Introduction: Several studies suggest that cardiac rehabilitation through physical exercise could reduce heart failure (HF) morbidity and mortality. Hypothesis: Here, we aimed to evaluate the association of physical activity with plasma levels of 92 proteins associated with cardiovascular disease (CVD) as well as risk of re-hospitalization and mortality in patients hospitalized for HF. Methods: Four-hundred-and-thirty-three patients hospitalized for HF (mean age 75 years; 32% women) were screened for physical activity derived from questionnaires in the Swedish national public health survey. The median follow-up time to death and re-hospitalization was 842 (IQR, 390-1433) and 155 (IQR, 42-583) days, respectively. Associations between baseline reported physical activity scores, mortality and re-hospitalization risk were analyzed using multivariable Cox regression analysis. Plasma samples from 295 study participants were analyzed with a proximity extension assay consisting of 92 proteins. Associations between proteins and physical activity were explored using a false discovery rate of 5%, and significant associations were taken forward to multivariate analyses. Results: A total of 206 patients (48%) reported moderate and regular physical activity throughout the week. In the fully adjusted Cox regression model, absence of moderate to regular physical activity was associated with increased mortality (HR 1.50; CI95% 1.11-2.03; p=0.008), but not with re-hospitalization risk (HR 1.05; CI95% 0.84-1.32; p=0.684). Physical active time below 1 h throughout the week was associated with increased risk of mortality (HR 1.82; CI95% 1.36-2.43; p<0.001)as well as re-hospitalization irrespective of cause (HR 1.26; CI95% 1.01-1.58; p=0.049). Sedentary lifestyle was associated with elevated plasma levels of 24 proteins, whereof several implicated in myocardial fibrosis, migration and apoptosis. Conclusions: Low weekly physical activity is associated with increased risk of mortality and re-hospitalization in hospitalized HF patients, independently of traditional risk factors. Further sedentary lifestyle was associated with elevated levels of several proteins earlier linked to myocardial fibrosis, migration and apoptosis.
Introduction: Even though treatment for heart failure (HF) has improved over recent decades, the mortality is still high, and the high re-hospitalization rate poses a huge economic burden to the society. Hypothesis: Here, we explored if proteomic profiles differed between high mortality risk/multiple hospitalized HF patients versus HF patients that survived without multiple hospitalizations. Methods: A multiplex protein panel was analysed in patients hospitalized for HF (The Swedish heart failure cohort (HARVEST-Malmö) discovery cohort: n=296; mean age 74.6 years; 30% women) and a replication cohort, the European MEDIA-DHF cohort (n=430). We characterized three mutually exclusive phenotypes of HF based on vital and hospitalization status (survivors without multiple hospitalizations (≥2; n=50); deceased without multiple hospitalizations (n=46) and multiply hospitalized but not dead (n=86), and explored associations between proteins and phenotype in multivariate logistic regressions. Results: In the discovery cohort, SCGB3A2 (OR 2.51 (1.14-5.52; p=0.023); elafin (OR 2.50 (1.01-6.14; p=0.047), GDF15 (OR 2.82 (1.07-7.42); p=0.036) and CHI3L1 (3.09 (1.42-6.72); p=0.004) presented with significant associations with death without multiple hospitalizations. GDF15 and CHI3L1 also presented with associations with multiple hospitalizations. SCGB3A2, elafin, In the replication cohort GDF15 and CHI3L1 were both associated with death without multiple hospitalizations (n=9) a model adjusted for age and sex. When associations between GDF15 and CHI3L1 and multiple hospitalizations were explored in the replication cohort, GDF15but not CHI3L1 presented with significant associations in a model adjusted for age and sex (p=0.005 and p=0.900, respectively), but the association was attenuated upon further adjustment (p=0.80). Conclusions: In two European hospitalized HF populations, we could show associations between GDF15 and CHI3L1 and a high-risk phenotype of HF in both the discovery and replication cohorts.
Introduction: Several biomarkers have been linked with incident heart failure (HF), but the pathophysiology of HF is complex and multifactorial. Hypothesis: We explored 92 biomarkers’ associations with left ventricular hypertrophy (LVH), prevalent LV diastolic dysfunction (LVDD), and incident HF in three European population-based cohorts. Methods: Profiling of 92 biomarkers was carried out in 1737 participants from the echocardiography subsample of the population-based cohort study, the Malmö Preventive Project (mean age 67 years, 29% women). The final study sample consisted of 1681 subjects for analyses of incident HF (n=130), and 1530 subjects for analyses of LVDD (n=109) and LVH (n=498). Multivariable Cox regression analyses excluding subjects with prevalent HF were carried out for incident HF. Multivariable logistic regression analyses excluding subjects with reduced or mid-range LV ejection fraction (<50%) were carried out for LVDD and LVH. Replication analyses of significant findings were carried out in the HOMAGE (562 cases of incident HF, 871 controls) and STANISLAS cohorts (304 cases of LVDD and 1668 controls; and 245 cases of LVH and 1681 controls). Results: In the multivariable model adjusted for clinical risk factors, six proteins were associated with incident HF (median follow-up time 12.6, interquartile range 10.9-13.6 years): ST2 (hazard ratio (HR) 1.40; 95% confidence interval (1.03-1.91); p=0.031), GDF-15 (HR 1.33 (1.00-1.77); p=0.048), AZU1 (HR 1.42 (1.10-1.82); p=0.006), MPO (HR 1.48 (1.02-2.15); p=0.041), Gal-4 (HR 1.37 (1.02-1.85); p=0.038) and NT-proBNP (HR 1.98 (1.66-2.36); p=2.1x10 -14 ) in the discovery cohort. In the replication cohort, ST2, GDF15, NT-proBNP and Gal-4 also displayed significant associations with incident HF. In analyses of DD, none of the associated proteins in the discovery cohort (AZU1; TR; PCSK9 and NT-proBNP) were replicated in the STANISLAS cohort. Among AZU1, PGLYRP1, and NT-proBNP, NT-proBNP was the only protein that was significantly associated with LVH in both cohorts. Conclusions: We replicated the association of ST2, GDF-15, NT-proBNP and Gal-4 with incident HF, whereas NT-proBNP was the only biomarker that was associated with LVH as well as incident HF in discovery and replication cohorts.
Introduction: Galectin-4 (Gal-4) is a small protein in the gastrointestinal tract. It has been implicated in diabetes mellitus, incident coronary events, incident heart failure as well as all-cause and cardiovascular mortality. However, possible associations of Gal-4 with stroke have not yet been examined. Hypothesis: We explored if Gal-4 is associated with prevalent and incident stroke in a large population cohort. Methods: Gal-4 was analyzed by the proximity extension assay technique in 1737 participants from a subsample of the population-based Malmö Preventive Project (mean age 67 years, 29% women). Stroke was defined as all strokes (ischemic, hemorrhagic and undefined). Multivariable logistic regression models were applied for prevalent stroke (n=72). Prior to analyses of incident stroke, cases of prevalent stroke were excluded. Multivariate Cox regression models were applied for incident stroke. Results: Gal-4 levels were significantly higher in subjects with prevalent stroke (p=0.003) than in subjects free from prevalent stroke. Gal-4 (per doubling of concentration) was significantly associated with prevalent stroke in age and sex adjusted models (odds ratio 1.49; 95% confidence interval (1.04-2.14); p=0.032), but the associations was no longer significant upon further adjustment for traditional risk factors for stroke (OR 1.22 (0.82-1.82), p=0.339). Further, each doubling in Gal-4 concentration was associated with higher risk of incident stroke (n=1604; 327 events; median follow up time 12.6 (interquartile range 10.0-13.6) years; hazard ratio 1.24 (1.02-1.49); p=0.027) in a model adjusted for BMI, systolic blood pressure, triglycerides, HDL-cholesterol, smoking, diabetes, prevalent coronary events and anti-hypertensive treatment. Conclusions: In a large population cohort, Gal-4 was associated with incident stroke during a follow-up of 12 years, further implicating a role of Gal-4 in both cardiovascular and metabolic disease.
Introduction: Anxiety and depression are common comorbid conditions in heart failure (HF), and there is growing evidence that they increase the risk of adverse outcomes, including rehospitalization and functional decline. Hypothesis: We aimed to determine if symptoms of anxiety and depression would predict mortality and rehospitalization in a Swedish prospective HF patient cohort. Methods: 387 patients hospitalized for HF (mean age 75 years; 32% women) were assessed using the Hospital Anxiety and Depression Scale (HADS) to measure symptoms of anxiety (HADS Anxiety) and depression (HADS Depression). The median follow-up time to death and rehospitalization was 665 (range,1737; interquartile range, 811) and 316 (range, 2069; interquartile range, 348) days, respectively. Relations between baseline HADS scores, mortality and rehospitalization risk were analyzed using multivariable Cox regression analysis adjusted for age, sex, body- mass index, smoking, prevalent atrial fibrillation, educational level, prevalent diabetes, NYHA-class at hospitalization and systolic blood pressure. Results: A total of 30 patients (8%) had signs of depression according to HADS Depression score >11 points. In the fully adjusted Cox regression model using continuous standardized values per 1 SD change, higher score on HADS Depression scale (HR,1.42; CI, 1.16-1.75; p=0.001) yielded significant associations with increased mortality whereas no associations were found for HADS Anxiety scale (HR, 1.04; CI, 0.86-1.26; p=0.719). Rehospitalization risk (n = 246; 64%) was not significantly associated with higher scores on HADS Depression scale (HR, 1.08; CI, 0.94-1.25; p=0.274) or HADS Anxiety scale (HR, 0.95; CI, 0.82-1.09; p=0.449). Conclusions: Higher scores on HADS Depression scale indicated increased mortality risk in hospitalized HF patients, independently of traditional risk factors. However, higher scores on HADS Anxiety scale did not herald increased risk of mortality or rehospitalization.
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