Vaccine responsiveness was inversely related to the CRP level in elderly participants, but not seniors, and those with congestive heart failure were less likely to achieve a 2-fold response (odds ratio, 0.08).
Further analysis revealed that MedDietScore differentially affected patients' prognosis according to heart failure phenotype, with short-term impact in HFrEF and HFmrEF patients yet longer positive outcomes in HFpEF and C-reactive protein potentially mediated these relations.
This study examined the individual and combined effect of N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity cardiac troponin T (hs-cTnT), interleukin-6 (IL-6), and hs-CRP on the prediction of heart failure incidence or progression in patients with type 2 diabetes.
After further adjustment for biomarkers (high-sensitivity C-reactive protein, lipoprotein-associated phospholipase A<sub>2</sub> activity, high-sensitivity troponin I, and B-type natriuretic peptide), IL-6 remained significantly associated with the risk of major adverse cardiovascular events (adj HR Q4:Q1 1.43, 95% CI 1.09-1.88) and cardiovascular death or heart failure (adj HR 1.79, 95% CI 1.22-2.63).
Female gender, history of heart failure or left ventricular ejection fraction <40%, and high levels (>1 mg/dL) of C-reactive protein (CRP) were independently associated with left atrial SEC/thrombosis.
To describe correlations and agreement between salivary and serum B-type natriuretic peptide (BNP), C-reactive protein (CRP), interleukin (IL)-6, and IL-10 and determine which biomarkers predict worse functional class in patients with heart failure (HF).
This study investigated the prospective influence of marital status, social support, depression, and C-reactive protein (CRP) on the mortality of patients with chronic HF.
We performed a cross-sectional analysis to investigate the relationships between inflammatory biomarkers [serum interleukin-6 (IL-6), C-reactive protein (hs-CRP) and serum amyloid A (SAA)] and median of 6 years follow-up for all-cause mortality and HF hospitalization among women with signs and symptoms of ischemia, non-obstructive CAD and preserved EF.
Presence of metabolic syndrome (MS) and its components, presence of heart failure, severity of CAD symptoms, severe past ventricular arrhythmia (sustained ventricular tachycardia [sVT] or ventricular fibrillation [VF]), lower left ventricle ejection fraction, higher left ventricle mass index, higher end-diastolic volume and higher number of smoking pack-years were significantly associated with higher WBC, CRP and IL-6.
The objective of the study was to determine whether GR haplotype 3 is associated with HF and whether this association is explained by low-grade inflammation (C-reactive protein).
In this study we investigated distribution of CRP, the Terminal Complement Complex (C5b-9) and macrophages (CD68) in the myocardium of patients suffering from non-ischaemic heart failure and their implication on clinical parameters.
We collected conventional (blood pressure, cholesterol, adiposity), lifestyle, and novel (C-reactive protein, CRP) risk factors at baseline in participants from the Scottish Health Surveys (n = 5946, 44.5% men, aged 53.6 +/- 12.4 years), who were followed up over an average of 7.1 years for cardiovascular disease (CVD) events (a composite of fatal and nonfatal events incorporating acute myocardial infarction, coronary artery bypass surgery, percutaneous coronary angioplasty, stroke, heart failure).
In group 1, patients with a G/G genotype had significantly higher levels of high-sensitivity C-reactive protein and white blood cell counts, and much higher incidences of multi-vessel disease, greater lesion lengths, advanced congestive heart failure (>or=class 3) and 30-day mortality, than patients with G/A or A/A genotypes (p values<0.05 in all cases).
The patient finally had a partial clinical response (reduction in fever and irritability) and complete laboratory response (improved C-reactive protein and serum amyloid A levels) to humanized anti-IL-6 receptor antibody (MRA), but died from congestive heart failure and interstitial pneumonia 2 months after initiation of therapy.