TY - JOUR
T1 - Association between statin treatment and LDL-cholesterol levels on the rate of ST-elevation myocardial infarction among patients with acute coronary syndromes
T2 - ACS Israeli Survey (ACSIS) 2002-2010
AU - Gottlieb, Shmuel
AU - Kolker, Shimon
AU - Shlomo, Nir
AU - Matetzky, Shlomi
AU - Leitersdorf, Eran
AU - Segev, Amit
AU - Goldenberg, Ilan
AU - Tzivoni, Dan
AU - Weisz, Giora
AU - Moriel, Mady
N1 - Publisher Copyright:
© 2016 Elsevier Ireland Ltd. All rights reserved.
PY - 2016/5/1
Y1 - 2016/5/1
N2 - Background STEMI is thought to occur as a result of a vulnerable coronary plaque rupture. Statins possess hypolipidemic and pleotropic effects that stabilize coronary plaque. We sought to determine the association between LDL-C levels, statin use prior to the index event on the type of acute coronary syndrome (ACS) presentation: STEMI vs. non-STEMI/unstable angina. Methods Data was drawn from the ACS Israeli Survey (ACSIS), a biennial prospective survey of ACS patients hospitalized in all CCU/Cardiology departments during 2002-2010. Results Among 6790 patients, 2760 (41%) reported statin use prior to the index ACS event. The proportion of STEMI was significantly lower among statin treated vs. statin naive patients (36% vs. 57%, p < 0.0001). At each LDL-C level, the proportion of STEMI was significantly lower only among statin treated patients (p < 0.0001). LDL-C < 70 mg/dL was associated with a lower proportion of STEMI only among statin treated but not among statin naive patients (33% vs. 57%, p < 0.0001). Multivariate analysis revealed that statin use was independently associated with a lower probability of presenting with STEMI (ORadj = 0.73, p = 0.007), but not LDL-C < 70 mg/dL (ORadj = 1.13, p = 0.32). Patients on high-intensity statin therapy (HIST) were less likely to present with STEMI as compared with low-intensity statin therapy (LIST) or statin naive patients (27%, 38%, 56%, respectively, p for trend < 0.0001; HIST ORadj = 0.28, p = 0.01; LIST ORadj = 0.48, p = 0.026). Conclusions Among patients admitted with ACS, statin use but not LDL-C level, was associated with a lower probability of presenting with STEMI. Patients on HIST had the lowest likelihood of presenting with STEMI.
AB - Background STEMI is thought to occur as a result of a vulnerable coronary plaque rupture. Statins possess hypolipidemic and pleotropic effects that stabilize coronary plaque. We sought to determine the association between LDL-C levels, statin use prior to the index event on the type of acute coronary syndrome (ACS) presentation: STEMI vs. non-STEMI/unstable angina. Methods Data was drawn from the ACS Israeli Survey (ACSIS), a biennial prospective survey of ACS patients hospitalized in all CCU/Cardiology departments during 2002-2010. Results Among 6790 patients, 2760 (41%) reported statin use prior to the index ACS event. The proportion of STEMI was significantly lower among statin treated vs. statin naive patients (36% vs. 57%, p < 0.0001). At each LDL-C level, the proportion of STEMI was significantly lower only among statin treated patients (p < 0.0001). LDL-C < 70 mg/dL was associated with a lower proportion of STEMI only among statin treated but not among statin naive patients (33% vs. 57%, p < 0.0001). Multivariate analysis revealed that statin use was independently associated with a lower probability of presenting with STEMI (ORadj = 0.73, p = 0.007), but not LDL-C < 70 mg/dL (ORadj = 1.13, p = 0.32). Patients on high-intensity statin therapy (HIST) were less likely to present with STEMI as compared with low-intensity statin therapy (LIST) or statin naive patients (27%, 38%, 56%, respectively, p for trend < 0.0001; HIST ORadj = 0.28, p = 0.01; LIST ORadj = 0.48, p = 0.026). Conclusions Among patients admitted with ACS, statin use but not LDL-C level, was associated with a lower probability of presenting with STEMI. Patients on HIST had the lowest likelihood of presenting with STEMI.
KW - Acute coronary syndrome
KW - LDL-C
KW - ST-elevation myocardial infarction
KW - Statins
UR - http://www.scopus.com/inward/record.url?scp=84964655321&partnerID=8YFLogxK
U2 - 10.1016/j.ijcard.2016.02.088
DO - 10.1016/j.ijcard.2016.02.088
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
AN - SCOPUS:84964655321
SN - 0167-5273
VL - 210
SP - 133
EP - 138
JO - International Journal of Cardiology
JF - International Journal of Cardiology
ER -