Study of lipid profile in acute myocardial infarction within 24 hours

  • Prashant Kumar Department of General Medicine Katihar Medical College, Katihar, Bihar, India.
  • Siddharth Singh Department of General Medicine AIIMS Patna, Bihar, India-801505.
  • Suresh Prasad Department of General Medicine Katihar Medical College, Katihar, Bihar, India.
  • Umesh Prasad Yadav Department of Biochemistry, All India Institute of Medical Sciences, Patna, Bihar, India
  • Pramod Kumar Agrawal Department of General Medicine Katihar Medical College, Katihar, Bihar, India.
Keywords: Acute myocardial infarction (AMI), Myocardium, Cardiac specific enzyme, Lipoproteins.


Background: Increased level of total cholesterol and LDL-cholesterol disturbs the endothelial function that may cause various cardio vascular disease and coronary heart disease. In addition, it can be expected, that hypercholesterolemia may unfavourably influence the course of the acute myocardial infarction. The aim of the study was to check whether patients with lipid levels above normal first 24 hours of myocardial infarction have an unfavorable clinical outcome.Methods: Study was designed on 60 patients (46-men and14-women) of different age groups admitted with myocardial infarction within first 24 hours of onset of symptoms. 20 normal healthy individuals with normal ECG and no family history of coronary heart disease were selected as control. The clinical history and physical examination confirmed the AMI by the cardiac specific enzyme Creatine Kinase (CK) and Creatine Kinase myocardial b fraction (CK-MB), Troponin (T) and ECG.  Blood samples were taken within 24 hours of acute myocardial infarction. Serum concentration of TC, TG, HDL-C were estimated by semi auto analyser. Analysis of variance (ANOVA) followed by Tukey’s post hoc test was done to evaluate the association between the mean values of serum samples and clinical outcome. A probability value p < 0.05 was considered statistically significant.Result: In the control group, the means of TC, TG, HDL-C, LDL-C and VLDL-C were found to be 172.2 mg/dl, 147.6 mg/dl, 45.52, 97.16 mg/dl and 29.52 mg/dl respectively. In the present case study, the mean TC was 208.53 mg/dl, mean TG was 168.73, mean HDL-C was 41.65 mg/dl, mean LDL-C was 133.13 mg/dl and mean VLDL-C was 33.74 mg/dl.Conclusion: We found that the occurrence of disease is more in male patient than the female and the male/female ratio was 3.28:1. The patients above the age of 60 years were more prone to develop myocardial infarction and the major risk factors were smoking, hypertension and diabetes. It has also been observed that most of the patients had high level of LDL-cholesterol and low level of HDL-cholesterol within 24 hours onset of myocardial infarction.DOI:10.21276/AABS.1677

Author Biography

Prashant Kumar, Department of General Medicine Katihar Medical College, Katihar, Bihar, India.
Department of General Medicine


1. Miller GJ, Miler NE: plasma HDL concentration and development of ischaemic heart disease: Lancet 1975;1:9-16.

2. Yokokawa H, Yasumura S, Tanno K et al. Serum low-density lipoprotein to high-density lipoprotein ratio as a predictor of future acute myocardial infarction among men in a. 2.7-year cohort study of a Japanese northern rural population. J Atheroscler Thromb. 2011;18:89-98.

3. Balci B. The modification of serum lipids after acute coronary syndrome and importance in clinical practice. Curr Cardiol Rev. 2011;7(4):272-276.

4. Nigam PK. Biochemical markers of myocardial injury. Indian J Clin Biochem. 2007;22:10-17.

5. Pitt B, Loscalzo J, Ycas J, Raichlen JS. Lipid levels after acute coronary syndromes. J Am Coll Cardiol. 2008;51:1440-1445.

6. Roubin RS, Barreiro PC, Roubín CF et al. High-sensitivity C-reactive protein predicts adverse outcomes after non-STsegmentelevation acute coronary syndrome regardless of GRACE risk score, but not after ST-segment elevation myocardial infarction. Rev Port Cardiol. 2013;32:117-122.

7. Swerdlow DI, Holmes MV, Kuchenbaecker KB et al. The interleukin-6 receptor as a target for prevention of coronary heart disease a mendelian randomisation analysis. Lancet. 2012;379:1214-1224.

8. Casas JP, Shah T, Hingorani AD, Danesh J, Pepys MB. C-reactive protein and coronary heart disease: a critical review. J Intern Med. 2008;264:295-314.

9. Bursi F, Weston SA, Killian JM et al. CRP and heart failure after myocardial infarction in the community. Am J Med. 2007;120:616-622.

10. Tarchalski J, Guzik P, Wysocki H. Correlation between the extent of coronary atherosclerosis and lipid profile. . Mol Cell Biochem. 2003;246(1-2):25-30.

11. Gorecki A, Bednarz B, Jaxa-Chamiec T et al. Lipid profile during the first 24 hours after myocardial infarction has significant prognostic value. Kardiol Pol. 2004;60(3): 229-236.

12. Ali I, Khan IU, Baloch MK, Mustafa G. Comparative lipid profile studies in cardiac and diabetic conditions. Pak J Pharm Sci. 2004;17(1):25-30.

13. Ferre N, Camps J, Fernandez-Ballart J, et al. Regulation of serum paraoxonase activity by genetic, nutritional, and lifestyle factors in the general population. Clin Chem. 2003;49:1491–1497.

14. Temelkova-Kurktschiev TS, Kurktschiev DP, Vladimirova-Kitova LG et al. Prevalence and type of dyslipidaemia in a population at risk for cardiovascular death in Bulgaria. Journal of Diabetology. 2009;51(2):22-26.

15. Volmink JA, Newton JN, Hicks NR et al. Coronary event and case fatality rates in an English population: results of the Oxford myocardial infarction incidence study. The Oxford Myocardial Infarction Incidence Study Group. Heart. 1998;80(1):4-40.

16. Tunstall-Pedoe H, Kuulasmaa K, Mähönen M et al. Contribution of trends in survival and coronary-event rates to changes in coronary heart disease mortality: 10-year results from 37 WHO MONICA project populations. Monitoring trends and determinants in cardiovascular disease. Lancet. 1998;8:1547-1557.

17. Lerner DJ and Kannel WB. Patterns of coronary heart disease morbidity and mortality in the sexes-A 26 years follow up of Framingham population. Am Heart J. 1986;111:383-390.

18. Lampe FC, Whincup PH, Wannamethee SG et al. The natural history of prevalent ischaemic heart disease in middle-aged men. Eur Heart J. 2000;21(13):1052-1062.

19. Nina RV, Gama ME, Santosh AM et al. Is the RACHS-1 (risk adjustment in congenital heart surgery) a useful tool in our scenario. Brito LM.Rev Bras cir Cardiovassc. 2007;4:425-431.

20. Borgel J, Schulz T, Bartels NK et al. Modifying effects of the R389G beta1-adrenoceptor polymorphism on resting heart rate and blood pressure in patients with obstructive sleep apnoea. Clin Sci (Lond). 2006;110(1):117-123.

21. Bartels NK, Borgel J, Wieczorek S, et al. Risk factors and myocardial infarction in patients with obstructive sleep apnea: impact of beta2-adrenergic receptor polymorphisms. BMC Med. 2007;1:1-5

22. Barrett Connor EL, Cohn BA, Wingard DL, and Edelstei SL. Why is diabetes mellitus a stronger risk factor for fatal ischaemic heart disease in women than in men. The Rancho Burnado study. JAMA. 1991;265:3249.

23. Shea S, Ottman R, Gabrielic et al. Family history- as an important risk factor for coronary heart disease. J Am Coll Cardiol 1984; 4:793-801

24. Mugge A, Hanefeld C, Böger RH. CARDIAC study investigators.. Plasma concentration of asymmetric dimethylarginine and the risk of coronary heart disease: rationale and design of the multicenter CARDIAC study. Atheroscler. 2003;4(4):29-32.

25. Wieczorek S, Arning L, Gizewski ER, Alheite I, Timmann D. Benign SCA14 phenotype in a German patient associated with a missense mutation in exon 3 of the PRKCG gene. Mov Disord. 2007;22(14):2135-2136.

26. Nikolaus S, Larisch R, Wirrwar A et al. Iodobenzamide binding to the rat dopamine D2 receptor in competition with haloperidol and endogenous dopamine--an in vivo imaging study with a dedicated small animalSPECT. Eur J Nucl Med Mol Imaging. 2005;32(11):1305-1310.

27. Hulley SB, Rosenman RH, Bawol RD, et al. Epidemiology as a guide to clinical decisions. The association between triglyceride and coronary heart disease. N Engl J Med. 1980;302:1383–1389.

28. William P, Castelli MD, Joseph T et al. HDL-cholesterol and other lipids in coronary heart disease the co-operative lipoprotein phenotyping study. Circulation. 1977;55: 767-772.
Original Article