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Relation of Low‐Density Lipoprotein Cholesterol With Microvascular Injury and Clinical Outcome in Revascularized ST‐Elevation Myocardial Infarction

BACKGROUND: Microvascular injury (MVI) after primary percutaneous coronary intervention for ST‐elevation myocardial infarction (STEMI) is a major determinant of adverse clinical outcome. Experimental data indicate an impact of hypercholesterolemia on MVI; however, there is a lack of clinical studies...

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Detalles Bibliográficos
Autores principales: Reindl, Martin, Reinstadler, Sebastian Johannes, Feistritzer, Hans‐Josef, Theurl, Markus, Basic, Daniel, Eigler, Christopher, Holzknecht, Magdalena, Mair, Johannes, Mayr, Agnes, Klug, Gert, Metzler, Bernhard
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5721881/
https://www.ncbi.nlm.nih.gov/pubmed/29018020
http://dx.doi.org/10.1161/JAHA.117.006957
Descripción
Sumario:BACKGROUND: Microvascular injury (MVI) after primary percutaneous coronary intervention for ST‐elevation myocardial infarction (STEMI) is a major determinant of adverse clinical outcome. Experimental data indicate an impact of hypercholesterolemia on MVI; however, there is a lack of clinical studies confirming this relation. We aimed to investigate the association of cholesterol concentrations on admission with MVI visualized by cardiac magnetic resonance imaging and clinical outcome in STEMI patients treated by primary percutaneous coronary intervention. METHODS AND RESULTS: In this prospective, observational study, we included 235 consecutive revascularized STEMI patients. Cholesterol (total cholesterol, low‐density lipoprotein [LDL], and high‐density lipoprotein cholesterol) and triglyceride concentrations were determined at presentation. Cardiac magnetic resonance scans were performed 2 (2–4) days after infarction to assess infarct characteristics, including MVI. Clinical end point was the occurrence of major adverse cardiac events (MACE) comprising all‐cause mortality, nonfatal reinfarction, and new congestive heart failure. Patients with MVI (n=129; 55%) showed higher levels of total cholesterol (204 [172–226] versus 185 [168–212] mg/dL; P=0.01) and LDL cholesterol (142 [113–166] versus 118 [103–149] mg/dL; P=0.001), whereas high‐density lipoprotein cholesterol and triglycerides did not differ significantly. In multivariable analysis, including all significant clinical and cardiac magnetic resonance determinants of MVI, LDL concentration emerged as an independent predictor of MVI (odds ratio, 1.02 [95% confidence interval, 1.01–1.02]; P=0.002). Furthermore, increased LDL cholesterol (>150 mg/dL) significantly predicted the occurrence of major adverse cardiac events (hazard ratio, 3.09 [95% confidence interval, 1.22–7.87]; P=0.01). CONCLUSIONS: In STEMI patients undergoing primary percutaneous coronary intervention, baseline LDL cholesterol concentrations were independently associated with MVI, revealing a clinically relevant link between LDL metabolism and MVI in acute STEMI.