Review
Copyright ©The Author(s) 2015.
World J Cardiol. Oct 26, 2015; 7(10): 609-620
Published online Oct 26, 2015. doi: 10.4330/wjc.v7.i10.609
Figure 1
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Figure 1 Low-density lipoprotein cholesterol levels on admission in patients with acute coronary syndrome[74]. LDL: Low-density lipoprotein.
Figure 2
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Figure 2 Pathogenic role of lipoprotein-associated phospholipase A2 in atherosclerosis development. LDL: Low-density lipoprotein; Lp-PLA2: Lipoprotein-associated phospholipase A2.
Figure 3
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Figure 3 Increased number of acute myocardial infarction depending on the variant gene Arg92His. A: The patients with variant gene GG (Arg92) have a greater number of infarcts compared to the other two variants; B: The Kaplan-Meyer curve shows a lower survival free from acute myocardial infarction in patients with variant GG (Arg92). AMI: Acute myocardial infarction.
Figure 4
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Figure 4 The Kaplan-Meyer curves underline a greater survival free from cardiovascular events (death, acute myocardial infarction) in patients with lower lipoprotein-associated phospholipase A2 activity. ACS: Acute coronary syndrome; CV: Cardiovascular.
Figure 5
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Figure 5 Relevance of measuring of lipoprotein-associated phospholipase A2 activity for risk stratification in adult patients with moderate cardiovascular risk (> 2 risk factors) or higher[80]. Lp-PLA2: Lipoprotein-associated phospholipase A2; LDL: Low-density lipoprotein; CAD: Coronary artery disease; CV: Cardiovascular.