| ObjectiveThere has been proved that proprotein convertase subtilisin/kexin type9(PCSK9)made the level of LDL-C in vivo increase through reducing the number of LDLR,thereby promoting the occurrence of atherosis and cardiovascular events,so PCSK9 plays an important role in the regulation of blood lipids.However,there were few literature reports about the dynamic changes about PCSK9 baseline levels in patients of acute ST-elevation myocardial infarction(STEMI)at hospital admission,at 1 week and 4weeks after atatins therapy.This study is designed to observe the change in the level of PCSK9 and blood lipid of patients with STEMI before statins therapy and at week 1 after statins therapy as well as 4 weeks.Methods167 cases of STEMI patient from the cardiovascular medicine department of Xuzhou Central Hospital who was attacked by the disease within 12 hours had been sequentially selected from 1st,Sep,2015 to 30 th,Jun,2016,and randomly divided into group A,B and C,they were treated with statins of different kinds,among which,59 patients were included into group A,where atorvastatin(20mg/d)was taken;55 patients were included into group B,where rosuvastatin(20mg/d)was taken;53 patients were included into group C,where simvastatin(20mg/d)and ezetimibe(10mg/d)were taken.Meanwhile,50 healthy adults were included as a control group.In STEMI group upon admission,as well as 1 and 4 weeks after statin therapy,and control group serum PCSK9,blood lipid,troponin I and other indices were determined.ResultsPCSK9 level of STEMI group on admission was 36.15±11.60 ng/ml,which is higher than that of control group17.01±8.57 ng/ml(P<0.001)but significantly declined 1 week after statin therapy18.86±1.84ng/ml(P<0.001)which was not significantly different from control group(P=0.108),and that at week 4 of statin therapy was significantly redused with group upon admission25.10±2.96ng/ml(P<0.001),but was much higher than that of 1week after statin therapy(P<0.001)and control group(P<0.001).The LDL-C level of STEMI group on admission was 2.92±0.76 mmol/L which is significantly higher than that of control group 2.48±0.80 mmol/L(P<0.001),which declined one week after statin therapy(2.42±0.65 mmol/L,P<0.001)and was not significantly different from control group(P=0.557);and that in STEMI group 4 weeks after statin therapy was further reduced compared with that of 1 week after statin therapy(2.14±0.39 mmol/L,P<0.001).The PCSK9 level of group A,B and C upon admission was respectively 36.85 ± 9.75ng/ml,35.95 ± 13.00ng/ml and 35.60 ± 12.11ng/ml,all of which wereclearly higher than that of group D(P<0.001).The PCSK9 level of group A,B and C on week 1 after admission was respectively 19.14±1.32 ng/ml,17.55±1.30 ng/ml and 19.92±2.02 ng/ml,all of which were clearly lower than the one upon admission(P<0.001),wherein,the level of group A and B approximated to that of group D(PAD=0.09,PBD=0.66),the level of group C was clearly higher than that of group D(P=0.02).The PCSK9 level of group A,B and C on week 4 after admission was respectively 25.73±1.87 ng/ml,27.31±2.46ng/ml and 22.45±2.04 ng/ml,all of which were lower than the ones upon admission(P<0.001),but higher than the ones on week 1 after admission(P<0.001),and were clearly higher than that of group D(P<0.001).The PCSK9 level of group C on week 4 was clearly lower than that of group A and B(P<0.001),PCSK9 level of group A was clearly lower than that of group B(P<0.001).ConclusionThe PCSK9 level of STEMI patients before and after taking statins has a dynamic change within 4 weeks,which culminates upon admission,and clearly goes down on week 1 after admission to the level of control group,at the time the LDL-C level also goes down clearly;on week 4,the PCSK9 level was still lower than the one upon admission but higher than the one on week 1 after admission;the LDL-C level of patients on week 4 after taking rosuvastatin was lower than that of patients who took atorvastatin,while their PCSK9 level was higher than that of patients who took atorvastatin,indicating that,the patients who took rosuvastatin had a better effect of lowering LDL-C level,but the lowered blood LDL-C concentration might facilitate the in vivo PCSK9 level to go up in a feedback manner,the elevated PCSK9 level re-regulates the plasma LDL-C level in a feedback manner.On week 4,The LDL-C level of patients who took atorvastatin alone was close to that of patients who took a combination of simvastatin with ezetimibe,but the PCSK9 level of patients after taking atorvastatin was clearly higher than that of patients who took a combination of simvastatin with ezetimibe,indicating that,the therapeutic method using statins alone might further accelerate the elevation of PCSK9 level as compared to the therapeutic strategy using a combination of statins with Cholesterol absorption inhibitor,thereby,playing a part in the process of cholesterol escape after statins therapy. |
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