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  1. THE ROLE OF BIOMARKER MACROPHAGE MIGRATION INHIBITORY FACTOR IN CARDIAC REMODELING PREDICTION IN PATIENTS WITH ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
    Vyshnevska IR, Storozhenko T, Kopytsya MP, Bila NV, Kis A, Kaaki M
    Wiad Lek, 2023;76(5 pt 1):911-919.
    PMID: 37326070 DOI: 10.36740/WLek202305104
    OBJECTIVE: The aim: To estimate the role of macrophage migration inhibitory factor and soluble ST2 in predicting the left ventricle remodeling six months after ST-segment elevation myocardial infarction.

    PATIENTS AND METHODS: Materials and methods: The study involved 134 ST-segment elevation myocardial infarction patients. Occurrence of post-percutaneous coronary (PCI) intervention epicardial blood flow of TIMI <3 or myocardial blush grade 0-1 along with ST resolution <70% within 2 hours after PCI was qualified as the no-reflow condition. Left ventricle remodeling was defined after 6-months as an increase in left ventricle end-diastolic volume and/or end-systolic volume by more than 10%.

    RESULTS: Results: A logistic regression formula was evaluated. Included biomarkers were macrophage migration inhibitory factor and sST2, left ventricle ejection fraction: Y=exp(-39.06+0.82EF+0.096ST2+0.0028MIF) / (1+exp(-39.06+0.82EF+0.096ST2+0.0028MIF)). The estimated range is from 0 to 1 point. Less than 0.5 determines an adverse outcome, and more than 0.5 is a good prognosis. This equation, with sensitivity of 77 % and specificity of 85%, could predict the development of adverse left ventricle remodeling six months after a coronary event (AUC=0.864, CI 0.673 to 0.966, p<0.05).

    CONCLUSION: Conclusions: A combination of biomarkers gives a significant predicting result in the formation of adverse left ventricular remodeling after ST-segment elevation myocardial infarction.

    Matched MeSH terms: Ventricular Remodeling/physiology
  2. The clinical benefit of cardiac resynchronization therapy for narrow QRS compared to broad QRS complex patients
    Yap LB, Qadir F, Nguyen ST, Ma SK, Koh KW, Muhammad Z, et al.
    Int J Cardiol, 2015 Mar 15;183:178-9.
    PMID: 25666128 DOI: 10.1016/j.ijcard.2015.01.042
    Matched MeSH terms: Ventricular Remodeling/physiology
  3. Fulltext Modulation of P2Y6R expression exacerbates pressure overload-induced cardiac remodeling in mice
    Shimoda K, Nishimura A, Sunggip C, Ito T, Nishiyama K, Kato Y, et al.
    Sci Rep, 2020 08 18;10(1):13926.
    PMID: 32811872 DOI: 10.1038/s41598-020-70956-5
    Cardiac tissue remodeling caused by hemodynamic overload is a major clinical outcome of heart failure. Uridine-responsive purinergic P2Y6 receptor (P2Y6R) contributes to the progression of cardiovascular remodeling in rodents, but it is not known whether inhibition of P2Y6R prevents or promotes heart failure. We demonstrate that inhibition of P2Y6R promotes pressure overload-induced sudden death and heart failure in mice. In neonatal cardiomyocytes, knockdown of P2Y6R significantly attenuated hypertrophic growth and cell death caused by hypotonic stimulation, indicating the involvement of P2Y6R in mechanical stress-induced myocardial dysfunction. Unexpectedly, compared with wild-type mice, deletion of P2Y6R promoted pressure overload-induced sudden death, as well as cardiac remodeling and dysfunction. Mice with cardiomyocyte-specific overexpression of P2Y6R also exhibited cardiac dysfunction and severe fibrosis. In contrast, P2Y6R deletion had little impact on oxidative stress-mediated cardiac dysfunction induced by doxorubicin treatment. These findings provide overwhelming evidence that systemic inhibition of P2Y6R exacerbates pressure overload-induced heart failure in mice, although P2Y6R in cardiomyocytes contributes to the progression of cardiac fibrosis.
    Matched MeSH terms: Ventricular Remodeling/physiology
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