Are there differences in acute phase inflammation markers regarding the type of heart failure?

This study aimed to determine if there are differences in inflammatory markers in the acute phase between systolic heart failure and heart failure with preserved systolic function. One hundred and thirty-one patients with acute heart failure were recruited consecutively. At admission, plasma fibrinogen, C-reactive protein, sialic acid, von Willebrand factor, vascular endothelial growth factor, interleukin-6 and NTproBNP were all evaluated. If the ejection fraction was 45% or over patients were included in the HF-PSF group; the remaining patients were included in the SHF group. The HF-PSF patients were older (72±10 vs 63±12 years, P<0.001), presented a higher rate of atrial fibrillation (56.1 vs 21.3%, P<0.001), and had a lower rate of hemoglobin (12.2±2 vs 13.3±2.1 g/dL, P<0.01). No significant differences were observed in the inflammation markers analyzed among SHF and HF-PSF groups. In the acute phase of heart failure there is a marked elevation of inflammatory markers but there are no differences in the inflammatory markers analyzed between the two different types of heart failure

Predictive value for death and rehospitalization of 30-day postdischarge B-type natriuretic peptide (BNP) in elderly patients with heart failure. Sub-analysis of Italian RED Study.

Abstract Background: Our aim was to determine if, in elderly heart failure (eHF) patients, serial B-type natriuretic peptide (BNP) assessments obtained during follow-up after hospital discharge could have prognostic utility for death and rehospitalizations. In eHF patients, BNP assessment at hospital discharge has been demonstrated to have a high prognostic value; however, its predictive role for future cardiovascular events in eHF patients, when assessed in the period after discharge, both for the correct timing and cut-off levels, has not been completely elucidated. Methods: This study is a monocentric subanalysis of the Italian RED (Rapid Emergency Department) study. We studied 180 consecutive patients admitted for acute HF through serial BNP assessments: at hospital arrival; at discharge; and at 30, 90, and 180 days follow-up outpatient visit. Results: Both a BNP >400 pg/mL at 30 days after discharge and the percentage variation of BNP from discharge to 30 days (Δ%BNP), compared with a BNP at discharge >400 pg/mL, showed a higher area under the curve (AUC) and odds ratio (OR) in predicting events [AUC=0.842, p<0.0001; OR 7.9 (3.3-19.0), p<0.001 for 30 days BNP and AUC=0.851, p<0.0001; OR 9.5 (4.065-22.572), p<0.0001 for Δ%BNP compared with AUC=0.638, p<0.002; OR 2.4 (1.1-5.3), p=0.032 for BNP at discharge]. Conclusions: In patients at a high risk for future events, BNP levels assessed 30 days after hospital discharge in the absence of signs and symptoms could be predictive of subsequent hospitalization and death. These patients should be considered for closer monitoring and treatment adjustment

Usefulness of Proneurotensin to Predict Cardiovascular and All-Cause Mortality in a United States Population (from the Reasons for Geographic and Racial Differences in Stroke Study)

Cardiovascular disease is a leading cause of death. Proneurotensin is a biomarker associated with the development of cardiovascular disease, cardiovascular mortality, and all-cause mortality. We assessed the association of fasting proneurotensin with mortal events by gender and race (black–white) in a US population. Using a case-cohort subpopulation of the Reasons for Geographic and Racial Differences in Stroke study, fasting proneurotensin was measured on a 1,046-person subcohort and in 651 participants with incident coronary heart disease. Higher proneurotensin was associated with all-cause mortality (hazard ratio [HR] 1.6 per interquartile range, 95% confidence interval [CI] 1.3 to 1.9) and cardiovascular mortality (HR 1.8, 95% CI 1.2 to 2.6). For all-cause and cardiovascular mortality, association was stronger in women (HR 1.9, 95% CI 1.4 to 2.6 and HR 2.5, 95% CI 1.4 to 4.7, respectively) than men (HR 1.4, 95% CI 1.0 to 1.8 and HR 1.4, 95% CI 0.9 to 2.3, respectively), although this difference was not significant. Proneurotensin predicted all-cause mortality in both races and was not predictive of cardiovascular mortality in whites but was in blacks. Proneurotensin was not associated with incident coronary heart disease events. Elevated proneurotensin levels predicted all-cause and cardiovascular mortality in both genders, with a trend toward stronger association in women. Associations were similar in blacks and whites. In conclusion, proneurotensin may be a useful biomarker for all-cause and cardiovascular mortality regardless of race, and it is potentially specific in women. © 201

Highlights of the Year in JACC 2010

Ventricular Dysfunction & Heart Failur

Highlights of the Year in JACC 2011

Cardiolog

Highlights of the Year in JACC 2013

Cardiolog

Supplementary Material for: Genetic Variants Are Not Associated with Outcome in Patients with Coronary Artery Disease and Left Ventricular Dysfunction: Results of the Genetic Substudy of the Surgical Treatment for Ischemic Heart Failure (STICH) Trials

<b><i>Objectives and Background:</i></b> We evaluated the ability of 23 genetic variants to provide prognostic information in patients enrolled in the Genetic Substudy of the Surgical Treatment for Ischemic Heart Failure (STICH) trials. <b><i>Methods:</i></b> Patients assigned to STICH Hypothesis 1 were randomized to medical therapy with or without coronary artery bypass grafting (CABG). Those assigned to STICH Hypothesis 2 were randomized to CABG or CABG with left ventricular reconstruction. <b><i>Results:</i></b> In patients assigned to STICH Hypothesis 2 (n = 714), no genetic variant met the prespecified Bonferroni-adjusted threshold for statistical significance (p < 0.002); however, several variants met nominal prognostic significance: variants in the β₂-adrenergic receptor gene (β₂-AR Gln27Glu) and in the A₁-adenosine receptor gene (A₁-717 T/G) were associated with an increased risk of a subject dying or being hospitalized for a cardiac problem (p = 0.027 and 0.031, respectively). These relationships remained nominally significant even after multivariable adjustment for prognostic clinical variables. However, none of the 23 genetic variants influenced all-cause mortality or the combination of death or cardiovascular hospitalization in the STICH Hypothesis 1 population (n = 532) by either univariate or multivariable analysis. <b><i>Conclusion:</i></b> We were unable to identify the predictive genotypes in optimally treated patients in these two ischemic heart failure populations

A proposal to standardize dyspnoea measurement in clinical trials of acute heart failure syndromes: The need for a uniform approach

Dyspnoea is the most common presenting symptom amongst patients with acute heart failure syndromes (AHFS). It is distressing to patients and therefore an important target for treatment in clinical practice, clinical trials, and for regulatory approval of novel agents. Despite its importance as a treatment target, no consensus exists on how to assess dyspnoea in this setting. There is a considerable uncertainty about the reproducibility of the various instruments used to measure dyspnoea, their ability to reflect changes in symptoms and whether they accurately reflect the patient&apos;s experience. Little attempt has been made to ensure consistent implementation with respect to patients&apos; posture during assessment or timing in relationship to therapy. There is also limited understanding of how rapidly and completely dyspnoea responds to standard therapy. A standardized method with which to assess dyspnoea is required for clinical trials of AHFS in order to ensure uniform collection of data on a key endpoint. We propose the Provocative Dyspnoea Assessment, a method of measurement that combines sequential dyspnoea provocation by positioning and walking with a dyspnoea self assessment using a five-point Likert scale, to yield a final Dyspnoea Severity Score. This proposed tool requires detailed validation but has face validity for the uniform assessment of dyspnoea. © The Author 2008