Equal clinical performance of a novel point-of-care cardiac troponin I (cTnI) assay with a commonly used high-sensitivity cTnI assay

Venge, Per; Lippen, Lian van; Blaschke, Sabine; Christ, Michael; Geier, Felicitas; Giannitsis, Evangelos; Hagström, Emil; Hausfater, Pierre; Khellaf, Mehdi; Mair, Johannes; Pariente, D.; Scharnhorst, Volkher; Semjonow, Véronique

doi:10.1016/j.cca.2017.03.023

Cited by 26 publications

(28 citation statements)

References 16 publications

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“…During myocardial ischemia, the membranes of cardiac muscle cells were damaged, leading to the release of myocardial enzymes and proteins including cTnI, cTnT, LDH, and Mb into peripheral blood. Therefore, detecting the levels of cTnI, cTnT, LDH, and Mb in peripheral blood can reflect the degree of myocardial ischemia necrosis 29. In our study, we observed that GB treatment downregulated the high levels of cTnI, cTnT, LDH, and Mb and also improved the damaged myocardial cells induced by I/R injury significantly, indicating that GB mitigated myocardial injury in myocardial I/R model rats.…”

Section: Discussionsupporting

confidence: 54%

<p>Ginkgolide B ameliorates myocardial ischemia reperfusion injury in rats via inhibiting endoplasmic reticulum stress</p>

Guo¹,

Zhang²,

Zhang³

et al. 2019

DDDT

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Purpose Ginkgolide B (GB) is a terpene lactone component found in Ginkgo biloba , which has a protective role on ischemia reperfusion (I/R) injury. This study was aimed at exploring the protective mechanism of GB on the myocardial I/R. Patients and methods Myocardial I/R model was established on Sprague Dawley rats. The levels of cardiac troponin I, cardiac troponin T, lactic dehydrogenase, and myoglobin were determined by a 200FR NEO automatic biochemical analyzer. Histological examination was performed through HE and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining. The expression levels of p-PERK, p-IRE1α, ATF6, p-AKT, and mTOR were detected by Western blot. Results The results exhibited that GB treatment suppressed the high levels of cardiac troponin I, cardiac troponin T, lactic dehydrogenase, and myoglobin and ameliorated the damaged and irregularly arranged myocardial cells induced by I/R injury significantly, indicating that GB could ameliorate myocardial I/R injury. Moreover, the high expression levels of endoplasmic reticulum (ER) stress key proteins caused by I/R injury were suppressed significantly by GB treatment, including p-PERK, p-IRE1α, and ATF6. GB treatment also decreased the number of apoptotic cells compared with I/R group. In addition, activation of ER stress by Tunicamycin treatment could counteract the protective effects of GB on I/R injury, suggesting that GB ameliorated myocardial I/R injury through inhibition of ER stress-induced apoptosis. Finally, the decreased p-AKT and p-mTOR expressions caused by I/R injury were upregulated by GB and inhibition of PI3K/AKT/mTOR pathway by LY294002 abolished the protective effects of GB on I/R injury, indicating that GB activated PI3K/AKT/mTOR pathway during I/R injury. Conclusion GB protected against myocardial I/R injury through inhibiting ER stress-induced apoptosis via PI3K/AKT/mTOR signaling pathway.

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Section: Discussionsupporting

confidence: 54%

<p>Ginkgolide B ameliorates myocardial ischemia reperfusion injury in rats via inhibiting endoplasmic reticulum stress</p>

Guo¹,

Zhang²,

Zhang³

et al. 2019

DDDT

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“…High myocardial specificity was required to detect the indexes of cTnI and cTnT and high sensitivity to determine the index of Mb in myocardial ischemic necrosis [ 26 ]. During myocardial ischemia, the integrity of the cardiac muscle cell membranes is damaged, causing myocardial enzymes and proteins, such as Mb, cTnI and cTnT, to be released into the peripheral blood.…”

Section: Discussionmentioning

confidence: 99%

Hyperbaric oxygen protects against myocardial reperfusion injury via the inhibition of inflammation and the modulation of autophagy

Chen

et al. 2017

Oncotarget

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Our previous study demonstrated that hyperbaric oxygen (HBO) preconditioning protected against myocardial ischemia reperfusion injury (MIRI) and improved myocardial infarction. However, HBO’s effect on MIRI-induced inflammation and autophagy remains unclear. In this study, we investigate the potential impact and underlying mechanism of HBO preconditioning on an MIRI-induced inflammatory response and autophagy using a ligation of the left anterior descending (LAD) coronary artery rat model. Our results showed that HBO restored myocardial enzyme levels and decreased the apoptosis of cardiomyocytes, which were induced by MIRI. Moreover, HBO significantly suppressed MIRI-induced inflammatory cytokines. This effect was associated with the inhibition of the TLR4-nuclear factor kappa-B (NF-κB) pathway. Interestingly, lower expression levels of microtubule-associated protein 1 light chain 3B (LC3B) and Beclin-1 were observed in the HBO-treatment group. Furthermore, we observed that HBO reduced excessive autophagy by activating the mammalian target of the rapamycin (mTOR) pathway, as evidenced by higher expression levels of threonine protein kinase (Akt) and phosphorylated-mTOR. In conclusion, HBO protected cardiomocytes during MIRI by attenuating inflammation and autophagy. Our results provide a new mechanistic insight into the cardioprotective role of HBO against MIRI.

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“…However, a 90.5% sensitivity and 94.4% NPV may be adequate for the purpose of triaging patients to a referral hospital based on a low-risk assessment. Furthermore, our data from the core-lab-PMHP suggests that as newer, more sensitive, POC cTn assays become available in the US, the sensitivity of the PMHP will improve [27,28]. In fact, in this cohort the core-lab-PMHP (the combination of a HEAR score with a core lab cTn measure from prehospital blood) achieved 100% sensitivity and NPV for 30-day MACE.…”

Section: Plos Onementioning

confidence: 84%

Prehospital use of a modified HEART Pathway and point-of-care troponin to predict cardiovascular events

et al. 2020

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The HEART Pathway is a validated risk stratification protocol for Emergency Department patients with chest pain that has yet to be tested in the prehospital setting. This study seeks to test the performance of a prehospital modified HEART Pathway (PMHP). A prospective cohort study of adults with chest pain without ST-segment elevation myocardial infarction was conducted at three EMS agencies between 12/2016-1/2018. To complete a PMHP assessment, paramedics drew blood, measured point-of-care (POC) troponin (i-STAT; Abbott Point of Care) and calculated a HEAR score. Patients were stratified into three groups: high-risk based on an elevated troponin, low-risk based on a HEAR score <4 with a negative troponin, or moderate risk for a HEAR score �4 with a negative troponin. Sensitivity, specificity, negative and positive predictive values of the PMHP for detection of major adverse cardiac events (MACE: cardiac death, MI, or coronary revascularization) at 30days were calculated. A total of 506 patients were accrued, with PMHP completed in 78.1% (395/506). MACE at 30-days occurred in 18.7% (74/395). Among these patients, 7.1% (28/ 395) were high risk yielding a specificity and PPV for 30-day MACE of 96.6% (95%CI: 94.0-98.3%) and 60.7% (95%CI: 40.6-78.6%) respectively. Low-risk assessments occurred in 31.4% (124/395), which were 90.5% (95%CI: 81.5-96.1%) sensitive for 30-day MACE with a NPV of 94.4% (95%CI: 88.7-97.7%). Moderate-risk assessments occurred in 61.5% (243/395), of which 20.6% had 30-day MACE. The PMHP is able to identify high-risk and low-risk groups with high specificity and negative predictive value for 30-day MACE.

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Equal clinical performance of a novel point-of-care cardiac troponin I (cTnI) assay with a commonly used high-sensitivity cTnI assay

Abstract: The Minicare cTnI POC assay may become useful for prompt and safe ruling-out of AMI in ED patients with suspected AMI using a guideline supported 0/3h sampling protocol.

Cited by 26 publications

References 16 publications

<p>Ginkgolide B ameliorates myocardial ischemia reperfusion injury in rats via inhibiting endoplasmic reticulum stress</p>

<p>Ginkgolide B ameliorates myocardial ischemia reperfusion injury in rats via inhibiting endoplasmic reticulum stress</p>

Hyperbaric oxygen protects against myocardial reperfusion injury via the inhibition of inflammation and the modulation of autophagy

Prehospital use of a modified HEART Pathway and point-of-care troponin to predict cardiovascular events

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