Effect of statins in cardiovascular diseases: a prospective observational study
Abstract
Cardiovascular diseases also called heart diseases which include a group of disorders of the heart and blood vessels. Cardiovascular diseases (CVDs) are the leading cause of death globally. The study was aimed to explore the effect of statins in cardiovascular diseases- chronic stable angina, acute coronary syndrome and in post PTCA patients by monitoring the lipid profile. The study was conducted in the Cardiology department in the Queen’s NRI Hospital. This is a prospective, non-interventional and observational study and 100 population attending Cardiology OPD & IPD in Queen’s NRI Hospital were recruited into the study with their informed consent. This research reported that the cardiovascular diseases in male with prevalence (63%) out of 100 patients and female with prevalence (37%) out of 100 and the prevalence of CSA is 15%, post PTCA is 21%, and ACS is 64% from a total estimation of the study. By using Paired T test the mean difference, estimated variance, standard error of difference, test statistic, test critical are calculated and the comparison between test statistic and critical value. The test statistic is greater than critical t value the alternate hypothesis is accepted by taking the level of significance α = 0.05 and p value less than 0.05 and there is a significant change in lipid profile parameters by using the statins and hence the study is statistically significant with positive outcome.
Downloads
References
2. Crisby M, Nordin-Fredriksson G, Shah PK, Yano J, Zhu J, Nilsson J. Pravastatin treatment increases collagen content and decreases lipid content, inflammation, metalloproteinases, and cell death in human carotid plaques: implications for plaque stabilization. Circulation. 2001; 103: 926–933.
3. Matsuda M, Korn BS, Hammer RE, Moon YA, Komuro R, Horton JD, Goldstein JL, Brown MS, Shimomura I. SREBP cleavage-activating protein (SCAP) is required for increased lipid synthesis in liver induced by cholesterol deprivation and insulin elevation. Genes Dev. 2001; 15: 1206–1216.
4. Chen L, Chester MR, Crook R, Kaski JC. Differential progression of complex culprit stenoses in patients with stable and unstable angina pectoris. J Am Coll Cardiol. 1996; 28: 597–603.
5. Libby P. What have we learned about the biology of atherosclerosis?: the role of inflammation. Am J Cardiol. 2001; 88: 3–6.
6. Aikawa M, Rabkin E, Voglic SJ, Shing H, Nagai R, Schoen FJ, Libby P. Lipid lowering promotes accumulation of mature smooth muscle cells expressing smooth muscle myosin heavy chain isoforms in rabbit atheroma. Circ Res. 1998; 83: 1015–1026.
7. Weitz-Schmidt G, Welzenbach K, Brinkmann V, Kamata T, Kallen J, Bruns C, Cottens S, Takada Y, Hommel U. Statins selectively inhibit leukocyte function antigen-1 by binding to a novel regulatory integrin site. Nat Med. 2001; 7: 687–692.
8. Ridker PM, Rifai N, Pfeffer MA, Sacks F, Braunwald E. Long-term effects of pravastatin on plasma concentration of C-reactive protein: the Cholesterol and Recurrent Events (CARE) Investigators. Circulation. 1999; 100: 230–235.
9. Guerin M, Lassel TS, Le Goff W, Farnier M, Chapman MJ. Action of atorvastatin in combined hyperlipidemia: preferential reduction of cholesteryl ester transfer from HDL to VLDL1 particles. Arterioscler Thromb Vasc Biol. 2000; 20: 189–197.
10. Colli S, Eligini S, Lalli M, Camera M, Paoletti R, Tremoli E. Vastatins inhibit tissue factor in cultured human macrophages: a novel mechanism of protection against atherothrombosis. Arterioscler Thromb Vasc Biol. 1997; 17: 265–272.
11. Friedman GD, Cutter GR, Donahue RP, Hughes GH, Hulley SB, Jacobs DR Jr, Liu K, Savage PJ. CARDIA: study design, recruitment, and some characteristics of the examined subjects. J Clin Epidemiol. 1988; 41: 1105–1116.
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
.