ArticleSisli Etfal Hastanesi tip bulteni2019
Is Cardiac Troponin I Valuable to Detect Low-Level Myocardial Damage in Congestive Heart Failure?
Article in Sisli Etfal Hastanesi tip bulteni, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Oxidative stress signaling in the pathogenesis of diabetic cardiomyopathy and the potential therapeutic role of antioxidant naringenin.Redox report : communications in free radical research · 2023Review
- Development of an Electrochemical Immunosensor for Detection of Cardiac Troponin I at the Point-of-Care.Biosensors · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesCongestive heart failure (CHF) is a heart disease with a growing incidence and prevalence. Creatine kinase-myocardial base (CK-MB) is generally used to determine myocardial damage; however, it is insufficiently sensitive to measure the relatively low level of myocardial damage that typically occurs in heart failure (HF). The use of cardiac troponins, which are far more sensitive and specific, has become common to identify myocardial damage and permits the detection of even minute amounts of damage. The aim of this study was to ascertain whether cardiac troponin I (cTnI) can be used to detect low-level myocardial damage occurring in CHF in real-life conditions.
methodsFifty patients with CHF symptoms (Group I) and 20 patients who were evaluated as normal (Group II) were included in this prospective study. The Framingham criteria were used to diagnose HF. Group I was divided into 3 subgroups according to the New York Heart Association classification of functional capacity: Class II, Group A; Class III, Group B, and Class IV, Group C. On the first day of admission, CK-MB and cTnI levels were measured and assessed quantitatively. The cTnI level was compared between these 3 subgroups and between Groups I and II. Linear regression analysis was performed to investigate the relationship between ejection fraction (EF) and cTnI.
resultsThe mean cTnI value was 0.084±0.07 ng/mL in Group I and 0.018±0.012 ng/mL in Group II (p=0.0001). The mean cTnI value was 0.047±0.016 ng/mL, 0.080±0.048 ng/mL, and 0.175± 0.102 ng/mL in Groups A, B, and C, respectively. The difference between the subgroups of Group I was statistically significant. In addition, it was observed that there was a significant difference in the EF (%) value between Groups I and II and between Groups A, B, and C. Linear regression analysis revealed an inverse relationship between EF and cTnI (r: -0.66) (p=0.0001).
conclusionAs the severity of HF increased, the cTnI serum level also increased. This increase was inversely related to the EF value. These results are consistent with other studies in the literature, suggesting that the cTnI level may be a useful marker in the diagnosis and evaluation of severity of HF.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.