Lipoprotein-Associated Phospholipase A2 Activity increase the Sensitivity of Framingham Score for detecting the incidence of Acute Myocardial Infarction in sub-population of Indonesian Male Patients

Andi Wahjono, Saifur Rohman, Miryanti Cahyaningtias, Rina Yudha, Yanna Indrayana, Mifetika lukitasari, Rusdianto Rusdianto, Aditya Kurniawan, Djanggan Sargowo, Sasmojo Widito, Dadang Hendrawan, Jayarani Fatimah Putri, widodo Ph.D

Abstract

Background: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an inflammatory biomarker of cardiovascular disease. Framingham score is currently a widely used risk stratification tool for detecting the incidence of acute myocardial infarction (AMI), although it is not very sensitive. Adding Lp-PLA2 to the Framingham score can raise the odds ratio (OR) for AMI, but requires further research.

Objectives: In this study, we examine the role of Lp-PLA2 in increasing the sensitivity of the Framingham score for detecting the incidence of AMI.

Methods: This study was a case-control study of 97 male patients, 60 of whom had AMI and were treated in the intensive care unit as test subjects, and 37 of whom were non-AMI patients with normal treadmill test used as controls.

Results:Lp-PLA2 activity was found to be higher in the AMI group than that in the control group (83.97 ± 27.15 nmol/ml/min vs. 55.04 ± 31.99 nmol/ml/min). Eighteen patients (30%) with AMI were included in the high-risk category according to the Framingham score; this number increased to 36 patients after the addition of Lp-PLA2 activity to the Framingham score. Analysis using a receiver operating characteristic (ROC) showed a cut-off value for Lp-PLA2 activity associated with AMI of approximately 74.21 nmol/ml/min with an accuracy of 67%. The OR for detecting AMI incidence increased after the addition of Lp-PLA2 activity from 1:01 (CI 95%, 0.414–2.48) to 4.67 (CI 95%, 1.88-11.61).

Conclusions:   The addition of Lp-PLA2 activity may increase the sensitivity of the Framingham score for detecting the incidence of AMI.

Full Text:

PDF

References

Ueshima, H., Sekikawa, A., Miura, K,, Turin, T.C., Takashima, N., Kita, Y., Watanabe, M., Kadota, A., Okuda, N., Kadowaki, T., Nakamura, Y., Okamura, T.. Cardiovascular disease and risk factors in Asia a selected review. Circulation. 2008; 118: 2702-9.

Melati, R., Basuki, E., Setianto, B., Relationship between job strain and myocardial infarction in the national cardiovascular center patients. Jurnal Kardiologi Indonesia. 2011; 29: 17-24.

Camm, A.J., Lüscher, T.F., Serruys, P., The ESC textbook of cardiovascular medicine: Blackwell publishing; 2006.

Lloyd-Jones, D.M., Cardiovascular risk prediction basic concepts, current status, and future directions. Circulation. 2010; 121: 1768-77.

Lee, G., Lee, L.C., Liu, C., Lim, S.L., Shi, L.M., Ong, H.Y., Lim, Y.T., Yeo, T.C., Framingham risk score inadequately predicts cardiac risk in young patients presenting with a first myocardial infarction. Ann Acad Med Singapore. 2010; 39: 163-7.

Berry, J.D., Lloyd-Jones, D.M., Garside, D.B., Greenland, P., Framingham risk score and prediction of coronary heart disease death in young men. American heart journal. 2007; 154: 80-6.

Colley, K.J., Wolfert, R.L., Cobble, M.E., Lipoprotein associated phospholipase A2: role in atherosclerosis and utility as a biomarker for cardiovascular risk. The EPMA journal. 2011; 2: 27-38.

Masson, W., Siniawski, D., Krauss, J., Cagide, A., Clinical applicability of the framingham 30-year risk score. Usefulness in cardiovascular risk stratification and the diagnosis of carotid atherosclerotic plaque. Revista Española de Cardiología (English Edition). 2011; 64: 305-11.

Zalewski, A., Macphee, C., Role of lipoprotein-associated phospholipase A2 in atherosclerosis biology, epidemiology, and possible therapeutic target. Arteriosclerosis, thrombosis, and vascular biology. 2005; 25: 923-31.

McIntyre, T.M., Prescott, S.M., Stafforini, D.M., The emerging roles of PAF acetylhydrolase. Journal of lipid research. 2009; 50: S255-S9.

Tsimikas, S., Tsironis, L.D., Tselepis, A.D., New insights into the role of lipoprotein (a)-associated lipoprotein-associated phospholipase A2 in atherosclerosis and cardiovascular disease. Arteriosclerosis, thrombosis, and vascular biology. 2007; 27: 2094-9.

Jenny, N.S., Lipoprotein-Associated Phospholipase A2 Novel Biomarker and Causal Mediator of Atherosclerosis? Arteriosclerosis, thrombosis, and vascular biology. 2006;26(11):2417-8.

Münzel, T., Gori, T., Lipoprotein-associated phospholipase A2, a marker of vascular inflammation and systemic vulnerability. European heart journal. 2009:ehp311.

Rosenson, R.S., Stafforini, D.M., Modulation of oxidative stress, inflammation, and atherosclerosis by lipoprotein-associated phospholipase A2. Journal of lipid research. 2012; 53:1767-82.

Madjid, M., Ali, M., Willerson, J.T., Lipoprotein-associated phospholipase A2 as a novel risk marker for cardiovascular disease: a systematic review of the literature. Texas Heart Institute Journal. 2010; 37: 25.

Kolodgie, F.D., Burke, A.P., Skorija, K.S., Ladich, E., Kutys, R., Makuria, A.T., Virmani, R., Lipoprotein-associated phospholipase A2 protein expression in the natural progression of human coronary atherosclerosis. Arteriosclerosis, thrombosis, and vascular biology. 2006; 26:2523-9.

Iribarren, C., Lipoprotein-associated phospholipase A2 and cardiovascular risk state of the evidence and future directions. Arteriosclerosis, thrombosis, and vascular biology. 2006; 26: 5-6.

Tselepis, A.D., Panagiotakos, D.B., Pitsavos, C., Tellis, C.C., Chrysohoou, C., Stefanadis, C., Smoking induces lipoprotein-associated phospholipase A2 in cardiovascular disease free adults: the ATTICA Study. Atherosclerosis. 2009; 206: 303-8.

Satoh, K., Imaizumi, T., Kawamura, Y., Yoshida, H., Takamatsu, S., Takamatsu, M., Increased activity of the platelet-activating factor acetylhydrolase in plasma low density lipoprotein from patients with essential hypertension. Prostaglandins. 1989; 37: 673-82.

Persson, M., Hedblad, B., Nelson, J.J., Berglund, G., Elevated Lp-PLA2 levels add prognostic information to the metabolic syndrome on incidence of cardiovascular events among middle-aged nondiabetic subjects. Arteriosclerosis, thrombosis, and vascular biology. 2007; 27: 1411-6.

Biancone, L., Cantaluppi, V., Del Sorbo, L., Russo, S., Tjoelker, L.W., Camussi, G., Platelet-activating factor inactivation by local expression of platelet-activating factor acetyl-hydrolase modifies tumor vascularization and growth. Clinical cancer research : an official journal of the American Association for Cancer Research. 2003; 9: 4214-20.

Hatoum, I.J., Nelson, J.J., Cook, N.R., Hu, F.B., Rimm, E.B., Dietary, lifestyle, and clinical predictors of lipoprotein-associated phospholipase A2 activity in individuals without coronary artery disease. The American journal of clinical nutrition. 2010; 91: 786-93.

Robins, S.J., Collins, D., Nelson, J.J., Bloomfield, H.E., Asztalos, B.F., Cardiovascular events with increased lipoprotein-associated phospholipase A2 and low high-density lipoprotein-cholesterol the veterans affairs hdl intervention trial. Arteriosclerosis, thrombosis, and vascular biology. 2008; 28: 1172-8.

Ning, L., Shuijun, L., Chen, Y., Shuiming. G., The Association between Lp-PLA2 activity and major cardiovascular events in acute coronary syndrome at the Chinese Community. Heart. 2010; 96: A118-A.

Corson, M.A., Jones, P.H., Davidson, M.H., Review of the evidence for the clinical utility of lipoprotein-associated phospholipase A2 as a cardiovascular risk marker. The American journal of cardiology. 2008; 101: S41-S50.

Guo, Y.L., and Li, J.J., Biomarkers for the prediction of acute ongoing arterial plaque rupture. Research Reports in Clinical Cardiology. 2013; 4.

Oei, H.H.S., van der Meer, I.M., Hofman, A., Koudstaal, P.J., Stijnen, T., Breteler, M.M., Witteman, J.C., Lipoprotein-associated phospholipase A2 activity is associated with risk of coronary heart disease and ischemic stroke the rotterdam study. Circulation. 2005; 111: 570-5.

Ridker, P.M., MacFadyen, J.G., Wolfert, R.L., Koenig, W., Relationship of lipoprotein-associated phospholipase A2 mass and activity with incident vascular events among primary prevention patients allocated to placebo or to statin therapy: an analysis from the JUPITER trial. Clinical chemistry. 2012; 58: 877-86.

Persson, M., Nilsson, J.Ã…., Nelson, J.J., Hedblad, B., Berglund, G., The epidemiology of Lp-PLA 2: distribution and correlation with cardiovascular risk factors in a population-based cohort. Atherosclerosis. 2007; 190: 388-96.

Liu, Y.S., Hu, X.B., Li, H.Z., Jiang, W.D., Wang, X., Lin, H., Qin, A.Q., Wang, Y.M., Zhao, T., Dong, Z.Q., Zhang, M., Lu, Q.H., Association of lipoprotein-associated phospholipase A2 with characteristics of vulnerable coronary atherosclerotic plaques. Yonsei medical journal. 2011; 52: 914-22.

Collaboration L-PS. Lipoprotein-associated phospholipase A 2 and risk of coronary disease, stroke, and mortality: collaborative analysis of 32 prospective studies. The Lancet. 2010; 375: 1536-44.

Packard, C.J., O'Reilly, D.S., Caslake, M.J., McMahon, A.D., Ford, I., Cooney, J., Macphee, C.H., Suckling, K.E., Krishna, M., Wilkinson, F.E., Rumley, A., Lowe, G.D., Lipoprotein-associated phospholipase A2 as an independent predictor of coronary heart disease. New England Journal of Medicine. 2000; 343: 1148-55.

Piñón, P., Kaski, J.C., Inflammation, Atherosclerosis, and Cardiovascular Disease Risk: PAPP-A, Lp-PLA2, and Cystatin C. New Insights or Redundant Information? Revista Española de Cardiología (English Edition). 2006; 59: 247-58.

Maiolino, G., Pedon, L., Cesari, M., Frigo, A.C., Wolfert, R.L., Barisa, M., Pagliani, L., Rossitto, G., Seccia, T.M., Zanchetta, M., Rossi, G.P., Lipoprotein-associated phospholipase A2 activity predicts cardiovascular events in high risk coronary artery disease patients. PloS one. 2012; 7: e48171.

Tsimikas, S., Willeit, J., Knoflach, M., Mayr, M., Egger, G., Notdurfter, M., Witztum, J.L., Wiedermann, C.J., Xu, Q., Kiechl, S.,,QW Lipoprotein-associated phospholipase A2 activity, ferritin levels, metabolic syndrome, and 10-year cardiovascular and non-cardiovascular mortality: results from the Bruneck study. European heart journal. 2009; 30: 107-15.

C.E. Koro, R.D. Modeling the cardiovascular burden associated with elevated Lp-PLA2. Available from: http://spo.escardio.org/eslides.

O’Donoghue, M., Morrow, D.A., Sabatine, M.S., Murphy, S.A., McCabe, C.H., Cannon, C.P., Braunwald, E., Lipoprotein-associated phospholipase A2 and its association with cardiovascular outcomes in patients with acute coronary syndromes in the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy–Thrombolysis In Myocardial Infarction) trial. Circulation. 2006; 113: 1745-52.

Acevedo, M., Varleta, P., Kramer, V., Valentino, G., Quiroga, T., Prieto, C., Parada, J., Adasme, M., Briones, L., Navarrete, C., Comparison of lipoprotein-associated phospholipase A2 and high sensitive c-reactive protein as determinants of metabolic syndrome in subjects without coronary heart disease: in search of the best predictor. International Journal of Endocrinology. 2014; 2015: 1-8.

Khalili, D., Hadaegh, F., Soori, H., Steyerberg, E.W., Bozorgmanesh, M., Azizi, F., Clinical Usefulness of the Framingham Cardiovascular Risk Profile Beyond Its Statistical Performance: The Tehran Lipid and Glucose Study. American Journal of Epidemiology. 2012; 176: 177-86.

Refbacks

  • There are currently no refbacks.


Bookmark and Share