| 1. |
- Corino, Valentina D.A., et al.
(författare)
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Non-invasive evaluation of the effect of metoprolol on the atrioventricular node during permanent atrial fibrillation
- 2014. - January
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Ingår i: Computing in Cardiology 2014. - : Oxford University Press (OUP). - 2325-8861. - 9781479943463 - 9781479943470 ; 41, s. 889-892
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Konferensbidrag (refereegranskat)abstract
- The aim of this study was to evaluate changes in AV nodal properties during administration of metoprolol, using a novel ECG-based method for parameter estimation. The AV nodal parameters account for the probability of an impulse not passing through the fast pathway, the absolute refractory periods of the slow and fast pathways (aRPs and aRPf), representing the functional refractory period, and related prolongation in the respective refractory periods. Twenty patients (age 71±8 years, 14 men) with permanent AF from the RATe control in Atrial Fibrillation (RATAF) database were included in this study. Recordings during baseline and metoprolol administration were analyzed. Furthermore, simulated RR series were generated mimicking metoprolol administration. During metoprolol administration, aRP was significantly prolonged in both pathways (aRPs: 342±39 vs. 408±81 ms, p<0.001; aRPf: 432±74 vs. 527±83 ms, p<0.001). Similar results were found for the simulated RR series: both aRPs and aRPf were significantly prolonged with metoprolol. The AV nodal parameters reflect expected changes after metoprolol administration, i.e., a prolongation in functional refractory period. The simulations suggest that aRP may serve as an estimate of the functional refractory period.
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| 2. |
- Johansson, Madeleine, et al.
(författare)
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Association of incident fragility fractures in patients hospitalised due to unexplained syncope and orthostatic hypotension
- 2021
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Ingår i: Europace. - : Oxford University Press (OUP). - 1532-2092. ; 23:Supplement 3
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Konferensbidrag (refereegranskat)abstract
- Background Fragility fractures are caused by low-energy insults such as falls from standing height or less and pose a growing health challenge as their incidence rises with increasing age. Impaired orthostatic blood pressure response and a number of cardiovascular biomarkers have been previously identified as risk factors for fractures. It is likely that severe episodes of syncope and orthostatic hypotension increase the risk of subsequent fragility fractures, however this relationship has not been thoroughly examined.PurposeTo investigate the relationship of hospital admissions due to unexplained syncope and OH with incident fragility fractures in a middle-aged population.MethodsWe analysed a large population-based prospective cohort of 30,446 middle-aged individuals (age, 57.5 ± 7.6; men, 39.8%). We included patients hospitalised due to unexplained syncope and OH. Cox regression analysis adjusted for age, sex, prevalent fractures, body mass index (BMI) were applied to assess the impact of unexplained syncope/OH hospitalisations on subsequent incident fragility fractures. Prevalent fractures occurring before syncope/OH hospitalisation were excluded (n = 39) as well as cases with no follow-up time after the event of syncope/OH (n= 8).ResultsThe mean follow-up from baseline to first incident fracture or end of follow-up was 17.8 + 6.5 years, and 8201 (27%) suffered incident fracture. The mean age of patients with unexplained syncope (n = 493) and OH patients (n = 406) at baseline was 61.5 ± 7.1 years (50.1%, male) and 62.6 ± 6.6 years (49.8% male), respectively. The mean time between baseline and first admission for syncope and OH was 12.3 ± 4.5 years, and the mean age at first hospitalisation was 74.4 ± 7.6 years. In the multivariable-adjusted Cox regression, the risk of subsequent incident fractures was increased among patients hospitalised due to unexplained syncope (HR: 1.20; 95% CI 1.03–1.40; p < 0.02) and OH (HR: 1.40; 95% CI 1.20–1.64; p < 0.001), respectively (Kaplan-Meier curves; Figure 1).ConclusionsPatients hospitalised due to unexplained syncope and OH demonstrate increased risk of subsequent fragility fractures. We suggest that patients who are hospitalised for unexplained syncope and OH should be clinically assessed for true syncope aetiology, systematically treated against fall risk, and evaluated for additional risk factors for fragility fractures.
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| 3. |
- Kharraziha, Isabella, et al.
(författare)
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Effect of aging on cerebral tissue oxygenation in relation to reflex syncope
- 2021
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Ingår i: Europace. - : Oxford University Press (OUP). - 1532-2092. ; 23:Supplement 3
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Konferensbidrag (refereegranskat)abstract
- Background: There is an increased susceptibility to syncope with aging attributed to age-related physiological impairments. Cerebral oxime-try non-invasively measures cerebral tissue oxygenation (SctO2) and has been shown to be valuable in syncope evaluation. SctO2 has beenfound to decrease with aging but it is unknown whether the decrease in SctO2 is related to increased susceptibility to syncope during ortho-static provocation. By measuring SctO2 during head up tilt test (HUT) we can study age-related differences in SctO2 and their impact ondeveloping reflex syncope.Purpose: To investigate the effect of age on the cerebral tissue oxygenation threshold for syncope and presyncope among patients withvasovagal syncope.Methods: Non-invasive haemodynamic monitoring and near-infrared spectroscopy (NIRS) were applied during head-up tilt (HUT) in 139vasovagal syncope patients (mean [SD] 45[17] years, 60% female), and 82 control patients with a normal response to HUT (45[18] years,61% female). Group differences in SctO2 and systolic blood pressure (SBP) during HUT in supine position, after 3 and 10 min of HUT, 30seconds prior to syncope ("presyncopal phase") and during syncope in different age groups (<30, 30-60 and >60 years) were comparedusing one-way ANOVA and Tukey"s multiple comparison test. Associations between age and SctO2 were studied using linear regressionmodels adjusted for sex and concurrent SBP.Results: Lower SctO2 in supine position was associated with increasing age among controls (B=-0.085, p = 0.010) but not among VVS pa-tients (B=-0.036, p = 0.114). No age-related differences in SctO2 were found after 3 and 10 minutes of HUT and during syncope. MeanSctO2 (%) during the presyncopal phase decreased over the advancing age groups (<30: 66.9 ± 6.2, 30-60: 64.5 ± 6.1, >60: 62.2 ± 5.8; p = 0.009 for inter-group comparison). In contrast, mean SBP during the presyncopal phase did not differ by age groups (<30: 85.6 ± 21.8, 30-60:77.6 ± 19.7, >60: 77.6 ± 20.8 mmHg, p = 0.133). Age was associated with lower SctO2 during the presyncopal phase after adjusting for sexand SBP (B = 0.096, p = 0.001).Conclusion: Older VVS patients have lower cerebral tissue oxygenation in the presyncopal phase compared with younger patients inde-pendently of systolic blood pressure. These results suggest either that with imminent reflex syncope cerebral tissue oxygenation diminishesmore with advancing age or that cerebral deoxygenation is better tolerated by older reflex syncope patients.
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| 4. |
- Nawaz, Sara, et al.
(författare)
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Novel inflammatory biomarkers in postural orthostatic tachycardia syndrome
- 2023
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Ingår i: Europace. - 1532-2092 .- 1099-5129. ; , s. 345-345
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Konferensbidrag (refereegranskat)abstract
- IntroductionPostural Orthostatic Tachycardia Syndrome (POTS) is a disorder characterized by excessive orthostatic tachycardia and orthostatic intolerance. While traditional inflammatory biomarkers tend to be normal, a subclinical inflammatory process may be present in POTS.PurposeWe aimed to analyse novel inflammatory biomarkers in POTS patients: Growth Differentiation Factor 15 (GDF15), Neutrophil Gelatinase Associated Lipocalin (NGAL), Intercellular Adhesion Molecule 1 (ICAM-1), Tumour Necrosis Factor Receptor 1 (TNFR1) and Tumour Necrosis Factor Receptor 2 (TNFR2) and compared them to healthy controls. These inflammatory biomarkers have been shown to be independent predictors of major adverse cardiovascular events in other populations.MethodsAn age- and sex-matched case-control study included 65 patients verified to have POTS by positive head-up tilt-testing and cardiovascular autonomic tests, and 65 healthy controls (mean age: 31.1 vs 31.5 years, 84% females) with negative active standing tests and no history of syncope, orthostatic intolerance, or endocrine disease. High-sensitivity chemiluminescence sandwich immunoassay was used to measure plasma levels of inflammatory biomarkers in a blinded fashion. Descriptive statistics compared groups and a univariate ANOVA was employed. Biomarker values were log-transformed. A score incorporating all biomarkers was generated to see if the totality of biomarkers discriminated POTS patients from controls.ResultsBaseline characteristics are displayed in Table 1. Mean levels of GDF15 (p=0.01), NGAL (p=0.003), ICAM-1 (p=0.04) and TNFR1 (p=0.03) were significantly higher in POTS vs controls, whereas TNFR2 (p=0.04) was significantly lower in POTS (p=0.04). The product of four upregulated biomarkers divided by TNFR2 produced a receiver operator curve (ROC) with an area under the curve (AUC) of 0.703 (pConclusionPOTS patients had increased GDF15, NGAL, TNFR1 and ICAM-1 levels and reduced TNFR2 levels suggesting underlying, yet undefined, subclinical inflammatory processes involving neutrophil and endothelial activation.
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