SP290ASSOCIATION BETWEEN LOW GRADE INFLAMMATION AND DIASTOLIC HEART FAILURE IN PREDIALYSIS PATIENTS. THE EFFECT OF ALDOSTERONE BLOCKADE

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii475-iii476
Author(s):  
Dimitris Xidakis ◽  
Ergini Antonaki ◽  
Kostas Kostakis ◽  
Maria Sfakianaki ◽  
Apostolos Papadogiannakis
2010 ◽  
Vol 95 (6) ◽  
pp. 2885-2891 ◽  
Author(s):  
Christian Otte ◽  
Stefan Wüst ◽  
Shoujun Zhao ◽  
Ludmila Pawlikowska ◽  
Pui-Yan Kwok ◽  
...  

Abstract Context: A common haplotype of the glucocorticoid receptor (GR) gene has been associated with increased susceptibility to coronary heart disease (CHD). Whether this haplotype predisposes to heart failure (HF) is unknown. Objective: 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). Design: In a prospective cohort study, participants were genotyped for common GR gene polymorphisms (ER22/23EK, BclI C/G, N363S, 9β A/G). Haplotype analyses were conducted. Setting: The study was conducted at one university medical center, two Veterans Affairs medical centers, and nine public health clinics. Patients: Patients included 526 white outpatients with stable CHD. Main Outcome Measures: Echocardiographic evidence of ventricular dysfunction, self-reported heart failure, and subsequent hospitalization for heart failure were measured. Results: After adjusting for age, sex, smoking, and body mass index, participants with two copies of haplotype 3 were more likely than those with 0 or 1 copy to report heart failure [hazard ratio (HR) 4.15, 95% confidence interval (CI) 1.5–11.3, P < 0.01], have systolic dysfunction (left ventricular ejection fraction <50%) (HR 3.0, 95% CI 0.9–9.9, P = 0.07), and be hospitalized for HF during a mean follow-up of 6 yr (HR 3.0, 95% CI 1.3–7.0, P = 0.01). These associations were attenuated after adjustment for higher C-reactive protein levels in patients with two copies of haplotype 3. Conclusions: We found that the GR gene haplotype 3 was associated with prevalent HF, systolic dysfunction, and subsequent HF hospitalization in patients with CHD. This association was partly mediated by low-grade inflammation.


2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Gorazd Kosir ◽  
Borut Jug ◽  
Marko Novakovic ◽  
Mojca Bozic Mijovski ◽  
Jus Ksela

Background. Heart failure (HF) is characterized by unfavorable prognosis. Disease trajectory of HF, however, may vary, and risk assessment of patients remains elusive. In our study, we sought to determine the prognostic impact of endocan—a novel biomarker of endothelial dysfunction and low-grade inflammation—in patients with heart failure. Methods. In outpatients with chronic HF, baseline values of endocan were determined and clinical follow-up for a minimum of 18 months obtained. A multivariate Cox proportional hazard model was built for HF-related death or hospitalization requiring inotropic support. Results. A total of 120 patients (mean age 71 years, 64% male, mean LVEF 36%) were included. During a mean follow-up of 656±109 days, 50 patients (41.6%) experienced an event. On Cox multivariate analysis, endocan values emerged as an independent predictor of HF prognosis (HR, 1.471 CI 95% 1.183-1.829, p=0.001, for each 1 ng/mL increase) even after adjustment for age, gender, HF etiology, LVEF, NYHA class, NT-proBNP, and exercise tolerance. Conclusions. Endocan is an independent predictor of HF-related events in chronic HF individuals and represents a promising tool for risk assessment of HF patients.


Endocrinology ◽  
2010 ◽  
Vol 151 (5) ◽  
pp. 2397-2398
Author(s):  
Christian Otte ◽  
Stefan Wüst ◽  
Shoujun Zhao ◽  
Ludmila Pawlikowska ◽  
Pui-Yan Kwok ◽  
...  

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Edoardo Bertero ◽  
Luca Carmisciano ◽  
Christian Jonasson ◽  
Christoph Maack ◽  
Pietro Ameri

Abstract Aims Conflicting data exist regarding the risk of cancer in patients with heart failure (HF). It was first reported that incident cancer is more common among patients with than without HF, whereas more recent studies indicate that this association is primarily driven by comorbidities. HF, cancer, and comorbidities, such as chronic kidney disease (CKD) and chronic obstructive pulmonary disease (COPD), share numerous risk factors, including a state of chronic low-grade inflammation reflected by elevated circulating levels of pro-inflammatory cytokines. The objective of this analysis was to assess whether chronic low-grade inflammation, as measured by levels of high-sensitivity C-reactive protein (hsCRP), and comorbidities mediate the association of HF with incident cancer. Methods We used data from the 3rd wave of the Nord-Trøndelag Health Study (HUNT3), a population-based study that enrolled 50 803 individuals ≥18-year-old between October 2006 and June 2008 in the Nord-Trøndelag County (Norway), and from the administrative health care records of the same region. Associations between baseline characteristics and the development of cancer were assessed using Cox proportional hazards regression models, using time from HUNT3 enrolment as the time scale. Analyses were performed using R statistical software, version 4.0.2. Results In HUNT3, hsCRP was measured in 47 571 individuals at the time of enrolment. Of these, we excluded 2308 patients because of missing information, leaving a cohort of 45 263 subjects. The prevalence of cardiovascular disease, comorbidities, and obesity was progressively higher with increasing concentrations of hsCRP. During a median follow-up of 12 years, there were 66/408 cases of incident cancer in patients with HF at baseline and 5024/47 163 in subjects without HF, with a more than 2-fold (HR 2.30; 95% CI 1.80–2.93; P < 0.001) increase in risk of developing cancer. After adjusting for age and sex, the excess risk decreased to 43% (HR 1.43; 95% CI 1.12–1.82). When including hsCRP in the model, the HF-related risk of cancer was 33% (HR 1.33; 95% CI 1.04–1.70; P = 0.022). Furthermore, when body mass index, CKD, COPD, and smoking and drinking habits were included in the model, the risk of cancer in HF patients compared to individuals without HF was no longer significant (HR 1.23; 95% CI 0.94–1.60; P = 0.127). Age, male sex, hsCRP, COPD, obesity, and smoking habits were all associated with an increased risk of cancer. Conclusions The increased risk of cancer in HF patients compared with the general population is at least in part explained by concomitant inflammation and comorbidities.


2013 ◽  
Vol 14 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Gabriele Fragasso ◽  
Roberto Spoladore ◽  
Francesco Maranta ◽  
Angelo Corti ◽  
Guido Lattuada ◽  
...  

2019 ◽  
Vol 3 (s1) ◽  
pp. 123-123
Author(s):  
Adeyinka Charles Adejumo ◽  
Olumuyiwa Ogundipe

OBJECTIVES/SPECIFIC AIMS: Chronically elevated cytokines from un-abating low-grade inflammation in heart failure (HF) results in Protein-Energy Malnutrition (PEM). However, the impact of PEM on clinical outcomes of admissions for HF exacerbations has not been evaluated in a national data. METHODS/STUDY POPULATION: From the 2012-2014 Nationwide Inpatient Sample (NIS) patient’s discharge records for primary HF admissions, we identified patients with concomitant PEM, and their demographic and comorbid factors. We propensity-matched PEM cohorts (32,771) to no-PEM controls (1:1) using a greedy algorithm-based methodology and estimated the effect of different clinical outcomes (SAS 9.4). RESULTS/ANTICIPATED RESULTS: There were 32,771 (~163,885) cases of PEM among the 541,679 (~2,708,395) primary admissions for HF between 2012 and 2014 in the US. PEM cases were older (PEM:76 vs. no-PEM:72 years), Whites (70.75% vs. 67.30%), and had higher comorbid burden, with Deyo-comorbidity index >3 (31.61% vs. 26.30%). However, PEM cases had lower rates of obesity, hyperlipidemia and diabetes. After propensity-matching, PEM was associated with higher mortality (AOR:2.48[2.31-2.66]), cardiogenic shock (3.11[2.79-3.46]), cardiac arrest (2.30[1.96-2.70]), acute kidney failure (1.49[1.44-1.54]), acute respiratory failure (1.57[1.51-1.64]), mechanical ventilation (2.72[2.50-2.97]). PEM also resulted in higher non-routine discharges (2.24[2.17-2.31]), hospital cost ($80,534[78,496-82,625] vs. $43,226[42,376-44,093]) and longer duration of admission (8.61[8.49-8.74] vs. 5.28[5.23-5.34] days). DISCUSSION/SIGNIFICANCE OF IMPACT: In the US, PEM is a common comorbidity among hospitalized HF subjects, and results in devastating health outcomes. Early identification and prevention of PEM in heart failure subjects during clinic visits and prompt treatment of PEM both in the clinic and during hospitalization are essential to decrease the excess burden of PEM.


Hematology ◽  
2020 ◽  
Vol 2020 (1) ◽  
pp. 478-486
Author(s):  
Kleber Yotsumoto Fertrin

Abstract While iron deficiency remains the most common cause of anemia worldwide, low iron stores are associated with symptoms regardless of the presence of typical microcytic, hypochromic anemia and may be hard to recognize in patients with concurrent inflammation. Diagnosing and treating iron deficiency become more of a challenge because markers of iron status are influenced by low-grade inflammation present in common conditions, such as chronic kidney disease, cirrhosis, or heart failure. Here I present a pragmatic way of interpreting diagnostic lab tests to help clinicians recognize patients who are most likely to benefit from iron supplementation, choose between oral and parenteral administration, and make personalized decisions when patients do not fit usual guidelines.


2019 ◽  
Vol 5 (2) ◽  
pp. 106-111 ◽  
Author(s):  
Edoardo Bertero ◽  
Pietro Ameri ◽  
Christoph Maack ◽  

The main focus of cardio-oncology has been the prevention and treatment of the cardiac toxicity of chemotherapy and radiotherapy. Furthermore, several targeted therapies have been associated with unexpected cardiotoxic side-effects. Recently, epidemiological studies reported a higher incidence of cancer in patients with heart failure (HF) compared with individuals without HF. On this basis, it has been proposed that HF might represent an oncogenic condition. This hypothesis is supported by preclinical studies demonstrating that hyperactivation of the sympathetic nervous system and renin–angiotensin–aldosterone system, which is a hallmark of HF, promotes cancer growth and dissemination. Another intriguing possibility is that the co-occurrence of HF and cancer is promoted by a common pathological milieu characterised by a state of chronic low-grade inflammation, which predisposes to both diseases. In this review, we provide an overview of the mechanisms underlying the bidirectional relationship between HF and cancer.


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