to target doses in the early post-discharge period, of guideline-directed medical therapy may improve both short- and long-term outcomes. Third, in chronic heart failure, medical treatment is often left unchanged, so the acute heart failure hospitalization presents an opportunity for implementation of therapy. The aim of this scientific statement by the Heart Failure Association of the European Society of Cardiology is to summarize recent findings that have implications for clinical management both in the pre-discharge and the early post-discharge phase after a hospitalization for acute heart failure

Education and certification on heart failure of the Heart Failure Association of the European Society of Cardiology

Heart failure (HF) is a devastating chronic and disabling disease with a wide variety of pharmaceutical and device treatment options which are becoming increasingly complex to implement. According to the Heart Failure Association (HFA) Atlas, a subspeciality resource aimed at sourcing contemporary data concerning the epidemiology and healthcare resources for HF, HF is prevalent in 17.20 patients per 1000 persons, accounting for 2671 HF hospitalizations per million inhabitants annually in Europe.1 HF patients also suffer from a high prevalence of non-cardiac comorbidities, which adds complexity to their HF treatment and can negatively impact prognosis.2 As a result, HF-related healthcare expenditure continues to rise, and healthcare organizations are becoming faced with the impossible challenge to provide the necessary financial and logistical support to this growing number of patients. In order to address these challenges, the HFA recently outlined the development of quality of care centres (QCC), in order to encourage multidisciplinary management of HF that will improve quality of care and survival.3 However, there remains a significant unmet need to train sufficient multidisciplinary teams lead by HF specialists to take care of this expanding group of HF patients. In order to ensure that the next generation of medically-qualified HF specialists will receive high-quality training, this consensus statement of the HFA outlines the requirements for a European training and certification programme for such specialists. The primary goal of this comprehensive educational programme is to increase the quality of patient-centred care related to HF

Cardiac Remodelling Part 1: From Cells and Tissues to Circulating Biomarkers:From cells and tissues to circulating biomarkers. A review from the Study Group on Biomarkers of the Heart Failure Association of the European Society of Cardiology

Cardiac remodelling refers to changes in left ventricular structure and function over time, with a progressive deterioration that may lead to heart failure (HF) development (adverse remodelling) or vice versa a recovery (reverse remodelling) in response to HF treatment. Adverse remodelling predicts a worse outcome, whilst reverse remodelling predicts a better prognosis. The geometry, systolic and diastolic function and electric activity of the left ventricle are affected, as well as the left atrium and on the long term even right heart chambers. At a cellular and molecular level, remodelling involves all components of cardiac tissue: cardiomyocytes, fibroblasts, endothelial cells and leucocytes. The molecular, cellular and histological signatures of remodelling may differ according to the cause and severity of cardiac damage, and clearly to the global trend toward worsening or recovery. These processes cannot be routinely evaluated through endomyocardial biopsies, but may be reflected by circulating levels of several biomarkers. Different classes of biomarkers (e.g. proteins, non-coding RNAs, metabolites and/or epigenetic modifications) and several biomarkers of each class might inform on some aspects on HF development, progression and long-term outcomes, but most have failed to enter clinical practice. This may be due to the biological complexity of remodelling, so that no single biomarker could provide great insight on remodelling when assessed alone. Another possible reason is a still incomplete understanding of the role of biomarkers in the pathophysiology of cardiac remodelling. Such role will be investigated in the first part of this review paper on biomarkers of cardiac remodelling

Cardiac remodelling – Part 2 : Clinical, imaging and laboratory findings. A review from the Study Group on Biomarkers of the Heart Failure Association of the European Society of Cardiology

In patients with heart failure, the beneficial effects of drug and device therapies counteract to some extent ongoing cardiac damage. According to the net balance between these two factors, cardiac geometry and function may improve (reverse remodelling, RR) and even completely normalize (remission), or vice versa progressively deteriorate (adverse remodelling, AR). RR or remission predict a better prognosis, while AR has been associated with worsening clinical status and outcomes. The remodelling process ultimately involves all cardiac chambers, but has been traditionally evaluated in terms of left ventricular volumes and ejection fraction. This is the second part of a review paper by the Study Group on Biomarkers of the Heart Failure Association of the European Society of Cardiology dedicated to ventricular remodelling. This document examines the proposed criteria to diagnose RR and AR, their prevalence and prognostic value, and the variables predicting remodelling in patients managed according to current guidelines. Much attention will be devoted to RR in patients with heart failure with reduced ejection fraction because most studies on cardiac remodelling focused on this setting

Effect of Nateglinide on the Incidence of Diabetes and Cardiovascular Events

BACKGROUND The ability of short-acting insulin secretagogues to reduce the risk of diabetes or cardiovascular events in people with impaired glucose tolerance is unknown. METHODS In a double-blind, randomized clinical trial, we assigned 9306 participants with impaired glucose tolerance and either cardiovascular disease or cardiovascular risk factors to receive nateglinide (up to 60 mg three times daily) or placebo, in a 2-by-2 factorial design with valsartan or placebo, in addition to participation in a lifestyle modification program. We followed the participants for a median of 5.0 years for incident diabetes (and a median of 6.5 years for vital status). We evaluated the effect of nateglinide on the occurrence of three coprimary outcomes: the development of diabetes; a core cardiovascular outcome that was a composite of death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure; and an extended cardiovascular outcome that was a composite of the individual components of the core composite cardiovascular outcome, hospitalization for unstable angina, or arterial revascularization. RESULTS After adjustment for multiple testing, nateglinide, as compared with placebo, did not significantly reduce the cumulative incidence of diabetes (36% and 34%, respectively; hazard ratio, 1.07; 95% confidence interval [CI], 1.00 to 1.15; P = 0.05), the core composite cardiovascular outcome (7.9% and 8.3%, respectively; hazard ratio, 0.94, 95% CI, 0.82 to 1.09; P = 0.43), or the extended composite cardiovascular outcome (14.2% and 15.2%, respectively; hazard ratio, 0.93, 95% CI, 0.83 to 1.03; P = 0.16). Nateglinide did, however, increase the risk of hypoglycemia. CONCLUSIONS Among persons with impaired glucose tolerance and established cardiovascular disease or cardiovascular risk factors, assignment to nateglinide for 5 years did not reduce the incidence of diabetes or the coprimary composite cardiovascular outcomes. (ClinicalTrials.gov number, NCT00097786.

Effect of valsartan on the incidence of diabetes and cardiovascular events

Background It is not known whether drugs that block the renin–angiotensin system reduce the risk of diabetes and cardiovascular events in patients with impaired glucose tolerance. Methods In this double-blind, randomized clinical trial with a 2-by-2 factorial design, we assigned 9306 patients with impaired glucose tolerance and established cardiovascular disease or cardiovascular risk factors to receive valsartan (up to 160 mg daily) or placebo (and nateglinide or placebo) in addition to lifestyle modification. We then followed the patients for a median of 5.0 years for the development of diabetes (6.5 years for vital status). We studied the effects of valsartan on the occurrence of three coprimary outcomes: the development of diabetes; an extended composite outcome of death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, hospitalization for heart failure, arterial revascularization, or hospitalization for unstable angina; and a core composite outcome that excluded unstable angina and revascularization. Results The cumulative incidence of diabetes was 33.1% in the valsartan group, as compared with 36.8% in the placebo group (hazard ratio in the valsartan group, 0.86; 95% confidence interval [CI], 0.80 to 0.92; P<0.001). Valsartan, as compared with placebo, did not significantly reduce the incidence of either the extended cardiovascular outcome (14.5% vs. 14.8%; hazard ratio, 0.96; 95% CI, 0.86 to 1.07; P=0.43) or the core cardiovascular outcome (8.1% vs. 8.1%; hazard ratio, 0.99; 95% CI, 0.86 to 1.14; P=0.85). Conclusions Among patients with impaired glucose tolerance and cardiovascular disease or risk factors, the use of valsartan for 5 years, along with lifestyle modification, led to a relative reduction of 14% in the incidence of diabetes but did not reduce the rate of cardiovascular events. (ClinicalTrials.gov number, NCT00097786.