Serial values for hematologic and biochemical analysis after myocardial infarction in rats

  • Lee, Mi-Jin (College of Veterinary Medicine & Bio-Safety Research Institute, Chonbuk National University) ;
  • Tae, Hyun-Jin (College of Veterinary Medicine & Bio-Safety Research Institute, Chonbuk National University) ;
  • Li, Ying-Hua (College of Veterinary Medicine & Bio-Safety Research Institute, Chonbuk National University) ;
  • Yu, Do-Hyeon (College of Veterinary Medicine & Bio-Safety Research Institute, Chonbuk National University) ;
  • Han, In-Ae (College of Veterinary Medicine & Bio-Safety Research Institute, Chonbuk National University) ;
  • Lee, Seok-Won (College of Veterinary Medicine & Bio-Safety Research Institute, Chonbuk National University) ;
  • Ahn, Dong-Choon (School of Veterinary Medicine, Kangwon National University) ;
  • Kim, In-Shik (College of Veterinary Medicine & Bio-Safety Research Institute, Chonbuk National University) ;
  • Park, Jin-Ho (College of Veterinary Medicine & Bio-Safety Research Institute, Chonbuk National University)
  • Published : 2008.06.30

Abstract

To diagnose acute myocardial infarction (MI), many cardiac markers have been used in hematologic and biochemical analysis, and many studies have been published for hematologic and biochemical analysis associated with human acute MI. However, after occurrence of acute MI, the serial investigation for values in hematologic and biochemical analysis including chronic MI has rarely been performed. To observe the change of the serial values in hematologic and biochemical analysis, we induced artificial MI. The left main descending artery (LMDA) of the left coronary artery was ligated during the progression (day 1, 3, 5, 7, 14 and 30) of MI. Total 66 Sprague-Dawley rats were divided into the sham group (n=24, thoracotomy without LMDA ligation) and the experimental (MI) group (n=42, with LMDA ligation). And all individual in each group was sacrified at day 1, 3, 5, 7, 14 and 30 for the hematologic and biochemical analysis. In comparison of hematologic analysis between the sham and MI groups, the mean values of red blood cell (RBCs), hemoglobin and hematocrit (HCT) showed a steady increase. In biochemical analysis, the mean values of glucose, cholesterol, total creatine kinase (CK) and isoenzyme MB, and lactate dehydrogenase (LDH) were increased in all MI groups compared with the sham groups. The results of this study suggest that early hematologic and biochemical mean values occurred after acute MI are similar to those of human acute MI. In conclusion, we could observe the alterations and serial values in hematologic and biochemical analysis to the extent of chronic status after acute MI.

Keywords

References

  1. Stephenson RB. 2007. Overview of cardiovascular function. In: Cunning‑ham JG, Klein BG. Textbook of vete‑rinary physiology. 4eds. Philadelphia, PA: Saunders:178‑191
  2. Herlitz J, Hjalmarson A. 1985. Predic‑tion of the severity of acute myocar‑dial infarction. Cardiology 72:174‑184
  3. Shebuski RJ. 2002. Utility of point‑of‑care diagnostic testing in patients 1. with chest pain and suspected acute myocardial infarction. Curr Opin Pharmacol 2:160‑164
  4. Morgan S, Smith H, Simpson I, et al. 1999. Prevalence and clinical charac‑teristics of left ventricular dysfunction among elderly patients in general prac‑tice setting: cross sectional survey. BMJ 318:368‑372 https://doi.org/10.1136/bmj.318.7180.372
  5. Wu AHB, Apple FS, Gibler WB, et al. 1999. National academy of clinical biochemistry standards of laboratory practice: Recommendations for the use of cardiac markers in coronary artery diseases. Clin Chem 45:1104‑1121
  6. Pekdemir M, Karaca I, Cevik Y, et al. 2006. The diagnostic value of QT dispersion for acute coronary synd‑rome in patients presenting with chest pain and nondiagnostic initial electro‑cardiograms. Mt Sinai J Med 73:813‑817
  7. Fontes JP, Goncalves M, Ribeiro VG. 1999. Serum markers for ischemic myocardial damage. Rev Port Cardiol 18:1129‑1136
  8. Matsui Y, Hashimoto H, Tsukamoto H, et al. 1989. Disappearance and ap‑pearance of isoenzymes of creatine kinase, lactate dehydrogenase and as‑partate aminotransferase in the myo‑cardium undergoing infarction. Cardiovasc Res 23:249‑253
  9. Okabe H. 1995. Aspartate aminotrans‑ferase. Nippon Rinsho 53:1141‑1145
  10. Cannon CP, McCabe CH, Wilcox RG, et al. 2001. Association of white blood cell count with increased mor‑tality in acute myocardial infarction and unstable angina pectoris. Am J Cardiol 87:636‑639 https://doi.org/10.1016/S0002-9149(00)01445-4
  11. Menon V, Lessard D, Yarzebski J, et al. 2003. Leukocytosis and adverse hospital outcomes after acute myo‑cardial infarction. Am J Cardiol 92:368‑372
  12. Kosiborod M, Smith GL, Radford MJ, et al. 2003. The prognostic impor‑tance of anemia in patients with heart failure. Am J Med 114:112‑119
  13. Mahmoodi MR, Kimiagar SM, Abadi AR. 2007. Is anemia an independent predictor of occurrence of acute co‑ronary syndrome? Results from the modares heart study. Am Heart Hos‑pital J 5:73‑79
  14. Ishihara M, Inoue I, Kawagoe T, et al. 2003. Impact of acute hyper‑glycemia on left ventricular function after reperfusion therapy in patients with a first anterior wall acute myo‑cardial infarction. Am Heart J 146:674‑678
  15. Kosiborod M, Rathore SS, Inzucchi SE, et al. 2005. Admission glucose and mortality in elderly patients hos‑pitalized with acute myocardial in‑farction: Implications for patients with and without recognized diabetes. Circulation 111:3078‑3086
  16. Swan JW, Anker SD, Walton C, et al. 1997. Insulin resistance in chro‑nic heart failure: relation to severity and etiology of heart failure. J Am Coll Cardiol 30:527‑532
  17. Ishihara M, Kojima S, Sakamoto T, et al. 2006. Usefulness of combined white blood cell count and plasma glucose for predicting in‑hospital out‑comes after acute myocardial infarction. Am J Cardiol 97:1558‑1563
  18. Aronson D, Suleiman M, Agmon Y, et al. 2007. Changes in haemoglobin levels during hospital course and long‑term outcome after acute myo‑cardial infarction. Eur heart J 28:1289‑1296
  19. Horwich TB, Fonarow GC, Hamilton MA, et al. 2002. Anemia is associ‑ated with worse symptoms, greater impairment in functional capacity and a significant increase in mortality in patients with advanced heart failure. J Am Coll Cardiol 39:780‑1786
  20. Archbold RA, Balami D, Al‑hajiri A, et al. 2006. Hemoglobin concent‑ration is an independent determinant of heart failure in acute coronary syndromes: cohort analysis of 2310 patients. Am Heart J 152:1091‑1095
  21. Aukrust P, Waehre T, Damas JK, et al. 2001. Inflammatory role of plate‑lets in acute coronary syndromes. Heart 86:605‑606
  22. Willoughby S, Holmes A, Loscalzo J. 2002. Platelets and cardio‑vascular disease. Eur J Cardiovas Nurs 1:273‑288
  23. Avramakis G, Papadimitraki E, Papa‑konstandinou D, et al. 2007. Plate‑lets and white blood cell subpopula‑tions among patients with myocardial infarction and unstable angina. Platelets 18:16‑23
  24. Iwashita M, Matsushita Y, Sasaki J, et al. 2004. Relation of serum total cholesterol and other risk factors to risk of coronary events in middle‑aged and elderly Japanese men with hypercholesterolemia. Circ J 68:405‑409
  25. Vega G, Martinez S, Jimenez PA, et al. 2007. Effect of cardio‑vascular risk factors on long‑term morbidity 1. and mortality following acute myocardial infarction. Rev Esp Cardiol 60:703‑713