BAB V KESIMPULAN, IMPLIKASI, dan SARAN
A. Kesimpulan Berdasarkan hasil-hasil penelitian yang dilakukan maka dapat diambil kesimpulan sebagai berikut : 1.
Pemberian Telmisartan 40 mg maupun Valsartan 80 selama 5 hari dapat menurunkan kadar HsCRP pada pasien infark miokard akut.
2.
Pemberian Telmisartan 40 mg selama 5 hari lebih baik dibandingkan pemberian Valsartan 80 mg selama 5 hari dalam menurunkan kadar HsCRP pada pasien infark miokard akut.
3.
Pemberian Telmisartan 40 mg selama 5 hari lebih kuat dalam menurunkan kadar tekanan darah dibandingkan pemberian Valsartan 80 mg selama 5 hari pada pasien infark miokard akut.
B. Implikasi Hasil penelitian ini telah menunjukkan bahwa pemberian telmisartan maupun valsartan pada pasien infark miokard akut dapat menurunkan inflamasi dan penurunan tekanan darah terlihat dari adanya penurunan kadar HsCRP dan penurunan tekanan darah pada pasien infark miokard akut. Hasil penelitian ini memberikan nilai-nilai kebaruan meliputi strategi, perspektif, dan kondisi baru dalam terapi tambahan terhadap penatalaksanaan infark miokard akut, sehingga meningkatkan luaran yang lebih baik pada pasien infark miokard akut.
C. Saran 1.
Penelitian dilakukan pada multicenter dengan jumlah sampel yang lebih banyak akan menambah kekuatan penelitian.
2.
Penelitian lebih lanjut terhadap luaran klinis seperti terjadinya infark miokard akut berulang, gagal jantung, atau kematian, serta pengamatan yang
lebih
lama.
DAFTAR PUSTAKA Adukauskiene D, Čiginskienė A, Adukauskaitė A, et al. 2016. Clinical relevance of high sensitivity C-reactive protein in cardiology. Medicina, vol.52, hlm.1–10.
Anzai T, Yoshikawa T, Shiraki H, et al. 1997. C-reactive protein as a predictor of infarct expansion and cardiac rupture after a first Q-wave acute myocardial infarction. Circulation, vol.96, hlm. 778-784.
Badan Penelitian dan Pengembangan Kesehatan Kementerian Kesehatan RI. 2013. Riset Kesehatan Dasar 2013. Jakarta: Kementerian Kesehatan RI. Hlm. 90-3.
Benge CD and Muldowney J. 2012. The pharmacokinetics and pharmacodynamics of valsartan in the post-myocardial infarction population. Expert Opin. Drug Metab. Toxicol, vol.8, hlm. 1469-148.
Black HR, Bailey , Zappe D, et al. 2009. Valsartan More Than a Decade of Experience. Drugs, vol. 69, hlm. 2393-2414.
Calabro P, Golia E, TH Yeh E. 2012. Role of c-reactive protein in acute myocardial infarction and stroke: Possible therapeutic approaches. Current pharmaceutical biotechnology, vol.13, hlm.4-16.
Cleland JG, Torabi A, Khan NK. 2005. Epidemiology and management of heart failure and left ventricular systolic dysfunction in the aftermath of a myocardial infarction. Heart, vol.91, hlm. 7–13.
Cowan BR, Young AA, Anderson C, et al. 2009. Left ventricular mass and volume with telmisartan, ramipril, or combination in patients with previous atherosclerotic events or with diabetes mellitus (from the ONgoing Telmisartan Alone and in Combination With Ramipril Global Endpoint Trial [ONTARGET]). Am J Cardiol, vol. 104,hlm. 1484-489
Dandona P, Kumar V, Aljada A, et al. 2003. Angiotensin II receptor blocker valsartan suppresses reactive oxygen species generation in leukocytes, nuclear factor-kB, in mononuclear cells of normal subjects: evidence of an antiinflammatory action. J Clin Endocrinol Metab, vol. 88, hlm. 4496–4501.
Dandona P, Dhindsa S, Ghanim H et al. 2007. Angiotensin II and inflammation: the effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockade. Journal of Human Hypertension, vol. 21, hlm. 20–27.
Del Fiorentino A, Cianchetti S, Celiet A, et al. 2009. The effect of angiotensin receptor blockers on C-reactive protein and other circulating infl ammatory indices in man. Vascular Health and Risk Management; vol.5, hlm. 233–242.
Frangogiannis NG, Smith CW, Entman ML. 2002. The inflammatory response in myocardial infarction. Cardiovasc Res; vol.53, hlm. 31–47.
Kumar, A dan Cannon, CP. 2009. Acute coronary syndromes: Diagnosis and management. Mayo Clinic Proceedings, vol. 84, hlm. 917-38.
Libby, P. 2012. Current concepts of the pathogenesis of the acute coronary syndromes. Circulation. vol. 104, hlm. 365-72.
Loo, B dan Martin, J, 1999. A role for changes inplatelet production in the cause of acute coronary syndromes. Journal of the American College of Cardiology: Arteriosclerosis, vol 19, hlm. 672-9. Ludwig AF and Kintscher U. 2015. Metabolic Effects of AT2R Stimulation in Adipose Tissue. In The Protective Arm of the Renin Angiotensin System. (hlm. 119-122). London : Elsevier.
McMurray J, Solomon S, Pieper K et al. 2006. The Effect of Valsartan, Captopril, or Both on Atherosclerotic Events After Acute Myocardial Infarction. JAM Coll Cardiol, vol. 47, hlm. 726-33.
Melamed KH and Goldhaber SZ. 2014. Inflammation and myocardial infarction. Circulation, vol. 130, hlm. e334–36
Mendis S, Thygesen K, Kuulasmaa K, et al. 2011. World health organization definition of myocardial infarction: 2008–09 revision. International journal of epideamiology, vol. 40, hlm. 139-146.
O'gara, P. T., Kushner, F. G., Ascheim, D. D., et al. 2013. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation, vol.127, hlm. e362-425.
Porto I, Vito LD, Maria GL, et al. 2009. Comparison of the Effects of RaAMIpril Versus TelAMIsartan on High-Sensitivity C-Reactive Protein and Endothelial Progenitor Cells After Acute Coronary Syndrome. J Am Coll Cardiol, vol.103, hlm. 1500 –1505.
Sastroasmoro S dan Ismael S, 1995. Dasar-Dasar Metodologi Penelitian Klinis. Jakarta, Binarupa Aksara.
Singh A, Jha KK, Mittal A, et al. 2013. A Review on: Telmisartan. J Sci & Inn Res, vol.2, hlm. 160-175. Sharif D, Hammoud M, Rasslan AS, et al. 2015. Very Early C-Reactive Protein Levels afterAcute Myocardial Infarction Predict Early Outcome and Late Prognosis. International Journal of Clinical Medicine, vol.6, hlm. 547-553.
Steg, P. G., James, S. K., Atar, et al. 2012. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J, vol.33, hlm. 2569-619.
Suleiman M, Khatib R, Agmon Y, et al. 2006. Early inflammation and risk of long-term development of heart failure and mortality in survivors of acute myocardial infarction predictive role of C-reactive protein. J Am Coll Cardiol, vol. 47, hlm. 962-968
Thygesen, K., Alpert, J. S., Jaffe, A. S., et al. 2012. Third universal definition of myocardial infarction. Circulation, vol. 126, hal. 2020-35.
Uehara K, Nomura M, Ozaki Y, et al. 2003. High-sensitivity C-reactive protein and left ventricular remodeling in patients with acute myocardial infarction. Heart Vessels,vol.18, hlm. 67–74.
Velazquez EJ, Francis GS, Armstrong PW, et al. 2004. An international perspective on heart failure and left ventricular systolic dysfunction complicating myocardial infarction: the VALLIANT Registry. Eur Heart J, vol.25, hlm. 1911–9.
Verdecchia P. 2005. Pre-clinical and clinical experience of telmisartan in cardiac remodelling. J Int Med Res, vol. 33, hlm. 12A-20A. Vito LD, Cautilli G, Vergallo, R et al. 2011. Telmisartan for the Prevention of Acute Coronary Syndrome in ACE-Inhibitor-Intolerant Patients. Int J Clin Rev, vol.12, hlm. 6.
Weir RA, McMurray JJ, Velazquez EJ. 2006. Epidemiology of heart failure and left ventricular systolic dysfunction after acute myocardial infarction: prevalence, clinical characteristics, and prognostic importance. Am J Cardiol, vol.97, hlm.13F–25F.
Yasunari K, Maeda K, Watanabe T, et al. 2004. Comparative effects of valsartan versus amlodipine on left ventricular mass and reactive oxygen species formation by monocytes
in hypertensive patients with left ventricular hypertrophy. J Am Coll Cardiol, vol. 43, hlm. 2116–2123.
Zou Z, Xi GL, Yuan HB, et al. 2009. Telmisartan versus angiotension- converting enzyme inhibitors in the treatment of hypertension: a meta-analysis of randomized controlled trials. J Hum Hypertens, vol. 23, hlm. 339–349.
