Depression and cancer: mechanisms and disease progression.

Development of a new predictive model for polypathological patients. The PROFUND index.

Guidelines for a Palliative Approach in Residential Aged Care

Context: Preventive medicine has historically favored reducing a risk factor by a small amount in the entire population rather than by a large amount in high-risk individuals. The use of multivariable risk prediction tools, however, may affect the relative merits of this strategy. Methods: This study uses risk factor data from the National Health and Nutrition Examination Survey III to simulate a population of more than 100 million Americans aged thirty or older with no history of CV disease. Three strategies that could affect CV events, CV mortality, and quality-adjusted life years were examined: (1) a population-based strategy that treats all individuals with a low- or moderate-intensity intervention (in which the low-intensity intervention represents a public health campaign with no demonstrable adverse effects), (2) a targeted strategy that treats individuals in the top 25 percent based on a single risk factor (LDL), and (3) a risk-targeted strategy that treats individuals in the top 25 percent based on overall CV risk (as predicted by a multivariable prediction tool). The efficiency of each strategy was compared while varying the intervention’s intensity and associated adverse effects, and the accuracy of the risk prediction tool. Findings: The LDL-targeted strategy and the low-intensity population-based strategy were comparable for CV events prevented over five years (0.79 million and 0.75 million, respectively), as were the risk-targeted strategy and

/pdf/the-relative-merits-of-population-based-and-targeted-2lzry7diz7.pdf

The Relative Merits of Population-Based and Targeted Prevention Strategies

Predictors of mortality in younger and older patients with heart failure and preserved or reduced left ventricular ejection fraction.

Prediction of Survival for Older Hospitalized Patients


 
 
 Circulating cellular communication network factor 1 (CCN1) improves risk stratification in ACS patients and, as we have recently shown, predicts all-cause mortality in patients with dilated cardiomyopathy (DCM). It was the aim of this study to evaluate whether the prognostic role of CCN1 is influenced by an inflammatory phenotype.
 
 
 
 Patients with a primary diagnosis of DCM, defined as LVEF <45% and an increased LVEDD (according to HENRY >117%), were included in this single-center study. Exclusion criteria comprised primary valvular diseases (≥second degree), acute myocarditis, active infectious diseases, pulmonary diseases, cancer, chronic alcoholism, and heart failure of other origins. CCN1 levels were determined in serum at study inclusion using an enzyme-linked immunosorbent assay. The primary endpoint was all-cause mortality during follow-up. An adjusted multivariable cox regression model was used to assess the association between CCN1 and all-cause mortality. We further analysed potential effect modifications by adding either an interaction term between CCN1 and DCMi diagnosis (DCMi vs. DCM). The Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC) score to predict all-cause mortality in HF patients was used as a reference model. The performance of CCN1 in combination with the MAGGIC score and NT-proBNP to predict all-cause mortality was assessed using Cox's proportional-hazards models
 
 
 
 A total of 283 predominantly male DCM patients (78.5% males) with a median age of 55.7 (interquartile range [IQR 48.2, 65.7]) years and predominantly recent onset of disease (3.8 [IQR 1.1, 20.5] months) with a severely reduced LVEF (31 [IQR 25, 37] %), increased LVEDD (67.0 [IQR 62.8, 72.0] mm), and normal eGFR (CKD-EPI) (90.9 [IQR73.9, 102.4] ml/min) were analyzed. During a median follow-up of 12.4 [IQR 10.5, 14.0] years, a total of 107 (37.8%) patients died. Patients in the highest CCN1 tertile had a significantly higher mortality risk than those in the lower tertile (HR 1.82; 95% CI 1.06, 3.14; P=0.030) in adjusted multivariable Cox regression models. Adding CCN1 to the MAGGIC risk score improved c-statistics for prognostic accuracy of all-cause mortality at 6 years (0.624 to 0.645, p=0.012), unlike NT-proBNP (0.624 to 0.630, p=0.123). Patients classified as DCMi (n=128) had significantly lower CCN1 levels compared with classical DCM (n=155) (154.9 (115.4–191.7) vs. 174.7 (130.0–241.0) pg/ml, P=0.022). Inflammation status (DCMi vs DCM) had no significant impact (P interaction = 0.28) on the association of CCN1 and all-cause mortality (Fig. 1).
 
 
 
 CCN1 independently predicts all-cause mortality in DCM patients and improves risk stratification beyond the MAGGIC score. In this pilot cohort, the inflammatory phenotype had no impact on prognostic discrimination. Data are currently analyzed in a validation cohort.
 
 
 
 Type of funding sources: Foundation. Main funding source(s): Kerckhoff Research Foundation


/pdf/impact-of-inflammatory-phenotype-on-prognostic-2laudw0r.pdf

Impact of inflammatory phenotype on prognostic discrimination for the novel biomarker cellular communication network factor 1 (CCN1) in patients with dilated cardiomyopathy


 
 
 We recently reported an independent prognostic ability of serum CCN1 to predict all-cause mortality in DCM, irrespective of its aetiology (inflammatory DCM (DCMi) or conventional DCM). Interestingly, CCN1 levels were lower in patients with DCMi than in patients with conventional DCM. In a murine model, miR-155, which has key functions in inflammation, repressed the expression of CCN1 and impeded its function in angiogenesis. In a recent study, patients with DCMi had higher miR-155 plasma levels than those with conventional DCM.
 
 
 
 The present study evaluated whether circulating levels of CCN1 and miR-155 are associated in order to provide insight into the underlying pathophysiology.
 
 
 
 Patients with a primary diagnosis of DCM, defined as LVEF <45% and an increased LVEDD (according to HENRY >117%), were included in this single-centre study. Exclusion criteria comprised primary valvular diseases (≥ second degree), acute myocarditis, active infectious diseases, pulmonary diseases, cancer, chronic alcoholism, and heart failure of other origins. CCN1 levels were determined in serum at study inclusion using an enzyme-linked immunosorbent assay. miR-155-5p was measured in serum using quantitative real-time PCR and normalized to a spike-in of miR-39-3p from C. elegans for analysis. The primary endpoint was all-cause mortality during follow-up. An adjusted multivariable Cox regression model (comprising age, sex, time of symptoms, LVEF, eGFR, CRP, and NT-proBNP) was used to assess the association between CCN1 or miR-155 with all-cause mortality.
 
 
 
 Among 283 patients in the DCM cohort with CCN1 data, miR-155 measurements were available for analysis in 270 patients. Among those, 77.4% were males at a median age of 55.3 [IQR 47.8, 64.7] years with 3.84 [IQR 1.1, 19.3] months since onset of disease who had severely reduced LVEF (31 [IQR 26, 37] %), elevated LVEDD (67 [IQR 62, 72] mm), and normal eGFR (CKD-EPI) (91.5 [IQR 74.01, 103.3] ml/min). During a median follow-up of 12.4 [IQR 10.5, 13.9] years, a total of 101 (37.4%) patients died.
 There was no significant difference in miR-155 levels between DCMi and conventional DCM (ΔCt: 14.84 vs 14.94, P = 0.60; and ΔΔCt values 1.68 vs 1.49, P = 0.42). A positive correlation was found for miR-155 (relative expression ΔΔCt values) with CCN1 in serum from patients with conventional DCM (rS = 0.251, p = 0.002) but not with DCMi (rS = 0.007, p = 0.94) (Figure 1). Unlike CCN1 (HR 1.11; 95% CI 1.04, 1.19; p = 0.002), miR-155 was not associated with all-cause mortality (HR 0.95; 95% CI 0.82, 1.11; P = 0.54) in adjusted multivariable Cox regression models.
 
 
 
 A differential correlation of miR-155 with CCN1 levels was found in patients with conventional DCM vs. those with DCMi, suggesting a potential role of these biomarkers only in conventional DCM. Further investigation of the pathophysiology of CCN1 in DCM is warranted, including -omics analyses.


Correlation of the novel biomarker cellular communication network factor 1 (CCN1) with miR-155 in serum of patients with dilated cardiomyopathy

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Prediction of Survival for Older Hospitalized Patients

Impact of inflammatory phenotype on prognostic discrimination for the novel biomarker cellular communication network factor 1 (CCN1) in patients with dilated cardiomyopathy

Correlation of the novel biomarker cellular communication network factor 1 (CCN1) with miR-155 in serum of patients with dilated cardiomyopathy