Page 147 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Elevated glucose levels impact microvascular function in STEMI
References
1. Dibra A, Mehilli J, Dirschinger J, et al. Thrombolysis in myocardial infarction myocardial perfusion grade in angiography correlates with myocardial salvage in patients with acute myocardial infarction treated with stenting or thrombolysis. J Am Coll Cardiol. 2003;41:925–9.
2. Tarantini G, Cacciavillani L, Corbetti F, et al. Duration of ischemia is a major determinant of transmurality and severe microvascular obstruction after primary angioplasty: a study performed with contrast-enhanced magnetic resonance. j Am Coll Cardiol. 2005;46:1229–35.
3. Ito H, Okamura A, Iwakura K, et al. Myocardial perfusion patterns related to thrombolysis in myocardial infarction perfusion grades after coronary angioplasty in patients with acute anterior wall myocardial infarction. Circulation. 1996;93:1993–9.
4. Bax M, de Winter RJ, Koch KT, et al. Time course of microvascular resistance of the infarct and noninfarct coronary artery following an anterior wall acute myocardial infarction. Am J Cardiol. 2006;97:1131–6.
5. Schäfer U, Kurz T, Jain D, et al. Impaired coronary flow and left ventricular dysfunction after mechanical recanalization in acute myocardial infarction: role of neurohumoral activation? Basic Res Cardiol. 2002;97:399–408.
6. Rezkalla SH, Kloner RA. Coronary no-reflow phenomenon. Curr Treat Options Cardiovasc Med. 2005;7:75–80.
7. Oliver MF, Opie LH. Effects of glucose and fatty acids on myocardial ischaemia and arrhythmias. Lancet. 1994;343:155–8.
8. Capes SE, Hunt D, Malmberg K, Gerstein HC. Stress hyperglycaemia and increased risk of death after myocardial infarction in patients with and without diabetes: a systematic overview. Lancet. 2000;355:773–8.
9. Vis MM, Sjauw KD, van der Schaaf RJ, et al. In patients with ST-segment elevation myocardial infarction with cardiogenic shock treated with percutaneous coronary intervention, admission glucose level is a strong independent predictor for 1-year mortality in patients without a prior diagnosis of diabetes. Am Heart J. 2007;154:1184–90.
10. Iwakura K, Ito H, Ikushima M, et al. Association between hyperglycemia and the no-reflow phenomenon in patients with acute myocardial infarction. J Am Coll Cardiol. 2003;41:1–7.
11. van de Hoef TP, Bax M, Meuwissen M, et al. Impact of coronary microvascular function on long-
term cardiac mortality in patients with acute ST-segment-elevation myocardial infarction. Circ 8 Cardiovasc Interv. 2013;6:207–15.
12. de Bruyne B, Bartunek J, Sys SU, et al. Simultaneous coronary pressure and flow velocity measurements in humans. Feasibility, reproducibility, and hemodynamic dependence of coronary flow velocity reserve, hyperemic flow versus pressure slope index, and fractional flow reserve. Circulation. 1996;94:1842–9.
13. Wieneke H, Haude M, Ge J, et al. Corrected coronary flow velocity reserve: a new concept for assessing coronary perfusion. J Am Coll Cardiol. 2000;35:1713–20.
14. van de Hoef TP, Nolte F, EchavarrÍa-Pinto M, et al. Impact of hyperaemic microvascular resistance on fractional flow reserve measurements in patients with stable coronary artery disease: insights from combined stenosis and microvascular resistance assessment. Heart. 2014;100:951–9.
15. Fearon WF, Shah M, Ng M, et al. Predictive value of the index of microcirculatory resistance in patients with ST-segment elevation myocardial infarction. J Am Coll Cardiol. 2008;51:560–5.
16. Díaz R, Paolasso EA, Piegas LS, et al. Metabolic modulation of acute myocardial infarction. The ECLA (Estudios Cardiológicos Latinoamérica) Collaborative Group. Circulation. 1998;98:2227–34.
17. de Alvaro C, Teruel T, Hernandez R, et al. Tumor necrosis factor alpha produces insulin resistance in skeletal muscle by activation of inhibitor kappaB kinase in a p38 MAPK-dependent manner. J Biol Chem. 2004;279:17070–8.
18. Kim J, Yeh DC, Ver M, et al. Phosphorylation of Ser24 in the pleckstrin homology domain of insulin receptor substrate-1 by Mouse Pelle-like kinase/interleukin-1 receptor-associated kinase: cross- talk between inflammatory signaling and insulin signaling that may contribute to insulin. J Biol Chem. 2005;280:23173–83.
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