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The prevention of stroke and restenosis of coronary arteries in patients with atrial fibrillation who have an acute coronary syndrome or undergo percutaneous coronary intervention relies on antithrombotic therapy. In a two-by-two factorial, randomized trial, apixaban plus clopidogrel was more effective than a vitamin K antagonist, with or without aspirin.

In this cardiovascular safety trial, lorcaserin facilitated sustained weight loss without a higher risk of major adverse cardiovascular events than that with placebo in a high-risk population of overweight or obese patients.

Background Congestion is the main cause of morbidity in patients with heart failure. Treatment of fluid overload is often challenging in everyday clinical practice. Objective The aim of this study was to determine the diuretic effect of acetazolamide in patients with exacerbations of chronic heart failure, in addition to their stable diuretic therapy. Methods This was a single-center, unblinded study. Patients hospitalized with chronic heart failure exacerbations, with left ventricular ejection fraction (EF) < 50% and signs of volume overload, with a stable dose of diuretics anticipated by the attending physician over the next 4 days, were considered eligible for the study. On day 1, patients were randomized to receive acetazolamide orally, once daily (dose-adjusted to body weight) or no treatment (control group) as add-on diuretic therapy, on days 2 and 3. Diuresis, natriuresis, fluid balance, and symptoms were assessed daily, up to day 4. Results Twenty patients (mean ± standard deviation age 72 ± 11.6 years; 85% men; mean EF 33.8 ± 11.4%; mean N-terminal pro-B-type natriuretic peptide 8064 ± 5593 pg/mL; mean intravenous furosemide dose 105 ± 55 mg) were enrolled. Diuresis, natriuresis, fluid balance, and symptoms were stable on days 1–4 in the control group. An increase in diuresis and natriuresis, and a greater change in fluid balance after administration of acetazolamide, were observed in patients randomized to acetazolamide. On day 4, there was a significant difference in fluid balance between the acetazolamide and control groups (−666 ± 1194 mL vs. +332 ± 705 mL; p   =  0.035), and dyspnea was lower in patients receiving acetazolamide (visual scale, p   <  0.001; 5-point Likert scale, 1.444 vs. 2.222; p   =  0.04) Conclusions In this pilot study, the addition of acetazolamide to the background diuretic regimen in patients with chronic heart failure exacerbations produced an additional diuretic effect and alleviation of dyspnea.

Exercise intolerance after acute myocardial infarction (AMI) is a predictor of worse prognosis, but its causes are complex and poorly studied. This study assessed the determinants of exercise intolerance using combined stress echocardiography and cardiopulmonary exercise testing (CPET-SE) in patients treated for AMI. We prospectively enrolled patients with left ventricular ejection fraction (LV EF) ≥40% for more than 4 weeks after the first AMI. Stroke volume, heart rate, and arteriovenous oxygen difference (A-VO 2 Diff) were assessed during symptom-limited CPET-SE. Patients were divided into four groups according to the percentage of predicted oxygen uptake (VO 2 ) (Group 1, <50%; Group 2, 50–74%; Group 3, 75–99%; and Group 4, ≥100%). Among 81 patients (70% male, mean age 58 ± 11 years, 47% ST-segment elevation AMI) mean peak VO 2 was 19.5 ± 5.4 mL/kg/min. A better exercise capacity was related to a higher percent predicted heart rate (Group 2 vs . Group 4, p <0.01), higher peak A-VO 2 Diff (Group 1 vs . Group 3, p <0.01) but without differences in stroke volume. Peak VO 2 and percent predicted VO 2 had a significant positive correlation with percent predicted heart rate at peak exercise (r = 0.28, p = 0.01 and r = 0.46, p < 0.001) and peak A-VO 2 Diff (r = 0.68, p <0.001 and r = 0.36, p = 0.001) but not with peak stroke volume. Exercise capacity in patients treated for AMI with LV EF ≥40% is related to heart rate response during exercise and peak peripheral oxygen extraction. CPET-SE enables non-invasive assessment of the mechanisms of exercise intolerance.

The goal of the global congestive heart failure (G-CHF) registry is to collect comparative international data on heart failure characteristics, management, and outcomes and to better understand the determinants that impact the clinical course of heart failure. G-CHF is a multicenter, prospective cohort study of adult patients with a new or prior clinical diagnosis of heart failure. We have enrolled 23,047 participants from 257 centers in 40 countries from 8 major geographic regions of the world, with recruitment ongoing. Approximately 4,000 participants will also participate in substudies to assess frailty, comorbidity, diet, barriers to care, biomarkers, and planned detailed echocardiographic analyses. Follow-up is planned for a period of 5 years. The primary outcome is cause-specific mortality. Key secondary outcomes include hospitalizations, quality of life, and major cardiovascular and noncardiovascular outcomes. A total of 31.9% of participants were enrolled as inpatients. Thus far, mean age of the cohort at baseline is 63.1 years, and 60.8% are male. Participants most commonly have heart failure with reduced ejection fraction (53.6%) followed by preserved ejection fraction (24.2%) and midrange ejection fraction (20.6%). The most common causes of heart failure are ischemic (37.8%) followed by hypertensive (20.0%), idiopathic (15.1%), and valvular disease (8.8%). G-CHF will provide a greater understanding of the characteristics of the global heart failure population, variations in its management, clinical outcomes, and what continues to impact morbidity and mortality in this high-risk population.

Higher growth differentiation factor 15 (GDF-15) concentrations are associated with cardiovascular (CV) and non-CV morbidity and mortality. However, information on associations between GDF-15 and the risk of specific CV and non-CV events in stable coronary heart disease (CHD) patients is limited. In 14 577 patients with stable CHD participating in the Stabilization of Atherosclerotic Plaque by Initiation of Darapladib Therapy Trial (STABILITY), GDF-15 and other prognostic biomarkers (N-terminal pro-B-type natriuretic peptide, high-sensitivity troponin T, cystatin C, and high-sensitivity C-reactive protein) were measured. In adjusted Cox regression models, the associations between GDF-15 and the composite CV end point [CV death, myocardial infarction (MI), and stroke], as well as other CV and non-CV events, were assessed. The median concentration (interquartile range) of GDF-15 at baseline was 1253 (915-1827) ng/L. The hazard ratio for the composite end point for the highest compared to the lowest quartile of GDF-15 was 1.8 (95% CI, 1.5-2.2); for CV death, 2.63 (1.9-3.6); for sudden death, 3.06 (1.9-4.8); for heart failure (HF) death, 4.3 (1.3-14); for cancer death, 2.5 (1.3-4.7); for hospitalization for HF, 5.8 (3.2-10); for MI 1.4 (95% CI, 1.1-1.9); and for stroke, 1.8 (95% CI, 1.1-2.8). After adjustment for other prognostic biomarkers, GDF-15 remained significantly associated with all outcomes except for MI. In stable CHD, GDF-15 was independently associated with CV, non-CV, and cancer mortality, as well as with MI and stroke. When also adjusting for other prognostic biomarkers, the associations to all fatal and nonfatal events were maintained except for MI. Information on GDF-15, therefore, might be helpful when assessing the risk of adverse outcomes in patients with stable CHD. ClinicalTrials.gov Identifier: NCT00799903.

Recently, associations between the biomarker galectin-3 and numerous pathological processes involved in heart failure (HF) and right ventricular (RV) function have been observed. We aimed to assess the long-term prognostic ability of galectin-3 and RV function parameters for all-cause mortality in HF patients treated with cardiac resynchronization therapy (CRT). We prospectively studied 63 symptomatic HF patients with a left ventricular (LV) ejection fraction (EF) ≤ 35%. The median serum galectin-3 concentration was 13.4 ng/mL (IQR 11.05, 17.15). A detailed assessment of LV and RV geometry and function was performed with echocardiography. CRT defibrillator implantation was achieved in all patients without major complications. The follow-up lasted 5 years. In the multivariable Cox regression model, independent predictors for all-cause mortality were log baseline galectin-3 and baseline RV function expressed as tricuspid annular plane systolic excursion with HR 2.96 ( p  = 0.037) and HR 0.88 ( p  = 0.023), respectively. Analysis of subgroups defined by galectin-3 concentration and CRT response showed that patients with high baseline galectin-3 concentrations and a lack of response to CRT had a significantly lower probability of survival. In our patient cohort, the baseline galectin-3 concentration and RV function were independent predictors of long-term all-cause mortality in HFrEF patients following CRT implantation.

Angiotensin receptor blockers (ARB) and angiotensin converting enzyme (ACE) inhibitors are known to reduce proteinuria. Their combination might be more effective than either treatment alone, but long-term data for comparative changes in renal function are not available. We investigated the renal effects of ramipril (an ACE inhibitor), telmisartan (an ARB), and their combination in patients aged 55 years or older with established atherosclerotic vascular disease or with diabetes with end-organ damage. The trial ran from 2001 to 2007. After a 3-week run-in period, 25 620 participants were randomly assigned to ramipril 10 mg a day (n=8576), telmisartan 80 mg a day (n=8542), or to a combination of both drugs (n=8502; median follow-up was 56 months), and renal function and proteinuria were measured. The primary renal outcome was a composite of dialysis, doubling of serum creatinine, and death. Analysis was by intention to treat. This study is registered with ClinicalTrials.gov, number NCT00153101. 784 patients permanently discontinued randomised therapy during the trial because of hypotensive symptoms (406 on combination therapy, 149 on ramipril, and 229 on telmisartan). The number of events for the composite primary outcome was similar for telmisartan (n=1147 [13·4%]) and ramipril (1150 [13·5%]; hazard ratio [HR] 1·00, 95% CI 0·92–1·09), but was increased with combination therapy (1233 [14.5%]; HR 1·09, 1·01–1·18, p=0·037). The secondary renal outcome, dialysis or doubling of serum creatinine, was similar with telmisartan (189 [2·21%]) and ramipril (174 [2·03%]; HR 1·09, 0·89–1·34) and more frequent with combination therapy (212 [2·49%]: HR 1·24, 1·01–1·51, p=0·038). Estimated glomerular filtration rate (eGFR) declined least with ramipril compared with telmisartan (−2·82 [SD 17·2] mL/min/1·73 m 2 vs −4·12 [17·4], p<0·0001) or combination therapy (−6·11 [17·9], p<0·0001). The increase in urinary albumin excretion was less with telmisartan (p=0·004) or with combination therapy (p=0·001) than with ramipril. In people at high vascular risk, telmisartan's effects on major renal outcomes are similar to ramipril. Although combination therapy reduces proteinuria to a greater extent than monotherapy, overall it worsens major renal outcomes. Boehringer-Ingelheim.

Galectin-3 (Gal-3), a biomarker of fibrosis, is involved in post-infarction remodelling, but its short-term prognostic value remains uncertain. This study aimed to evaluate the prognostic value of Gal-3 for new-onset heart failure (HF) in first acute myocardial infarction (MI) during the in-hospital phase following MI and to assess its association with advanced echocardiographic indices of myocardial and atrial dysfunction, including left ventricular global longitudinal strain (LVGLS) and left atrial reservoir strain. In this prospective study, 105 consecutive patients with STEMI/NSTEMI (mean age 61 ± 11 years) were enrolled. New-onset HF, defined by symptoms, elevated NT-proBNP, and echocardiographic LV dysfunction, developed in 34 patients (32%) during follow-up of a median of 10 [8–13] days. Median serum Gal-3 concentration was 11.6 [9.5–13.5] ng/mL. Gal-3 correlated with echocardiographic indices of myocardial and atrial dysfunction (p = 0.001). Receiver operating characteristic analysis showed moderate discriminative ability (AUC = 0.712; cut-off > 10.9 ng/mL). In multivariable regression, both Gal-3 and LVGLS independently predicted HF, and their combination improved discrimination (AUC = 0.833). In conclusion, Gal-3, particularly when combined with LVGLS, is a valuable early prognostic marker of new-onset HF during the in-hospital phase of acute MI. The combined assessment of Gal-3 and GLS provides a novel, translational biomarker–imaging approach to post-MI prognosis.

Background The development of coronary artery disease (CAD) is the result of complex interactions between environmental and genetic factors. While the former is well known, the genetic factors that predispose individuals to the development of CAD are still under investigation. The aim of our study was to investigate whether single nucleotide polymorphisms (SNPs) in the gene encoding the receptor for advanced glycation end products ( RAGE ), specifically rs2070600 G/A and rs184003 G/T, may determine predisposition to acute coronary syndrome (ACS) and severity of coronary artery disease (CAD) in the Polish population. Methods Two RAGE SNPs were genotyped in 336 patients with a history of acute coronary syndrome (ACS): 175 < 50 years, 161 ≥ 50 years, and 160 ethnically, age- and sex-matched controls via the restriction fragment length polymorphism method. Allele frequencies were compared between groups via the chi 2 test on a 2 × 2 contingency table. Genotype distribution was analyzed assuming three modes of inheritance: dominant, codominant, or recessive. The values of the variables between the study groups were compared using Student’s t-test or the Mann-Whitney U test, as appropriate. Results For the rs184003 G/T polymorphism, the frequency of genotypes containing the T allele (GT + TT) was significantly greater in patients with a history of ACS than in healthy age- and sex-matched controls (28.87% vs. 11.25%, p  < 0.0001, OR = 3.2 [95% CI: 1.86–5.52]). Moreover, individuals possessing this allele had lower high-density lipoprotein (HDL) cholesterol levels (mean 1.02 mmol/l vs. 1.14 mmol/l, p  = 0.01) and higher median troponin I concentrations at the time of ACS (32.2 ng/ml vs. 24.4 ng/ml, p  = 0.04). These genotypes were also significantly less common in patients with ACS before the age of 50 than in those diagnosed later (20.0% vs. 38.5%, p  = 0.0002, OR = 0.4 [95%CI: 0.25–0.65]). In the case of rs2070600 G/A polymorphism, the genotype and allele frequencies were not significantly different between the study groups and subgroups. Conclusions Our findings suggest that the rs184003 SNP in the RAGE gene may play a role in determining genetic susceptibility to CAD and ACS in the Polish population. However, they do not support the hypothesis that the studied SNPs impact the incidence of ACS at a young age.