Association between P2Y1 and P2Y12 polymorphisms and acute myocardial infarction and ADP-induced platelet aggregation

The objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI) in the Quanzhou population and to determine associations between P2Y1 and P2Y12 genotypes and ADP-induced platelet aggregation in this population. All su...

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Published inBMC cardiovascular disorders Vol. 23; no. 1; pp. 41 - 8
Main Authors Su, Chunyan, Zhang, Zhishan, Chen, Jintu, Tian, Mengcha, Wu, Conglian, Zhang, Tao
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 21.01.2023
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ISSN1471-2261
1471-2261
DOI10.1186/s12872-023-03075-4

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Abstract The objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI) in the Quanzhou population and to determine associations between P2Y1 and P2Y12 genotypes and ADP-induced platelet aggregation in this population. All subjects were screened for P2Y1 (c.1622A > G) and P2Y12 (H1/H2, c.34C > T) polymorphisms by direct DNA sequencing. The maximal platelet aggregation rate (MAR) in AMI patients (n = 61) and healthy control subjects (n = 50) was measured by a PL-12 platelet function analyzer, and adenosine diphosphate (ADP) (5 μmol/L) was used as an agonist. The haploid H2 allele in the P2Y12 gene was more frequent in patients with AMI than in control subjects (OR 1.887, P = 0.005). The P2Y12 H2 haplotype was significantly associated with AMI in the codominant (P = 0.008), dominant (OR 2.103, P = 0.003), and overdominant models (OR 2.133, P = 0.003). After adjusting for potential confounders, H2 haplotype carriers had a 2.132-fold increased risk for AMI (OR 2.132, P = 0.012) compared with noncarriers. Moreover, we observed that the ADP-induced MAR in the carriers of the H2 haplotype from the control group was somewhat higher than that in noncarriers of this group (P = 0.020). However, we failed to demonstrate that the P2Y1 H1/H2 polymorphism affected ADP-induced MAR in AMI patients. Additionally, P2Y1 c.1622A > and P2Y12 c.34C > T polymorphisms were not associated with the risk of AMI or ADP-induced MAR in either group. Therefore, our results suggest that the P2Y12 H2 haplotype was associated with a higher risk of AMI, while its effect on increased ADP-induced platelet aggregation remains to be investigated. Thus, the P2Y12 H2 haplotype may be a potential marker for AMI.
AbstractList BackgroundThe objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI) in the Quanzhou population and to determine associations between P2Y1 and P2Y12 genotypes and ADP-induced platelet aggregation in this population.MethodsAll subjects were screened for P2Y1 (c.1622A > G) and P2Y12 (H1/H2, c.34C > T) polymorphisms by direct DNA sequencing. The maximal platelet aggregation rate (MAR) in AMI patients (n = 61) and healthy control subjects (n = 50) was measured by a PL-12 platelet function analyzer, and adenosine diphosphate (ADP) (5 μmol/L) was used as an agonist.ResultsThe haploid H2 allele in the P2Y12 gene was more frequent in patients with AMI than in control subjects (OR 1.887, P = 0.005). The P2Y12 H2 haplotype was significantly associated with AMI in the codominant (P = 0.008), dominant (OR 2.103, P = 0.003), and overdominant models (OR 2.133, P = 0.003). After adjusting for potential confounders, H2 haplotype carriers had a 2.132-fold increased risk for AMI (OR 2.132, P = 0.012) compared with noncarriers. Moreover, we observed that the ADP-induced MAR in the carriers of the H2 haplotype from the control group was somewhat higher than that in noncarriers of this group (P = 0.020). However, we failed to demonstrate that the P2Y1 H1/H2 polymorphism affected ADP-induced MAR in AMI patients. Additionally, P2Y1 c.1622A > and P2Y12 c.34C > T polymorphisms were not associated with the risk of AMI or ADP-induced MAR in either group.ConclusionsTherefore, our results suggest that the P2Y12 H2 haplotype was associated with a higher risk of AMI, while its effect on increased ADP-induced platelet aggregation remains to be investigated. Thus, the P2Y12 H2 haplotype may be a potential marker for AMI.
The objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI) in the Quanzhou population and to determine associations between P2Y1 and P2Y12 genotypes and ADP-induced platelet aggregation in this population. All subjects were screened for P2Y1 (c.1622A > G) and P2Y12 (H1/H2, c.34C > T) polymorphisms by direct DNA sequencing. The maximal platelet aggregation rate (MAR) in AMI patients (n = 61) and healthy control subjects (n = 50) was measured by a PL-12 platelet function analyzer, and adenosine diphosphate (ADP) (5 μmol/L) was used as an agonist. The haploid H2 allele in the P2Y12 gene was more frequent in patients with AMI than in control subjects (OR 1.887, P = 0.005). The P2Y12 H2 haplotype was significantly associated with AMI in the codominant (P = 0.008), dominant (OR 2.103, P = 0.003), and overdominant models (OR 2.133, P = 0.003). After adjusting for potential confounders, H2 haplotype carriers had a 2.132-fold increased risk for AMI (OR 2.132, P = 0.012) compared with noncarriers. Moreover, we observed that the ADP-induced MAR in the carriers of the H2 haplotype from the control group was somewhat higher than that in noncarriers of this group (P = 0.020). However, we failed to demonstrate that the P2Y1 H1/H2 polymorphism affected ADP-induced MAR in AMI patients. Additionally, P2Y1 c.1622A > and P2Y12 c.34C > T polymorphisms were not associated with the risk of AMI or ADP-induced MAR in either group. Therefore, our results suggest that the P2Y12 H2 haplotype was associated with a higher risk of AMI, while its effect on increased ADP-induced platelet aggregation remains to be investigated. Thus, the P2Y12 H2 haplotype may be a potential marker for AMI.
The objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI) in the Quanzhou population and to determine associations between P2Y1 and P2Y12 genotypes and ADP-induced platelet aggregation in this population. All subjects were screened for P2Y1 (c.1622A > G) and P2Y12 (H1/H2, c.34C > T) polymorphisms by direct DNA sequencing. The maximal platelet aggregation rate (MAR) in AMI patients (n = 61) and healthy control subjects (n = 50) was measured by a PL-12 platelet function analyzer, and adenosine diphosphate (ADP) (5 [mu]mol/L) was used as an agonist. The haploid H2 allele in the P2Y12 gene was more frequent in patients with AMI than in control subjects (OR 1.887, P = 0.005). The P2Y12 H2 haplotype was significantly associated with AMI in the codominant (P = 0.008), dominant (OR 2.103, P = 0.003), and overdominant models (OR 2.133, P = 0.003). After adjusting for potential confounders, H2 haplotype carriers had a 2.132-fold increased risk for AMI (OR 2.132, P = 0.012) compared with noncarriers. Moreover, we observed that the ADP-induced MAR in the carriers of the H2 haplotype from the control group was somewhat higher than that in noncarriers of this group (P = 0.020). However, we failed to demonstrate that the P2Y1 H1/H2 polymorphism affected ADP-induced MAR in AMI patients. Additionally, P2Y1 c.1622A > and P2Y12 c.34C > T polymorphisms were not associated with the risk of AMI or ADP-induced MAR in either group. Therefore, our results suggest that the P2Y12 H2 haplotype was associated with a higher risk of AMI, while its effect on increased ADP-induced platelet aggregation remains to be investigated. Thus, the P2Y12 H2 haplotype may be a potential marker for AMI.
The objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI) in the Quanzhou population and to determine associations between P2Y1 and P2Y12 genotypes and ADP-induced platelet aggregation in this population.BACKGROUNDThe objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI) in the Quanzhou population and to determine associations between P2Y1 and P2Y12 genotypes and ADP-induced platelet aggregation in this population.All subjects were screened for P2Y1 (c.1622A > G) and P2Y12 (H1/H2, c.34C > T) polymorphisms by direct DNA sequencing. The maximal platelet aggregation rate (MAR) in AMI patients (n = 61) and healthy control subjects (n = 50) was measured by a PL-12 platelet function analyzer, and adenosine diphosphate (ADP) (5 μmol/L) was used as an agonist.METHODSAll subjects were screened for P2Y1 (c.1622A > G) and P2Y12 (H1/H2, c.34C > T) polymorphisms by direct DNA sequencing. The maximal platelet aggregation rate (MAR) in AMI patients (n = 61) and healthy control subjects (n = 50) was measured by a PL-12 platelet function analyzer, and adenosine diphosphate (ADP) (5 μmol/L) was used as an agonist.The haploid H2 allele in the P2Y12 gene was more frequent in patients with AMI than in control subjects (OR 1.887, P = 0.005). The P2Y12 H2 haplotype was significantly associated with AMI in the codominant (P = 0.008), dominant (OR 2.103, P = 0.003), and overdominant models (OR 2.133, P = 0.003). After adjusting for potential confounders, H2 haplotype carriers had a 2.132-fold increased risk for AMI (OR 2.132, P = 0.012) compared with noncarriers. Moreover, we observed that the ADP-induced MAR in the carriers of the H2 haplotype from the control group was somewhat higher than that in noncarriers of this group (P = 0.020). However, we failed to demonstrate that the P2Y1 H1/H2 polymorphism affected ADP-induced MAR in AMI patients. Additionally, P2Y1 c.1622A > and P2Y12 c.34C > T polymorphisms were not associated with the risk of AMI or ADP-induced MAR in either group.RESULTSThe haploid H2 allele in the P2Y12 gene was more frequent in patients with AMI than in control subjects (OR 1.887, P = 0.005). The P2Y12 H2 haplotype was significantly associated with AMI in the codominant (P = 0.008), dominant (OR 2.103, P = 0.003), and overdominant models (OR 2.133, P = 0.003). After adjusting for potential confounders, H2 haplotype carriers had a 2.132-fold increased risk for AMI (OR 2.132, P = 0.012) compared with noncarriers. Moreover, we observed that the ADP-induced MAR in the carriers of the H2 haplotype from the control group was somewhat higher than that in noncarriers of this group (P = 0.020). However, we failed to demonstrate that the P2Y1 H1/H2 polymorphism affected ADP-induced MAR in AMI patients. Additionally, P2Y1 c.1622A > and P2Y12 c.34C > T polymorphisms were not associated with the risk of AMI or ADP-induced MAR in either group.Therefore, our results suggest that the P2Y12 H2 haplotype was associated with a higher risk of AMI, while its effect on increased ADP-induced platelet aggregation remains to be investigated. Thus, the P2Y12 H2 haplotype may be a potential marker for AMI.CONCLUSIONSTherefore, our results suggest that the P2Y12 H2 haplotype was associated with a higher risk of AMI, while its effect on increased ADP-induced platelet aggregation remains to be investigated. Thus, the P2Y12 H2 haplotype may be a potential marker for AMI.
Abstract Background The objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI) in the Quanzhou population and to determine associations between P2Y1 and P2Y12 genotypes and ADP-induced platelet aggregation in this population. Methods All subjects were screened for P2Y1 (c.1622A > G) and P2Y12 (H1/H2, c.34C > T) polymorphisms by direct DNA sequencing. The maximal platelet aggregation rate (MAR) in AMI patients (n = 61) and healthy control subjects (n = 50) was measured by a PL-12 platelet function analyzer, and adenosine diphosphate (ADP) (5 μmol/L) was used as an agonist. Results The haploid H2 allele in the P2Y12 gene was more frequent in patients with AMI than in control subjects (OR 1.887, P = 0.005). The P2Y12 H2 haplotype was significantly associated with AMI in the codominant (P = 0.008), dominant (OR 2.103, P = 0.003), and overdominant models (OR 2.133, P = 0.003). After adjusting for potential confounders, H2 haplotype carriers had a 2.132-fold increased risk for AMI (OR 2.132, P = 0.012) compared with noncarriers. Moreover, we observed that the ADP-induced MAR in the carriers of the H2 haplotype from the control group was somewhat higher than that in noncarriers of this group (P = 0.020). However, we failed to demonstrate that the P2Y1 H1/H2 polymorphism affected ADP-induced MAR in AMI patients. Additionally, P2Y1 c.1622A > and P2Y12 c.34C > T polymorphisms were not associated with the risk of AMI or ADP-induced MAR in either group. Conclusions Therefore, our results suggest that the P2Y12 H2 haplotype was associated with a higher risk of AMI, while its effect on increased ADP-induced platelet aggregation remains to be investigated. Thus, the P2Y12 H2 haplotype may be a potential marker for AMI.
Background The objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI) in the Quanzhou population and to determine associations between P2Y1 and P2Y12 genotypes and ADP-induced platelet aggregation in this population. Methods All subjects were screened for P2Y1 (c.1622A > G) and P2Y12 (H1/H2, c.34C > T) polymorphisms by direct DNA sequencing. The maximal platelet aggregation rate (MAR) in AMI patients (n = 61) and healthy control subjects (n = 50) was measured by a PL-12 platelet function analyzer, and adenosine diphosphate (ADP) (5 [mu]mol/L) was used as an agonist. Results The haploid H2 allele in the P2Y12 gene was more frequent in patients with AMI than in control subjects (OR 1.887, P = 0.005). The P2Y12 H2 haplotype was significantly associated with AMI in the codominant (P = 0.008), dominant (OR 2.103, P = 0.003), and overdominant models (OR 2.133, P = 0.003). After adjusting for potential confounders, H2 haplotype carriers had a 2.132-fold increased risk for AMI (OR 2.132, P = 0.012) compared with noncarriers. Moreover, we observed that the ADP-induced MAR in the carriers of the H2 haplotype from the control group was somewhat higher than that in noncarriers of this group (P = 0.020). However, we failed to demonstrate that the P2Y1 H1/H2 polymorphism affected ADP-induced MAR in AMI patients. Additionally, P2Y1 c.1622A > and P2Y12 c.34C > T polymorphisms were not associated with the risk of AMI or ADP-induced MAR in either group. Conclusions Therefore, our results suggest that the P2Y12 H2 haplotype was associated with a higher risk of AMI, while its effect on increased ADP-induced platelet aggregation remains to be investigated. Thus, the P2Y12 H2 haplotype may be a potential marker for AMI. Keywords: Acute myocardial infarction, P2Y1 gene, P2Y12 gene, Polymorphism, Platelet aggregation
ArticleNumber 41
Audience Academic
Author Tian, Mengcha
Chen, Jintu
Wu, Conglian
Zhang, Zhishan
Su, Chunyan
Zhang, Tao
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CitedBy_id crossref_primary_10_31083_j_rcm2512462
crossref_primary_10_18705_2782_3806_2024_4_4_295_312
crossref_primary_10_1016_j_intimp_2024_112222
Cites_doi 10.1007/s12687-017-0293-9
10.1161/01.ATV.0000148708.44691.27
10.1016/j.ijcard.2007.12.118
10.1186/s12883-019-1271-0
10.1111/j.1538-7836.2006.01869.x
10.1097/MD.0000000000006553
10.1016/0378-1119(96)00027-3
10.1161/01.STR.0000169922.79281.a5
10.1016/j.thromres.2012.06.024
10.1016/j.ihj.2013.02.012
10.1161/01.CIR.0000085073.69189.88
10.1055/a-0622-8110
10.18632/oncotarget.19991
10.1016/j.atherosclerosis.2007.07.001
10.1007/s11033-010-0628-7
10.1016/j.thromres.2013.06.020
10.1038/aps.2016.41
10.2147/NDT.S171213
10.1111/j.1751-553X.2012.01420.x
10.25011/cim.v43i3.34597
10.1590/1806-9282.20220033
10.2217/14622416.8.6.577
10.1097/MBC.0b013e32835e98bf
10.1186/1471-2350-8-59
10.1371/journal.pone.0001523
10.3109/09537104.2012.693992
10.1124/pr.58.3.3
10.1016/j.thromres.2011.02.019
10.1016/j.bcp.2012.01.003
10.2478/bjmg-2014-0072
10.1080/14017431.2019.1590628
10.1172/JCI20986
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Issue 1
Keywords Platelet aggregation
P2Y1 gene
Acute myocardial infarction
P2Y12 gene
Polymorphism
Language English
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References X Yi (3075_CR12) 2017; 8
C Léon (3075_CR9) 1996; 171
RY Zee (3075_CR18) 2008; 197
X Liang (3075_CR24) 2020; 43
R Priyadharsini (3075_CR1) 2017; 8
X Yi (3075_CR4) 2019; 19
K Zhao (3075_CR34) 2019; 69
MP Abbracchio (3075_CR14) 2006; 58
AA Timur (3075_CR2) 2012; 34
RT Dorsam (3075_CR15) 2004; 113
U Cavallari (3075_CR17) 2007; 8
SL Hetherington (3075_CR6) 2005; 25
S Ziegler (3075_CR16) 2005; 36
R Liu (3075_CR30) 2016; 37
SJ Lu (3075_CR3) 2018; 14
N Zoheir (3075_CR8) 2013; 24
KK Shalia (3075_CR21) 2013; 65
N Azarpira (3075_CR23) 2010; 38
I Isordia-Salas (3075_CR19) 2012; 130
R Kar (3075_CR22) 2013; 24
KA Kim (3075_CR7) 2013; 132
P Fontana (3075_CR5) 2003; 108
Q Li (3075_CR20) 2007; 8
N Martinelli (3075_CR27) 2008; 3
I Yildiz (3075_CR25) 2022; 68
M Lordkipanidzé (3075_CR10) 2011; 128
D Sibbing (3075_CR11) 2006; 4
M Li (3075_CR32) 2017; 96
F Gao (3075_CR13) 2011; 124
S Namazi (3075_CR31) 2012; 83
T Çınar (3075_CR26) 2019; 53
H Hassani Idrissi (3075_CR29) 2017; 2017
P Staritz (3075_CR28) 2009; 133
HM Sen (3075_CR33) 2014; 17
References_xml – volume: 8
  start-page: 127
  issue: 2
  year: 2017
  ident: 3075_CR1
  publication-title: J Commun Genet
  doi: 10.1007/s12687-017-0293-9
– volume: 25
  start-page: 252
  issue: 1
  year: 2005
  ident: 3075_CR6
  publication-title: Arterioscler Thromb Vasc Biol
  doi: 10.1161/01.ATV.0000148708.44691.27
– volume: 133
  start-page: 341
  issue: 3
  year: 2009
  ident: 3075_CR28
  publication-title: Int J Cardiol
  doi: 10.1016/j.ijcard.2007.12.118
– volume: 19
  start-page: 44
  issue: 1
  year: 2019
  ident: 3075_CR4
  publication-title: BMC Neurol
  doi: 10.1186/s12883-019-1271-0
– volume: 4
  start-page: 912
  issue: 4
  year: 2006
  ident: 3075_CR11
  publication-title: J Thrombosis Haemostasis JTH
  doi: 10.1111/j.1538-7836.2006.01869.x
– volume: 96
  issue: 14
  year: 2017
  ident: 3075_CR32
  publication-title: Medicine
  doi: 10.1097/MD.0000000000006553
– volume: 171
  start-page: 295
  issue: 2
  year: 1996
  ident: 3075_CR9
  publication-title: Gene
  doi: 10.1016/0378-1119(96)00027-3
– volume: 124
  start-page: 1731
  issue: 11
  year: 2011
  ident: 3075_CR13
  publication-title: Chin Med J
– volume: 36
  start-page: 1394
  issue: 7
  year: 2005
  ident: 3075_CR16
  publication-title: Stroke
  doi: 10.1161/01.STR.0000169922.79281.a5
– volume: 130
  start-page: e67
  issue: 3
  year: 2012
  ident: 3075_CR19
  publication-title: Thromb Res
  doi: 10.1016/j.thromres.2012.06.024
– volume: 65
  start-page: 158
  issue: 2
  year: 2013
  ident: 3075_CR21
  publication-title: Indian Heart J
  doi: 10.1016/j.ihj.2013.02.012
– volume: 108
  start-page: 989
  issue: 8
  year: 2003
  ident: 3075_CR5
  publication-title: Circulation
  doi: 10.1161/01.CIR.0000085073.69189.88
– volume: 69
  start-page: 23
  issue: 1
  year: 2019
  ident: 3075_CR34
  publication-title: Drug Res
  doi: 10.1055/a-0622-8110
– volume: 8
  start-page: 70811
  issue: 41
  year: 2017
  ident: 3075_CR12
  publication-title: Oncotarget
  doi: 10.18632/oncotarget.19991
– volume: 197
  start-page: 694
  issue: 2
  year: 2008
  ident: 3075_CR18
  publication-title: Atherosclerosis
  doi: 10.1016/j.atherosclerosis.2007.07.001
– volume: 38
  start-page: 4873
  issue: 8
  year: 2010
  ident: 3075_CR23
  publication-title: Mol Biol Rep
  doi: 10.1007/s11033-010-0628-7
– volume: 132
  start-page: 221
  issue: 2
  year: 2013
  ident: 3075_CR7
  publication-title: Thromb Res
  doi: 10.1016/j.thromres.2013.06.020
– volume: 37
  start-page: 882
  issue: 7
  year: 2016
  ident: 3075_CR30
  publication-title: Acta Pharmacol Sin
  doi: 10.1038/aps.2016.41
– volume: 14
  start-page: 2225
  year: 2018
  ident: 3075_CR3
  publication-title: Neuropsychiatr Dis Treat
  doi: 10.2147/NDT.S171213
– volume: 34
  start-page: 473
  issue: 5
  year: 2012
  ident: 3075_CR2
  publication-title: Int J Lab Hematol
  doi: 10.1111/j.1751-553X.2012.01420.x
– volume: 43
  start-page: E33
  issue: 3
  year: 2020
  ident: 3075_CR24
  publication-title: Clin Invest Med
  doi: 10.25011/cim.v43i3.34597
– volume: 68
  start-page: 802
  issue: 6
  year: 2022
  ident: 3075_CR25
  publication-title: Rev Assoc Med Bras
  doi: 10.1590/1806-9282.20220033
– volume: 2017
  start-page: 9532471
  year: 2017
  ident: 3075_CR29
  publication-title: Genet Res Int
– volume: 8
  start-page: 577
  issue: 6
  year: 2007
  ident: 3075_CR20
  publication-title: Pharmacogenomics
  doi: 10.2217/14622416.8.6.577
– volume: 24
  start-page: 525
  issue: 5
  year: 2013
  ident: 3075_CR8
  publication-title: Blood Coagul Fibrinolysis Int J Haemostasis Thrombosis
  doi: 10.1097/MBC.0b013e32835e98bf
– volume: 8
  start-page: 59
  year: 2007
  ident: 3075_CR17
  publication-title: BMC Med Genet
  doi: 10.1186/1471-2350-8-59
– volume: 3
  issue: 2
  year: 2008
  ident: 3075_CR27
  publication-title: PLoS ONE
  doi: 10.1371/journal.pone.0001523
– volume: 24
  start-page: 297
  issue: 4
  year: 2013
  ident: 3075_CR22
  publication-title: Platelets
  doi: 10.3109/09537104.2012.693992
– volume: 58
  start-page: 281
  issue: 3
  year: 2006
  ident: 3075_CR14
  publication-title: Pharmacol Rev
  doi: 10.1124/pr.58.3.3
– volume: 128
  start-page: 47
  issue: 1
  year: 2011
  ident: 3075_CR10
  publication-title: Thromb Res
  doi: 10.1016/j.thromres.2011.02.019
– volume: 83
  start-page: 903
  issue: 7
  year: 2012
  ident: 3075_CR31
  publication-title: Biochem Pharmacol
  doi: 10.1016/j.bcp.2012.01.003
– volume: 17
  start-page: 37
  issue: 2
  year: 2014
  ident: 3075_CR33
  publication-title: Balkan J Med Genet
  doi: 10.2478/bjmg-2014-0072
– volume: 53
  start-page: 83
  issue: 2
  year: 2019
  ident: 3075_CR26
  publication-title: Scand Cardiovasc J
  doi: 10.1080/14017431.2019.1590628
– volume: 113
  start-page: 340
  issue: 3
  year: 2004
  ident: 3075_CR15
  publication-title: J Clin Investig
  doi: 10.1172/JCI20986
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Snippet The objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI) in the...
Background The objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI)...
BackgroundThe objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI) in...
Abstract Background The objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial...
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StartPage 41
SubjectTerms Acute myocardial infarction
Adenosine diphosphate
Adenosine Diphosphate - pharmacology
Blood Platelets
Body mass index
Cardiovascular disease
Cholesterol
Diabetes
DNA sequencing
Gene polymorphism
Haplotypes
Heart attacks
High density lipoprotein
Humans
Hypertension
Myocardial infarction
Myocardial Infarction - diagnosis
Myocardial Infarction - genetics
P2Y1 gene
P2Y12 gene
Platelet Aggregation
Platelet Aggregation Inhibitors - pharmacology
Polymorphism
Polymorphism, Genetic
Regression analysis
Risk factors
Stroke
Vein & artery diseases
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Title Association between P2Y1 and P2Y12 polymorphisms and acute myocardial infarction and ADP-induced platelet aggregation
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Volume 23
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