Clinical InvestigationPrognostic Value of Serum Tenascin-C Levels on Long-Term Outcome After Acute Myocardial Infarction
Section snippets
Study Population
We initially studied a prospective series of 250 patients with first AMI who underwent primary PCI at Yokosuka Kyosai Hospital from January 2005 to February 2008. Inclusion criteria for the study patients were: 1) chest pain >30 minutes in duration and presenting to hospital within 12 hours after onset of symptoms; 2) ST-segment elevation >0.1 mV in 2 contiguous electrocardiographic leads; 3) total occlusion of the infarct-related artery; 4) elevated creatine kinase–MB (CK-MB) isoenzymes within
Patient Characteristics
The 239 patients included in the study comprised 184 men and 55 women with an overall mean age of 67 ± 11 years. Baseline clinical characteristics of the patients are summarized in Table 1.
Comparison of Clinical Characteristics and LV Parameters Between MACE and Non-MACE Groups
Of the 239 patients, 54 patients (22.6%) suffered MACE during the follow-up period. MACE included 23 (9.2%) cardiac deaths and 31 (13%) episodes of heart failure. Clinical characteristics of the study patients suffering MACE and those without are shown in Table 2. There were no significant differences in sex,
Discussion
The major important findings in this are as follows. First, serum TN-C level measured in patients on day 5 after admission for AMI has a prognostic value similar to that of plasma BNP level, the predictive biomarker of prognosis after AMI. Second, the incorporation of a combination of serum TN-C and plasma BNP levels with the established prognostic markers improved risk stratification for MACE and cardiac death, as evidenced by a substantial increase in the C-statistics and IDI values.
Conclusion
Inclusion of serum TN-C level measured on day 5 after admission for AMI is potentially useful in addition to established prognostic markers for early risk stratification of patients after AMI. Identification of this and other biomarkers will lead to more aggressive follow-up and medical intervention as potential strategies to prevent MACE and cardiac deaths.
Disclosures
None.
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2021, Current Problems in CardiologyCitation Excerpt :However, the added clinical value of CRP testing among AAS patients remains uncertain. Tenascin-C (TN-C) (adhesive glycoprotein, constituent of the extracellular matrix) is thought to play a leading role in cardiovascular tissue remodeling, including coronary atherosclerotic plaque, abdominal aortic aneurysm, acute myocardial infarction, myocarditis and VTE.69-73 In type B-AAD patients, raised TN-C levels have been associated with in-hospital mortality.74
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2019, American Heart JournalCitation Excerpt :However, we should note that c-statistic is considered as a conservative statistic, and this amount of improvement is shown for many novel predictors. For example, even cardiac markers at the time of MI demonstrated similar degree of improvement in c-statistic for secondary outcomes after MI in previous studies.56-58 There are several clinical and pathophysiological implications from our study.
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2019, Experimental GerontologyCitation Excerpt :More recently, our group demonstrated that TNC itself induces MMP-2 and at lower levels MMP-9 expression as well as upregulates the expression of hypertrophic markers such as ANP and BNP in H9c2 cardiomyoblasts (Podesser et al., 2018). Clinical studies demonstrated that high TNC levels in blood are associated with worse cardiac functional outcome after MI (Sato et al., 2006; Sato et al., 2012). Collectively, these results indicate that TNC plays a critical role in post-MI remodeling as well as in the hypertrophy of the non-infarcted myocardium (Imanaka-Yoshida et al., 2001; Nishioka et al., 2010; Tamaoki et al., 2005).
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2016, Advanced Drug Delivery ReviewsCitation Excerpt :This highlights the multifunctional role of TN-C in cardiac remodeling, which involves the recruitment of myofibroblasts, collagen fiber formation, and angiogenesis that promote repair, as well as the creation of a de-adhesive state, upregulation of MMPs, and enhancement of inflammation that contribute to fibrosis [19]. As such, TN-C is a reported biomarker for a number of cardiovascular diseases, including: dilated cardiomyopathy, coronary plaque rupture, heart failure, and acute myocardial infarction [161–166]. For cardiovascular imaging, a labeled TN-C antibody has been used to noninvasively detect remodeling in rats after infarction, and could potentially be used to look for left ventricular remodeling, which can lead to heart failure in humans [167].
Extracellular matrix-mediated cellular communication in the heart
2016, Journal of Molecular and Cellular CardiologyCitation Excerpt :Additionally, ablation of TNC in mice leads to delayed myofibroblast recruitment to the site of injury [162]. Following cardiac insult, TNC is released into the bloodstream, leading to its development as a reliable biomarker that can predict the degree of cardiac remodeling and subsequent mortality in humans [163–166]. The increase in TNC following cardiac injury is exacerbated by the action of several factors released in pathologic cardiac remodeling, such as TGF-β and FGF-2, therefore suggesting a role of this glycoprotein in regulating inflammation and fibrosis.
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