You are here

Home » Content

Carvedilol and Metoprolol in Acute Myocardial Infarction Early Effect of Oxidized LDL and Paraoxonase-1 Activity

Akut Miyokard İnfarktüsünde Karvedilol ve Metoprolol’ün Okside LDL ve Paraoksonaz-1

Journal Name:

  • Abant Tıp Dergisi

Publication Year:

  • 2013

Key Words:

Keywords (Original Language):

Author NameUniversity of AuthorFaculty of Author
Abstract (2. Language): 
Amaç: Bu çalışmanın amacı akut miyokard infarktüsü (AMİ) geçiren hastalarda dört haftalık karvedilol ve metoprolol tedavisinin okside düşük yoğunluklu lipoprotein (LDL) düzeyi ve paraoksanaz-1 (PON-1) aktivitesi üzerine etkisini araştır-maktır. Yöntem: Çalışmaya AMİ tanısı konulan 31 hasta ve kontrol grubunu oluşturacak 15 olgu alındı. AMİ grubundan 15 has-taya karvedilol ve 16 hastaya metoprolol tedavisi verilerek çalışma iki guruba randomize edildi. Çalışmanın sonunda başvuru ve kontrol vizitinde alınan ve saklanan kan örnekle-rinden okside LDL’nin ve PON-1 aktivitesinin başvuru (tedavi öncesi) ve tedavi sonrası 1 aylık sonuçlarına bakıldı. Bulgular: Hasta grubunda kontrol grubuna kıyasla başlangıç HDL düzeyi ve PON-1 aktivitesi anlamlı derecede düşük olarak saptandı. Okside LDL düzeyi hasta grubunda kontrol grubuna göre daha yüksekti. Hasta grubunda 1 aylık karvedi-lol (p=0,008) ve metoprolol (p Sonuç: AMİ geçiren hastalarda diğer çalışmalara paralel olarak, okside LDL' nin arttığı ve HDL-K düzeyi ile PON-1 aktivitesinin azaldığı gösterildi. Antioksidan özellikleri nede-niyle Karvedilol’ün PON-1 aktivitesini arttırmada Metopro-lol’e göre daha üstün olması beklenebilir. Fakat bir aylık süre bunu göstermek için yeterli olmayabilir.
Bookmark/Search this post with
Abstract (Original Language): 
Objective: The aim of this study to investigate the effects of Carvedilol and Metoprolol on oxidized low density lipopro-tein (oxLDL) and paraoxonase-1 (PON-1) activity in patients with acute myocardial infarction who were treated with these agents for four weeks. Method: 31 patients with AMI and 15 healhty subjects for control group were contained. 15 patients of AMI group were given Carvedilol treatment and the remained 16 were given Metoprolol treatment and the study was randomized to two groups. At the end of the study oxLDL and PON-1 activity levels were studied from the blood samples taken at admission (pre treatment) and samples taken after one month treatment. Results: In patient group initial high density lipoprotein (HDL) level and PON-1 activity were found significantly lower but oxLDL level was higher in patient group compared to control group. The oxLDL levels were found to decrease in patient group after Carvedilol(p=0,008) and Metoprolol (p Conclusion: In paralel to other studies we showed that oxLDL is increased and HDL and PON-1 activity is decreased in patients with AMI. Carvedilol may be expected to be superior to Metoprolol due to its antioxidant effect in incre-asing PON-1 acitvity. But one month period may not be enough to determine this effect.
FULL TEXT (PDF): 
PDF icon arastirmax-carvedilol-and-metoprolol-acute-myocardial-infarction-early-effect-oxidized-ldl-and-paraoxonase-1-activity.pdf
  • 3
179
184
  • English

REFERENCES

References: 

1.Ross R. The pathogenesis of atherosclerosis: A perspec- tive for the 1990s. Nature 1993; 362(6423):801-9
2.Carmena R, Ascaso JF, Camejo G, Varela G, Hurt-Camejo E, Ordovas JM, et al. Effect of olive and sunflower oils on low density lipoprotein level, composition, size, oxidation and interaction with arterial proteoglycans. Atherosclero-sis. 1996;125(2):243-55.
3.Tsimikas S, Brilakis ES, Miller ER, McConnell JP, Lennon RJ, Kornman KS, et al. Oxidized phospholipids, Lp(a) lipo-protein, and coronary artery disease. N Engl J Med 2005; 353(1):46-57
4.Mackness MI, Arrol S, Durrington PN. Paraoxonase prevents accumulation of lipoperoxides in low-density lipoprotein. FEBS Lett 1991;286(1-2): 152–4.
5.Mackness MI, Mackness B, Durrington PN, Connelly PW, HegeleRA. Paraoxonase: biochemistry, genetics and rela-tionship to plasmalipoproteins. Curr Opin Lipidol 1996;7(2): 69–76.
6.Aviram M, Rosenblat M, Billecke S, Erogul J, Sorenson R, Bisgaier CL, et al. Human serum paraoxonase is inactivat-ed by oxidized low density lipoprotein and preserved by antioxidants. Free Radic Biol Med 1999;26(7-8): 892–904.
7.Eckerson HW, Wyte CM, La Du BN. The human serum paraoxonase/ arylesterase polymorphism. Am J Hum Genet 1983; 35(6): 1126-38.
8.Yusuf S, Sleight P, Rosi PRF, Ramsdale D, Peto R, Furze L, et al. Reduction in infarct size, arrhythmias, chest pain,
and morbidity by early intravenous beta-blockade in suspected acute myocardial infarction. Circulation 1983; 67 (6 Pt 2): I32-41.
9.Feuerstein GZ, Hamburger SA, Smith EF, Bril A, Ruffolo RR, Myocardial protection with Carvedilol. J Cardiovasc Pharmacol 1992; 19:S138-41.
10.McElveen J, Mackness MI, Colley CM, Peard T, Warner S, Walker CH. Distribution of paraoxon hydrolytic activity in the serum of patients after myocardial infarction. Clin Chem1986; 32(4): 671-3.
11.Ombres D, Pannitteri G, Montali A, Candeloro A, Sec-careccia F, Campagna F, et al. The Gln-Argl92 polymor-phism of human paraoxonase gene ıs not associated with coronary artery disease in Italian patients. Arterioscler Thromb Vasc Biol 1998;18(10):1611-6.
12.Aviram M, Hardak E, Vaya J, Mahmood S, Milo S, Hoffman A, et al. Human serum paraoxonases (PON1) Q and R selectively decrease lipid peroxides in human coro-nary and carotid atherosclerotic lesions. Circulation 2000; 101(21): 2510-7.
13.Aviram M, Rosenblat M, Bisgair CL, Newton RS, Primo-Parmo SL, La Du BN Paraoxonase inhibits high density lipoprotein (HDL) oxidation and preserves its functions: a possible peroxidative role for paraoxonase. J Clin Invest 1998; 101(8): 1581-90.
14.Watson AD, Berliner JA, Hama SY, La Du BN, Faull KF, Fogelman AM, et al. Protective effect of high density
Albayrak S et al.
Carvedilol and Metoprolol in AMI
Abant Med J 2013; 2(3):179-184
184
lipoprotein associated paraoxonase. Inhibition of the biological activity of minimally oxidized low density lipo-protein. J Clin Invest 1995;96(6):2882–91.
15.Ehara S, Ueda M, Naruko T, Haze K, Itoh A, Otsuka M, et al. Elevated levels of oxidized low density lipoprotein show a positive relationship with the severity of acute coronary syndromes. Circulation 2001;103(15):1955–60.
16.Holvet P, Vanhaecke J, Janssens S, Van de Werf F, Collen D. Oxidized LDL and Malondialdehyde-Modified LDL in Patients With Acute Coronary Syndromes and Stable Coronary Artery Disease. Circulation 1998;9(15)8:1487-1494.
17.Halliwell B, Gutteridge JM, Cross CE, Free radi-cals,antioxidants, and human disease: where are we now? J Lab Clin Med 1992:119(6):598-620.
18.Devasagayam TP, Tilac JC, Boloor KK Sane KS, Ghaskadbi SS, Lele RD. Free radicals and antioxidants in human health: curent status and future prospects. J Assoc Phisicians India 2004;52: 794-804.
19.Serdar Z, Serdar Z, Altın A, Albayrak S. et al. The rela-tion between oxidant and antioxidant parameters and severity of acute coronary syndromes. Acta Cardiol 2007; 62(4):373-80.
20.Jialal I, Vega G, Grundy S. Physiological levels of ascor-bate inhibit the oxidative modification of LDL. Atheroscle-rosis 1990;82(3):185–91.
21.Aviram M, Rosenblat M, Bisgair CL, Newton RS, Primo-Parmo SL, La Du BN Paraoxonase inhibits high density lipoprotein (HDL) oxidation and preserves its functions: a possible peroxidative role for paraoxonase. J Clin Invest 1998; 101(8): 1581-90.
22.Castelli WP, Garrison RJ, Wilson PW, Abbott RD, Ka-lousdian S, Kannel WB. Incidence of coronary heart dis-ease and lipoprotein cholesterol levels. The Framingham Study. J Am Med Assoc 1986;256(20):2835–8.

Thank you for copying data from http://www.arastirmax.com