Prognostic relevance of the interaction between short-term, metronome-paced heart rate variability, and inflammation: results from the population-based CARLA cohort study
Abstract:A change in TNF-α levels or the autonomic nervous system influences the mortality risk through both entities simultaneously. Thus, TNF-α and HRV need to be considered when predicating mortality.
“…When comparing our data to theirs, our control group was younger and with more female donors, and we observed lower levels of sTNFR1 but higher levels of sTNFR2, but in both studies, the sTNFR levels in the patients were significantly higher than in the control group. However, it has to be noted that the levels of sTNFR1 reported by us and others 16 – 18 in STEMI patients are relatively similar to the ones reported in prospective studies in patients with stable CAD 7 , 8 , 20 , and also to levels reported in population-based studies in older adults 9 , 11 – 13 . Thus, the level of sTNFR1 may not be of diagnostic interest on the population level in this age group.…”
Section: Discussionsupporting
confidence: 85%
“…For sTNFR2, only one study report values as high as ours 8 , while the other studies that included this marker 7 , 11 , 12 , 16 – 18 , 20 report levels more similar to the ones in our control group. The reason for this is unclear, all these studies have used ELISA kits from the same manufacturer, and even though analyses have been performed in plasma in some 12 , 13 , 18 , 20 and in serum in others 10 , 12 , 16 , 17 this did not seem to have created any consistent differences in levels. Also, we did not observe any differences in levels between the investigated time points, while Nilsson et al 18 report increased levels at 24 h and Paccalet et al shows increasing levels up to 48 h followed by a decrease towards admission levels after one month 16 .…”
Section: Discussionmentioning
confidence: 99%
“…In prospective studies, high levels of sTNFRs have been associated with cardiovascular events and increased mortality both in patients with stable coronary artery disease 7 , 8 , non-calcified atherosclerotic plaque 9 , and diabetes 10 . It has also been associated with increased risk for heart failure 11 , incident myocardial infarction 12 and cardiovascular death 13 in population-based studies. Increased levels have also been found in patients with recurrent ventricular arrhythmia 14 or recurrent myocardial infarction 15 after coronary stenting.…”
The soluble tumor necrosis factor receptors (sTNFR1 and sTNFR2) are suggested to play dual roles on physiological and pathophysiological actions of TNF-α. The aim of this study was to investigate the dynamic changes of these biomarkers in patients with ST-segment elevation myocardial infarction (STEMI). Blood was collected from 165 STEMI patients at admission, 1–3 days and 3 months after percutaneous coronary intervention (PCI) and from 40 healthy blood donors. sTNFR1 and sTNFR2 were measured with ELISA. The plasma levels of both sTNFR1 and sTNFR2 were significantly higher than in healthy donors at all three time points. We found no significant differences in sTNFR1 or sTNFR2 when comparing patients with patent versus occluded culprit vessels, or between patients having a thrombus aspiration or not. Survival analysis was performed comparing patients with levels of biomarkers above and below the median values at that time point. We found significant differences in survival for sTNFR2 in acute samples (p = 0.0151) and for both sTNFR1 and sTNFR2 in samples 1–3 days after PCI (p = 0.0054 and p = 0.0003, respectively). Survival analyses suggest that sTNFR1 or sTNFR2 could be promising markers to predict mortality in STEMI patients after PCI.
“…When comparing our data to theirs, our control group was younger and with more female donors, and we observed lower levels of sTNFR1 but higher levels of sTNFR2, but in both studies, the sTNFR levels in the patients were significantly higher than in the control group. However, it has to be noted that the levels of sTNFR1 reported by us and others 16 – 18 in STEMI patients are relatively similar to the ones reported in prospective studies in patients with stable CAD 7 , 8 , 20 , and also to levels reported in population-based studies in older adults 9 , 11 – 13 . Thus, the level of sTNFR1 may not be of diagnostic interest on the population level in this age group.…”
Section: Discussionsupporting
confidence: 85%
“…For sTNFR2, only one study report values as high as ours 8 , while the other studies that included this marker 7 , 11 , 12 , 16 – 18 , 20 report levels more similar to the ones in our control group. The reason for this is unclear, all these studies have used ELISA kits from the same manufacturer, and even though analyses have been performed in plasma in some 12 , 13 , 18 , 20 and in serum in others 10 , 12 , 16 , 17 this did not seem to have created any consistent differences in levels. Also, we did not observe any differences in levels between the investigated time points, while Nilsson et al 18 report increased levels at 24 h and Paccalet et al shows increasing levels up to 48 h followed by a decrease towards admission levels after one month 16 .…”
Section: Discussionmentioning
confidence: 99%
“…In prospective studies, high levels of sTNFRs have been associated with cardiovascular events and increased mortality both in patients with stable coronary artery disease 7 , 8 , non-calcified atherosclerotic plaque 9 , and diabetes 10 . It has also been associated with increased risk for heart failure 11 , incident myocardial infarction 12 and cardiovascular death 13 in population-based studies. Increased levels have also been found in patients with recurrent ventricular arrhythmia 14 or recurrent myocardial infarction 15 after coronary stenting.…”
The soluble tumor necrosis factor receptors (sTNFR1 and sTNFR2) are suggested to play dual roles on physiological and pathophysiological actions of TNF-α. The aim of this study was to investigate the dynamic changes of these biomarkers in patients with ST-segment elevation myocardial infarction (STEMI). Blood was collected from 165 STEMI patients at admission, 1–3 days and 3 months after percutaneous coronary intervention (PCI) and from 40 healthy blood donors. sTNFR1 and sTNFR2 were measured with ELISA. The plasma levels of both sTNFR1 and sTNFR2 were significantly higher than in healthy donors at all three time points. We found no significant differences in sTNFR1 or sTNFR2 when comparing patients with patent versus occluded culprit vessels, or between patients having a thrombus aspiration or not. Survival analysis was performed comparing patients with levels of biomarkers above and below the median values at that time point. We found significant differences in survival for sTNFR2 in acute samples (p = 0.0151) and for both sTNFR1 and sTNFR2 in samples 1–3 days after PCI (p = 0.0054 and p = 0.0003, respectively). Survival analyses suggest that sTNFR1 or sTNFR2 could be promising markers to predict mortality in STEMI patients after PCI.
“…In addition, higher HRV might predict more prolonged survival in cancer patients due to the effect of vagus nerve activity on cancer progression. Evidence also showed that the interaction of HRV and inflammatory mediators such as TNF-α and IL-6 is associated with cardiovascular mortality in a population-based CARLA cohort study [ 25 ]. Moreover, the release of inflammatory cytokines and chemokines following TBI can alter sleep [ 26 , 27 , 28 , 29 , 30 , 31 ].…”
To identify a screening tool for poor self-reported sleep quality at 12 weeks according to non-invasive measurements and patients’ characteristics in the first week after mild traumatic brain injury (mTBI), data from 473 mTBI participants were collected and follow-ups were performed at 12 weeks. Patients with previous poor self-reported sleep quality prior to the injury were excluded. Patients were then divided into two groups at 12 weeks according to the Pittsburgh Sleep Quality Index based on whether or not they experienced poor sleep quality. The analysis was performed on personal profiles and heart rate variability (HRV) for 1 week. After analyzing the non-invasive measurements and characteristics of mTBI patients who did not complain of poor sleep quality, several factors were found to be relevant to the delayed onset of poor sleep quality, including age, gender, and HRV measurements. The HRV–age–gender (HAG) index was proposed and found to have 100% sensitivity (cut-off, 7; specificity, 0.537) to predicting whether the patient will experience poor sleep quality after mTBI at the 12-week follow-up. The HAG index helps us to identify patients with mTBI who have no sleep quality complaints but are prone to developing poor self-reported sleep quality. Additional interventions to improve sleep quality would be important for these particular patients in the future.
“…Several studies demonstrated increased all-cause and cardiovascular mortality in patients with various diseases and higher levels of sTNF-R1 [ 7 – 12 ]. In the general population, elevated levels of sTNF-R1 were associated with all-cause and cardiovascular mortality after adjustment for lifestyle factors, inflammation due to chronic diseases, and established cardiovascular risk factors [ 13 – 15 ].…”
Aims
Single measurements of higher levels of soluble tumor necrosis factor receptor I (sTNF-R1) have been shown to be associated with increased risk of mortality. However, up to date, little is known about the underlying temporal dynamics of sTNF-R1 concentrations and their relation with mortality. We aimed to characterize the effect of changes in sTNFR-1 levels on all-cause and cardiovascular mortality, independent from other established risk factors for mortality, including other inflammatory markers.
Methods
We used data of the population based cohort study CARLA and included 1408 subjects with sTNF-R1 measured at baseline (2002–2006) and first follow-up (2007–2010). Cox proportional hazard models were used to assess the association of baseline and follow-up sTNF-R1 measurements with all-cause and cardiovascular mortality during ~10 years since the first follow-up after adjusting for relevant confounders.
Results
Based on 211 deaths among 1408 subjects, per each doubling of the baseline sTNF-R1, the risk of all-cause mortality was increased by about 30% (Hazard ratio 1.28, 95% Confidence Interval 0.6–2.7), while per each doubling of the follow-up level of sTNF-R1 mortality was 3-fold (3.11, 1.5–6.5) higher in a model including both measurements and adjusting for confounders. The results were mainly related to the cardiovascular mortality (5.9, 2.1–16.8 per each doubling of follow up sTNF-R1 value).
Conclusion
Solely the follow-up value, rather than its change from baseline, predicted future mortality. Thus, while sTNF-R1 levels are associated with mortality, particularly cardiovascular, over a long-time period in the general population, if they change, the earlier measurements play no or little role.
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