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Acute cardioprotective effects of erythropoietin in infant rabbits are mediated by activation of protein kinases and potassium channels.

Basic research in cardiology

[No authors listed]
PMID: 27519302
Basic Res Cardiol. 2004 May;99(3):239. doi: 10.1007/s00395-004-0464-9.

No abstract available.

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Acute cardioprotective effects of erythropoietin in infant rabbits are mediated by activation of protein kinases and potassium channels. Basic Res Cardiol. 2004;99(3):239doi: 10.1007/s00395-004-0464-9.
(2004). Acute cardioprotective effects of erythropoietin in infant rabbits are mediated by activation of protein kinases and potassium channels. Basic research in cardiology, 99(3), 239. https://doi.org/10.1007/s00395-004-0464-9
"Acute cardioprotective effects of erythropoietin in infant rabbits are mediated by activation of protein kinases and potassium channels." Basic research in cardiology vol. 99,3 (2004): 239. doi: https://doi.org/10.1007/s00395-004-0464-9
Acute cardioprotective effects of erythropoietin in infant rabbits are mediated by activation of protein kinases and potassium channels. Basic Res Cardiol. 2004 May;99(3):239. doi: 10.1007/s00395-004-0464-9. PMID: 27519302.
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Erratum to: Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation.

Basic research in cardiology

Meyer-Roxlau S, Lämmle S, Opitz A, Künzel S, Joos JP, Neef S, Sekeres K, Sossalla S, Schöndube F, Alexiou K, Maier LS, Dobrev D, Guan K, Weber S, El-Armouche A.
PMID: 28688054
Basic Res Cardiol. 2017 Sep;112(5):51. doi: 10.1007/s00395-017-0638-x.

No abstract available.

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Meyer-Roxlau S, Lämmle S, Opitz A, et al. Erratum to: Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation. Basic Res Cardiol. 2017;112(5):51doi: 10.1007/s00395-017-0638-x.
Meyer-Roxlau, S., Lämmle, S., Opitz, A., Künzel, S., Joos, J. P., Neef, S., Sekeres, K., Sossalla, S., Schöndube, F., Alexiou, K., Maier, L. S., Dobrev, D., Guan, K., Weber, S., & El-Armouche, A. (2017). Erratum to: Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation. Basic research in cardiology, 112(5), 51. https://doi.org/10.1007/s00395-017-0638-x
Meyer-Roxlau, Stefanie, et al. "Erratum to: Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation." Basic research in cardiology vol. 112,5 (2017): 51. doi: https://doi.org/10.1007/s00395-017-0638-x
Meyer-Roxlau S, Lämmle S, Opitz A, Künzel S, Joos JP, Neef S, Sekeres K, Sossalla S, Schöndube F, Alexiou K, Maier LS, Dobrev D, Guan K, Weber S, El-Armouche A. Erratum to: Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation. Basic Res Cardiol. 2017 Sep;112(5):51. doi: 10.1007/s00395-017-0638-x. PMID: 28688054.
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Erratum to: High field magnetic resonance imaging of rodents in cardiovascular research.

Basic research in cardiology

Vanhoutte L, Gerber BL, Gallez B, Po C, Magat J, Balligand JL, Feron O, Moniotte S.
PMID: 27492500
Basic Res Cardiol. 2016 Sep;111(5):55. doi: 10.1007/s00395-016-0572-3.

No abstract available.

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Vanhoutte L, Gerber BL, Gallez B, et al. Erratum to: High field magnetic resonance imaging of rodents in cardiovascular research. Basic Res Cardiol. 2016;111(5):55doi: 10.1007/s00395-016-0572-3.
Vanhoutte, L., Gerber, B. L., Gallez, B., Po, C., Magat, J., Balligand, J. L., Feron, O., & Moniotte, S. (2016). Erratum to: High field magnetic resonance imaging of rodents in cardiovascular research. Basic research in cardiology, 111(5), 55. https://doi.org/10.1007/s00395-016-0572-3
Vanhoutte, Laetitia, et al. "Erratum to: High field magnetic resonance imaging of rodents in cardiovascular research." Basic research in cardiology vol. 111,5 (2016): 55. doi: https://doi.org/10.1007/s00395-016-0572-3
Vanhoutte L, Gerber BL, Gallez B, Po C, Magat J, Balligand JL, Feron O, Moniotte S. Erratum to: High field magnetic resonance imaging of rodents in cardiovascular research. Basic Res Cardiol. 2016 Sep;111(5):55. doi: 10.1007/s00395-016-0572-3. PMID: 27492500.
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4-hydroxytamoxifen does not deteriorate cardiac function in cardiomyocyte-specific MerCreMer transgenic mice.

Basic research in cardiology

Heinen A, Gödecke S, Flögel U, Miklos D, Bottermann K, Spychala A, Gödecke A.
PMID: 33544211
Basic Res Cardiol. 2021 Feb 05;116(1):8. doi: 10.1007/s00395-020-00841-9.

Conditional, cell-type-specific transgenic mouse lines are of high value in cardiovascular research. A standard tool for cardiomyocyte-restricted DNA editing is the αMHC-MerCreMer/loxP system. However, there is an ongoing debate on the occurrence of cardiac side effects caused by unspecific...

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Heinen A, Gödecke S, Flögel U, et al. 4-hydroxytamoxifen does not deteriorate cardiac function in cardiomyocyte-specific MerCreMer transgenic mice. Basic Res Cardiol. 2021;116(1):8doi: 10.1007/s00395-020-00841-9.
Heinen, A., Gödecke, S., Flögel, U., Miklos, D., Bottermann, K., Spychala, A., & Gödecke, A. (2021). 4-hydroxytamoxifen does not deteriorate cardiac function in cardiomyocyte-specific MerCreMer transgenic mice. Basic research in cardiology, 116(1), 8. https://doi.org/10.1007/s00395-020-00841-9
Heinen, Andre, et al. "4-hydroxytamoxifen does not deteriorate cardiac function in cardiomyocyte-specific MerCreMer transgenic mice." Basic research in cardiology vol. 116,1 (2021): 8. doi: https://doi.org/10.1007/s00395-020-00841-9
Heinen A, Gödecke S, Flögel U, Miklos D, Bottermann K, Spychala A, Gödecke A. 4-hydroxytamoxifen does not deteriorate cardiac function in cardiomyocyte-specific MerCreMer transgenic mice. Basic Res Cardiol. 2021 Feb 05;116(1):8. doi: 10.1007/s00395-020-00841-9. PMID: 33544211; PMCID: PMC7864833.
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Regulatory B cells improve ventricular remodeling after myocardial infarction by modulating monocyte migration.

Basic research in cardiology

Jiao J, He S, Wang Y, Lu Y, Gu M, Li D, Tang T, Nie S, Zhang M, Lv B, Li J, Xia N, Cheng X.
PMID: 34302556
Basic Res Cardiol. 2021 Jul 24;116(1):46. doi: 10.1007/s00395-021-00886-4.

Overactivated inflammatory responses contribute to adverse ventricular remodeling after myocardial infarction (MI). Regulatory B cells (Bregs) are a newly discovered subset of B cells with immunomodulatory roles in many immune and inflammation-related diseases. Our study aims to determine whether...

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Jiao J, He S, Wang Y, et al. Regulatory B cells improve ventricular remodeling after myocardial infarction by modulating monocyte migration. Basic Res Cardiol. 2021;116(1):46doi: 10.1007/s00395-021-00886-4.
Jiao, J., He, S., Wang, Y., Lu, Y., Gu, M., Li, D., Tang, T., Nie, S., Zhang, M., Lv, B., Li, J., Xia, N., & Cheng, X. (2021). Regulatory B cells improve ventricular remodeling after myocardial infarction by modulating monocyte migration. Basic research in cardiology, 116(1), 46. https://doi.org/10.1007/s00395-021-00886-4
Jiao, Jiao, et al. "Regulatory B cells improve ventricular remodeling after myocardial infarction by modulating monocyte migration." Basic research in cardiology vol. 116,1 (2021): 46. doi: https://doi.org/10.1007/s00395-021-00886-4
Jiao J, He S, Wang Y, Lu Y, Gu M, Li D, Tang T, Nie S, Zhang M, Lv B, Li J, Xia N, Cheng X. Regulatory B cells improve ventricular remodeling after myocardial infarction by modulating monocyte migration. Basic Res Cardiol. 2021 Jul 24;116(1):46. doi: 10.1007/s00395-021-00886-4. PMID: 34302556; PMCID: PMC8310480.
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Connexin 43 phosphorylation by casein kinase 1 is essential for the cardioprotection by ischemic preconditioning.

Basic research in cardiology

Hirschhäuser C, Lissoni A, Görge PM, Lampe PD, Heger J, Schlüter KD, Leybaert L, Schulz R, Boengler K.
PMID: 33751227
Basic Res Cardiol. 2021 Mar 22;116(1):21. doi: 10.1007/s00395-021-00861-z.

Myocardial connexin 43 (Cx43) forms gap junctions and hemichannels, and is also present within subsarcolemmal mitochondria. The protein is phosphorylated by several kinases including mitogen-activated protein kinase (MAPK), protein kinase C (PKC), and casein kinase 1 (CK1). A reduction...

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Hirschhäuser C, Lissoni A, Görge PM, et al. Connexin 43 phosphorylation by casein kinase 1 is essential for the cardioprotection by ischemic preconditioning. Basic Res Cardiol. 2021;116(1):21doi: 10.1007/s00395-021-00861-z.
Hirschhäuser, C., Lissoni, A., Görge, P. M., Lampe, P. D., Heger, J., Schlüter, K. D., Leybaert, L., Schulz, R., & Boengler, K. (2021). Connexin 43 phosphorylation by casein kinase 1 is essential for the cardioprotection by ischemic preconditioning. Basic research in cardiology, 116(1), 21. https://doi.org/10.1007/s00395-021-00861-z
Hirschhäuser, Christine, et al. "Connexin 43 phosphorylation by casein kinase 1 is essential for the cardioprotection by ischemic preconditioning." Basic research in cardiology vol. 116,1 (2021): 21. doi: https://doi.org/10.1007/s00395-021-00861-z
Hirschhäuser C, Lissoni A, Görge PM, Lampe PD, Heger J, Schlüter KD, Leybaert L, Schulz R, Boengler K. Connexin 43 phosphorylation by casein kinase 1 is essential for the cardioprotection by ischemic preconditioning. Basic Res Cardiol. 2021 Mar 22;116(1):21. doi: 10.1007/s00395-021-00861-z. PMID: 33751227; PMCID: PMC7985055.
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Atg5 knockdown induces age-dependent cardiomyopathy which can be rescued by repeated remote ischemic conditioning.

Basic research in cardiology

Wang F, He Q, Gao Z, Redington AN.
PMID: 34319513
Basic Res Cardiol. 2021 Jul 28;116(1):47. doi: 10.1007/s00395-021-00888-2.

Altered autophagy is implicated in several human cardiovascular diseases. Remote ischemic conditioning (RIC) is cardioprotective in multiple cardiovascular injury models and modifies autophagy signaling, but its effect in cardiomyopathy induced by gene manipulation has not been reported. To investigate...

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Wang F, He Q, Gao Z, et al. Atg5 knockdown induces age-dependent cardiomyopathy which can be rescued by repeated remote ischemic conditioning. Basic Res Cardiol. 2021;116(1):47doi: 10.1007/s00395-021-00888-2.
Wang, F., He, Q., Gao, Z., & Redington, A. N. (2021). Atg5 knockdown induces age-dependent cardiomyopathy which can be rescued by repeated remote ischemic conditioning. Basic research in cardiology, 116(1), 47. https://doi.org/10.1007/s00395-021-00888-2
Wang, Fangfei, et al. "Atg5 knockdown induces age-dependent cardiomyopathy which can be rescued by repeated remote ischemic conditioning." Basic research in cardiology vol. 116,1 (2021): 47. doi: https://doi.org/10.1007/s00395-021-00888-2
Wang F, He Q, Gao Z, Redington AN. Atg5 knockdown induces age-dependent cardiomyopathy which can be rescued by repeated remote ischemic conditioning. Basic Res Cardiol. 2021 Jul 28;116(1):47. doi: 10.1007/s00395-021-00888-2. PMID: 34319513; PMCID: PMC8316897.
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Mechanism of the switch from NO to H.

Basic research in cardiology

Juguilon C, Wang Z, Wang Y, Enrick M, Jamaiyar A, Xu Y, Gadd J, Chen CW, Pu A, Kolz C, Ohanyan V, Chen YR, Hardwick J, Zhang Y, Chilian WM, Yin L.
PMID: 35024970
Basic Res Cardiol. 2022 Jan 13;117(1):2. doi: 10.1007/s00395-022-00910-1.

Coronary microvascular dysfunction is prevalent among people with diabetes and is correlated with cardiac mortality. Compromised endothelial-dependent dilation (EDD) is an early event in the progression of diabetes, but its mechanisms remain incompletely understood. Nitric oxide (NO) is the...

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Juguilon C, Wang Z, Wang Y, et al. Mechanism of the switch from NO to H. Basic Res Cardiol. 2022;117(1):2doi: 10.1007/s00395-022-00910-1.
Juguilon, C., Wang, Z., Wang, Y., Enrick, M., Jamaiyar, A., Xu, Y., Gadd, J., Chen, C. W., Pu, A., Kolz, C., Ohanyan, V., Chen, Y. R., Hardwick, J., Zhang, Y., Chilian, W. M., & Yin, L. (2022). Mechanism of the switch from NO to H. Basic research in cardiology, 117(1), 2. https://doi.org/10.1007/s00395-022-00910-1
Juguilon, Cody, et al. "Mechanism of the switch from NO to H." Basic research in cardiology vol. 117,1 (2022): 2. doi: https://doi.org/10.1007/s00395-022-00910-1
Juguilon C, Wang Z, Wang Y, Enrick M, Jamaiyar A, Xu Y, Gadd J, Chen CW, Pu A, Kolz C, Ohanyan V, Chen YR, Hardwick J, Zhang Y, Chilian WM, Yin L. Mechanism of the switch from NO to H. Basic Res Cardiol. 2022 Jan 13;117(1):2. doi: 10.1007/s00395-022-00910-1. PMID: 35024970.
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Mitochondrial nucleoid in cardiac homeostasis: bidirectional signaling of mitochondria and nucleus in cardiac diseases.

Basic research in cardiology

Feng Y, Huang W, Paul C, Liu X, Sadayappan S, Wang Y, Pauklin S.
PMID: 34392401
Basic Res Cardiol. 2021 Aug 14;116(1):49. doi: 10.1007/s00395-021-00889-1.

Metabolic function and energy production in eukaryotic cells are regulated by mitochondria, which have been recognized as the intracellular 'powerhouses' of eukaryotic cells for their regulation of cellular homeostasis. Mitochondrial function is important not only in normal developmental and...

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Feng Y, Huang W, Paul C, et al. Mitochondrial nucleoid in cardiac homeostasis: bidirectional signaling of mitochondria and nucleus in cardiac diseases. Basic Res Cardiol. 2021;116(1):49doi: 10.1007/s00395-021-00889-1.
Feng, Y., Huang, W., Paul, C., Liu, X., Sadayappan, S., Wang, Y., & Pauklin, S. (2021). Mitochondrial nucleoid in cardiac homeostasis: bidirectional signaling of mitochondria and nucleus in cardiac diseases. Basic research in cardiology, 116(1), 49. https://doi.org/10.1007/s00395-021-00889-1
Feng, Yuliang, et al. "Mitochondrial nucleoid in cardiac homeostasis: bidirectional signaling of mitochondria and nucleus in cardiac diseases." Basic research in cardiology vol. 116,1 (2021): 49. doi: https://doi.org/10.1007/s00395-021-00889-1
Feng Y, Huang W, Paul C, Liu X, Sadayappan S, Wang Y, Pauklin S. Mitochondrial nucleoid in cardiac homeostasis: bidirectional signaling of mitochondria and nucleus in cardiac diseases. Basic Res Cardiol. 2021 Aug 14;116(1):49. doi: 10.1007/s00395-021-00889-1. PMID: 34392401; PMCID: PMC8364536.
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Epigenetic regulation of cardiac electrophysiology in atrial fibrillation: HDAC2 determines action potential duration and suppresses NRSF in cardiomyocytes.

Basic research in cardiology

Lugenbiel P, Govorov K, Syren P, Rahm AK, Wieder T, Wunsch M, Weiberg N, Manolova E, Gramlich D, Rivinius R, Finke D, Lehmann LH, Schweizer PA, Frank D, El Tahry FA, Bruehl C, Heimberger T, Sandke S, Weis T, Most P, Schmack B, Ruhparwar A, Karck M, Frey N, Katus HA, Thomas D.
PMID: 33630168
Basic Res Cardiol. 2021 Feb 25;116(1):13. doi: 10.1007/s00395-021-00855-x.

Atrial fibrillation (AF) is associated with electrical remodeling, leading to cellular electrophysiological dysfunction and arrhythmia perpetuation. Emerging evidence suggests a key role for epigenetic mechanisms in the regulation of ion channel expression. Histone deacetylases (HDACs) control gene expression through...

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Lugenbiel P, Govorov K, Syren P, et al. Epigenetic regulation of cardiac electrophysiology in atrial fibrillation: HDAC2 determines action potential duration and suppresses NRSF in cardiomyocytes. Basic Res Cardiol. 2021;116(1):13doi: 10.1007/s00395-021-00855-x.
Lugenbiel, P., Govorov, K., Syren, P., Rahm, A. K., Wieder, T., Wunsch, M., Weiberg, N., Manolova, E., Gramlich, D., Rivinius, R., Finke, D., Lehmann, L. H., Schweizer, P. A., Frank, D., El Tahry, F. A., Bruehl, C., Heimberger, T., Sandke, S., Weis, T., Most, P., Schmack, B., Ruhparwar, A., Karck, M., Frey, N., Katus, H. A., & Thomas, D. (2021). Epigenetic regulation of cardiac electrophysiology in atrial fibrillation: HDAC2 determines action potential duration and suppresses NRSF in cardiomyocytes. Basic research in cardiology, 116(1), 13. https://doi.org/10.1007/s00395-021-00855-x
Lugenbiel, Patrick, et al. "Epigenetic regulation of cardiac electrophysiology in atrial fibrillation: HDAC2 determines action potential duration and suppresses NRSF in cardiomyocytes." Basic research in cardiology vol. 116,1 (2021): 13. doi: https://doi.org/10.1007/s00395-021-00855-x
Lugenbiel P, Govorov K, Syren P, Rahm AK, Wieder T, Wunsch M, Weiberg N, Manolova E, Gramlich D, Rivinius R, Finke D, Lehmann LH, Schweizer PA, Frank D, El Tahry FA, Bruehl C, Heimberger T, Sandke S, Weis T, Most P, Schmack B, Ruhparwar A, Karck M, Frey N, Katus HA, Thomas D. Epigenetic regulation of cardiac electrophysiology in atrial fibrillation: HDAC2 determines action potential duration and suppresses NRSF in cardiomyocytes. Basic Res Cardiol. 2021 Feb 25;116(1):13. doi: 10.1007/s00395-021-00855-x. PMID: 33630168.
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Thiol-based redox-active proteins as cardioprotective therapeutic agents in cardiovascular diseases.

Basic research in cardiology

Andreadou I, Efentakis P, Frenis K, Daiber A, Schulz R.
PMID: 34275052
Basic Res Cardiol. 2021 Jul 17;116(1):44. doi: 10.1007/s00395-021-00885-5.

Thiol-based redox compounds, namely thioredoxins (Trxs), glutaredoxins (Grxs) and peroxiredoxins (Prxs), stand as a pivotal group of proteins involved in antioxidant processes and redox signaling. Glutaredoxins (Grxs) are considered as one of the major families of proteins involved in...

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Andreadou I, Efentakis P, Frenis K, et al. Thiol-based redox-active proteins as cardioprotective therapeutic agents in cardiovascular diseases. Basic Res Cardiol. 2021;116(1):44doi: 10.1007/s00395-021-00885-5.
Andreadou, I., Efentakis, P., Frenis, K., Daiber, A., & Schulz, R. (2021). Thiol-based redox-active proteins as cardioprotective therapeutic agents in cardiovascular diseases. Basic research in cardiology, 116(1), 44. https://doi.org/10.1007/s00395-021-00885-5
Andreadou, Ioanna, et al. "Thiol-based redox-active proteins as cardioprotective therapeutic agents in cardiovascular diseases." Basic research in cardiology vol. 116,1 (2021): 44. doi: https://doi.org/10.1007/s00395-021-00885-5
Andreadou I, Efentakis P, Frenis K, Daiber A, Schulz R. Thiol-based redox-active proteins as cardioprotective therapeutic agents in cardiovascular diseases. Basic Res Cardiol. 2021 Jul 17;116(1):44. doi: 10.1007/s00395-021-00885-5. PMID: 34275052.
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Intravenous metoprolol during ongoing STEMI ameliorates markers of ischemic injury: a METOCARD-CNIC trial electrocardiographic study.

Basic research in cardiology

Díaz-Munoz R, Valle-Caballero MJ, Sanchez-Gonzalez J, Pizarro G, García-Rubira JC, Escalera N, Fuster V, Fernández-Jiménez R, Ibanez B.
PMID: 34279726
Basic Res Cardiol. 2021 Jul 19;116(1):45. doi: 10.1007/s00395-021-00884-6.

Besides its protective effect against neutrophil-mediated injury at reperfusion, intravenous (IV) metoprolol was recently shown to reduce the progression of ischemic injury in a pig model of ST-segment elevation myocardial infarction (STEMI). Here, we tested the hypothesis that IV...

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Díaz-Munoz R, Valle-Caballero MJ, Sanchez-Gonzalez J, et al. Intravenous metoprolol during ongoing STEMI ameliorates markers of ischemic injury: a METOCARD-CNIC trial electrocardiographic study. Basic Res Cardiol. 2021;116(1):45doi: 10.1007/s00395-021-00884-6.
Díaz-Munoz, R., Valle-Caballero, M. J., Sanchez-Gonzalez, J., Pizarro, G., García-Rubira, J. C., Escalera, N., Fuster, V., Fernández-Jiménez, R., & Ibanez, B. (2021). Intravenous metoprolol during ongoing STEMI ameliorates markers of ischemic injury: a METOCARD-CNIC trial electrocardiographic study. Basic research in cardiology, 116(1), 45. https://doi.org/10.1007/s00395-021-00884-6
Díaz-Munoz, Raquel, et al. "Intravenous metoprolol during ongoing STEMI ameliorates markers of ischemic injury: a METOCARD-CNIC trial electrocardiographic study." Basic research in cardiology vol. 116,1 (2021): 45. doi: https://doi.org/10.1007/s00395-021-00884-6
Díaz-Munoz R, Valle-Caballero MJ, Sanchez-Gonzalez J, Pizarro G, García-Rubira JC, Escalera N, Fuster V, Fernández-Jiménez R, Ibanez B. Intravenous metoprolol during ongoing STEMI ameliorates markers of ischemic injury: a METOCARD-CNIC trial electrocardiographic study. Basic Res Cardiol. 2021 Jul 19;116(1):45. doi: 10.1007/s00395-021-00884-6. PMID: 34279726.
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