Baseline Troponin T level in stroke and its association with stress cardiomyopathy

Liesirova, Kai Timo; Abela, Eugenio; Pilgrim, Thomas; Bickel, Laura; Meinel, Thomas; Meisterernst, Julia Anne; Verma, Renuka; Sarıkaya, Hakan; Heldner, Mirjam Rachel; Dobrocky, Tomas; Siqueira, Erick; El-Koussy, Marwan; Fischer, Urs; Gralla, Jan; Arnold, Marcel; Mattle, Heinrich; Hsieh, Kety; Jung, Simon

doi:10.1371/journal.pone.0209764

Cited by 9 publications

(9 citation statements)

References 23 publications

(26 reference statements)

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“…Interestingly, TF positively correlated with D-dimer and troponin levels (Fig. e3A and B), which have been previously suggested as indicators of CVS and TCM risk respectively [35,36]. Although more evidence is needed to confirm TF role as a prognostic biomarker for aSAH complications, this data sow the seeds for further investigations in this context.…”

Section: Serum Tissue Factor Correlated With Asah Functional Outcomesupporting

confidence: 65%

NLRP3 Inflammasome Overactivation in Patients with Aneurysmal Subarachnoid Hemorrhage

Nanwani-Nanwani

García-Tovar²,

Alfaro³

et al. 2022

Transl. Stroke Res.

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Aneurysmal subarachnoid hemorrhage (aSAH) is an uncommon and severe subtype of stroke leading to the loss of many years of productive life. We analyzed NLRP3 activity as well as key components of the inflammasome cascade in monocytes and plasma from 28 patients with aSAH and 14 normal controls using flow cytometry, western blot, ELISA, and qPCR technologies. Our data reveal that monocytes from patients with aSAH present an overactivation of the NLRP3 inflammasome, which results in the presence of high plasma levels of interleukin (IL)-1β, IL-18, gasdermin D, and tissue factor. Although further research is needed, we propose that serum tissue factor concentration might be a useful prognosis biomarker for clinical outcome, and for Tako-Tsubo cardiomyopathy and cerebral vasospasm prediction. Remarkably, MCC-950 inhibitor effectively blocks NLRP3 activation in aSAH monocyte culture and supresses tissue factor release to the extracellular space. Finally, our findings suggest that NLRP3 activation could be due to the release of erythrocyte breakdown products to the subarachnoid space during aSAH event. These data define NLRP3 activation in monocytes from aSAH patients, indicating systemic inflammation that results in serum TF upregulation which in turns correlates with aSAH severity and might serve as a prognosis biomarker for aSAH clinical outcome and for cerebral vasospasm and Tako-Tsubo cardiomyopathy prediction.

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Section: Serum Tissue Factor Correlated With Asah Functional Outcomesupporting

confidence: 65%

NLRP3 Inflammasome Overactivation in Patients with Aneurysmal Subarachnoid Hemorrhage

Nanwani-Nanwani

García-Tovar²,

Alfaro³

et al. 2022

Transl. Stroke Res.

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“…The initial injury to the brain often increases the intracranial pressure through a local mass effect and diffuse cerebral oedema, and this increase in intracranial pressure leads to a complex interaction with the neuroendocrine response by activating the autonomic system, with the further release of catecholamine. The systemic release of catecholamine often leads to an increase in arterial blood pressure [40] , 41. , [42] .…”

Section: Discussionmentioning

confidence: 99%

Survival status and predictors of mortality among traumatic brain injury patients in an Ethiopian hospital: A retrospective cohort study

Amare

Tesfaye

Ali

et al. 2021

African Journal of Emergency Medicine

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Introduction Traumatic brain injury is a major global public health problem causing substantial mortality among the adult population. Hence, this study aimed to determine the predictors of mortality among adult traumatic brain injury patients in Felegehiwot Comprehensive Specialized Hospital in Northwest Ethiopia during 2020. Methods A retrospective cohort study was conducted at Felegehiwot Comprehensive Specialized Hospital using anonymized patient data obtained from chart review. Descriptive statistics were used to summarise the patient characteristics. The Kaplan–Meier survival curve and log-rank test were used to test for differences in survival status among groups. The Cox proportional hazards regression model was used at the 5% level of significance to determine the net effect of each explanatory variable on time to death. Results In total, 338 patients aged ≥15 years and diagnosed with traumatic brain injury were included in the analysis. Among these patients, 103 (30.45%) died, giving a crude death rate of 25.53 per 1000 (95% CI: 21.05–30.98) person-days of follow-up. The overall median survival time was 44 days. The independent predictors of mortality after diagnosis of traumatic brain injury were admission Glasgow coma scale score ≤ 8 (adjusted hazard ratio (AHR): 4.85; 95% confidence interval (CI): 1.73–13.62), bilateral non-reactive pupils at admission (AHR: 2.00 (95% CI: 1.10–3.71), elevated systolic blood pressure at admission (AHR: 0.31; 95% CI:0.11–0.86), elevated diastolic blood pressure at admission (AHR: 3.54; 95% CI: 1.33–9.43), and haematoma evacuation (AHR: 0.42; 95% CI: 0.16–0.90). Discussion The Survival status of traumatic brain injury patients was relatively low in this study. Glasgow coma scale score, bilateral non-reactive pupils, and elevated blood pressure were significant predictors of mortality. Further prospective follow-up studies that include residence and occupation are recommended.

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“…A basic model included hs‐cTnT as dependent variable and VO 2peak , randomization group, and testing centre (by a categorical variable) as independent variables. The model was then further adjusted with predefined clinical variables selected based on previous literature, that is, age, 1,5 sex, 1,5 creatinine concentration, 1,17 N‐terminal pro‐brain natriuretic peptide (NT‐proBNP), 1 LVEDD, 13 New York Heart Association (NYHA) functional class, 18 LVEF, 18 HR peak , 18 workload, 18 and HF treatment, defined as treatment (yes/no) with angiotensin II receptor blockers, angiotensin‐converting enzyme inhibitors, and/or beta‐blockers. For adjustment variables with repeated measurements, that is, creatinine, NT‐proBNP, LVEDD, LVEF, HR peak , and workload, the values for each time point were included.…”

Section: Methodsmentioning

confidence: 99%

Exercise training and high‐sensitivity cardiac troponin T in patients with heart failure with reduced ejection fraction

et al. 2021

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Aims Whether an exercise training intervention is associated with reduction in long-term high-sensitivity cardiac troponin T (hs-cTnT) concentration (a biomarker of subclinical myocardial injury) in patients with heart failure with reduced ejection fraction (HFrEF) is unknown. The aims were to determine (i) the effect of a 12 week endurance exercise training intervention with different training intensities on hs-cTnT in stable patients with HFrEF (left ventricular ejection fraction ≤ 35%) and (ii) associations between hs-cTnT and peak oxygen uptake (VO 2peak ). Methods and results In this sub-study of the SMARTEX-HF trial originally including 261 patients from nine European centres, 213 eligible patients were included after withdrawals and appropriate exclusions [19% women, mean age 61.2 years (standard deviation: 11.9)], randomized to high-intensity interval training (HIIT; n = 77), moderate continuous training (MCT; n = 63), or a recommendation of regular exercise (RRE; n = 73). Hs-cTnT measurements and clinical data acquired before (BL) and after a 12 week exercise training intervention (12 weeks) and at 1 year follow-up (1 year) were analysed using multivariable mixed models. Baseline hs-cTnT was above the 99th percentile upper reference limit of 14 ng/L in 35 (48%), 35 (56%), and 49 (64%) patients in the RRE, MCT, and HIIT groups, respectively. Median hs-cTnT was 16 ng/L at BL, 14 ng/L at 12 weeks, and 14 ng/L at 1 year. Hs-cTnT was statistically significantly reduced at 12 weeks in a model adjusted for randomization group, centre and VO 2peak , and after further adjustment in the final model that also included age, sex, creatinine concentrations, N-terminal pro-brain natriuretic peptide, smoking, and heart failure treatment. The mean reduction from BL to 12 weeks in the final model was 1.1 ng/L (95% confidence interval: 1.0-1.2 ng/L, P < 0.001), and the reduction was maintained at 1 year with a mean reduction from BL to 1 year of 1.1 ng/L (95% confidence interval: 1.0-1.1 ng/L, P = 0.025). Randomization group was not associated with hs-cTnT at any time point (overall test: P = 0.20, MCT vs. RRE: P = 0.81, HIIT vs. RRE: P = 0.095, interaction time × randomization group: P = 0.88). Independent of time point, higher VO 2peak correlated with lower hs-cTnT (mean reduction over all time points: 0.2 ng/L per increasing mL•kg À1 •min À1 , P = 0.002), without between-group differences (P = 0.19). Conclusions In patients with stable HFrEF, a 12 week exercise intervention was associated with reduced hs-cTnT in all groups when adjusted for clinical variables. Higher VO 2peak correlated with lower hs-cTnT, suggesting a positive long-term effect of increasing VO 2peak on subclinical myocardial injury in HFrEF, independent of training programme.

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Baseline Troponin T level in stroke and its association with stress cardiomyopathy

Cited by 9 publications

References 23 publications

NLRP3 Inflammasome Overactivation in Patients with Aneurysmal Subarachnoid Hemorrhage

NLRP3 Inflammasome Overactivation in Patients with Aneurysmal Subarachnoid Hemorrhage

Survival status and predictors of mortality among traumatic brain injury patients in an Ethiopian hospital: A retrospective cohort study

Exercise training and high‐sensitivity cardiac troponin T in patients with heart failure with reduced ejection fraction

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