THE ROLE OF ECHOCARDIOGRAPHY IN THE DIAGNOSIS OF CORONARY HEART DISEASE AND MONITORING OF TRIMETAZIDIN THERAPY IN PATIENTS WITH CORONARY HEART DISEASE
Keywords:
Coronary heart disease, myocardial infarction, atherosclerosis, echocardiography, trimetazidinAbstract
Coronary heart disease (CHD) is one of the most common diseases with high mortality worldwide. Therefore, in order to improve the quality and increase the life expectancy of mankind, it is important to improve the methods of diagnosis, treatment and prevention of coronary heart disease. The purpose of our study is to conduct a diagnostic analysis of the heart of patients who have suffered a myocardial infarction using EchoCG and to identify the structural and functional features of coronary heart disease. In addition, using these features to analyze the therapeutic efficacy of trimetazidin after treatment of these patients. We found that after treatment of patients with coronary artery disease with trimetazidin, the results of EchoCG showed mainly positive changes in markers associated with functional features of the heart, and to a lesser extent we found structural changes.
References
Walker C.A., Spinale F.G. The structure and function of the cardiac myocyte: A review of fundamental concepts. J. Thorac. Cardiovasc. Surg. 1999;118:375–382. doi: 10.1016/S0022-5223(99)70233-3.
Pittman R.N. Regulation of Tissue Oxygenation. Morgan & Claypool Life Sciences; San Rafael, CA, USA: 2011. Integrated Systems Physiology: From Molecule to Function to Disease. [Google Scholar]
Ribeiro A.J.S., Ang Y.-S., Fu J.-D., Rivas R.N., Mohamed T.M.A., Higgs G.C., Srivastava D., Pruitt B.L. Contractility of single cardiomyocytes differentiated from pluripotent stem cells depends on physiological shape and substrate stiffness. Proc. Natl. Acad. Sci. USA. 2015;112:12705–12710. doi: 10.1073/pnas.1508073112.
Langer G.A., Frank J.S., Rich T.L., Orner F.B. Calcium exchange, structure, and function in cultured adult myocardial cells. Am. J. Physiol. 1987;252:H314–H324. doi: 10.1152/ajpheart.1987.252.2.H314.
Langer G.A., Frank J.S., Philipson K.D. Ultrastructure and calcium exchange of the sarcolemma, sarcoplasmic reticulum and mitochondria of the myocardium. Pharmacol. Ther. 1982;16:331–376. doi: 10.1016/0163-7258(82)90006-7.
McCain M.L., Parker K.K. Mechanotransduction: The role of mechanical stress, myocyte shape, and cytoskeletal architecture on cardiac function. Pflüg. Arch.- Eur. J. Physiol. 2011;462:89–104. doi: 10.1007/s00424-011-0951-4.
Powers J.D., Yuan C.-C., McCabe K.J., Murray J.D., Childers M.C., Flint G.V., Moussavi-Harami F., Mohran S., Castillo R., Zuzek C., et al. Cardiac myosin activation with 2-deoxy-ATP via increased electrostatic interactions with actin. Proc. Natl. Acad. Sci. USA. 2019;116:11502–11507. doi: 10.1073/pnas.1905028116.
Moran A., Forouzanfar M., Sampson U., Chugh S., Feigin V., Mensah G. The epidemiology of cardiovascular diseases in sub-Saharan Africa: The Global Burden of Diseases, Injuries and Risk Factors 2010 Study. Prog. Cardiovasc. Dis. 2013;56:234–239. doi: 10.1016/j.pcad.2013.09.019.
Lauer M.S. Advancing cardiovascular research. Chest. 2012;141:500–505. doi: 10.1378/chest.11-2521.
Institute of Medicine (US) Committee on Social Security Cardiovascular Disability Criteria. Cardiovascular Disability: Updating the Social Security Listings. Washington (DC): National Academies Press (US); 2010. 7, Ischemic Heart Disease. Available from: https://www.ncbi.nlm.nih.gov/books/NBK209964/
Arslan F, de Kleijn DP, Pasterkamp G. Innate immune signaling in cardiac ischemia. Nat Rev Cardiol 8: 292-300, 2011.
Jennings RB, Steenbergen C Jr. Nucleotide metabolism and cellular damage in myocardial ischemia. Annu Rev Physiol 47: 727-749, 1985.
Frangogiannis NG. Pathophysiology of Myocardial Infarction. Compr Physiol. 2015 Sep 20;5(4):1841-75. doi: 10.1002/cphy.c150006. PMID: 26426469.
Bialik S, Geenen DL, Sasson IE, Cheng R, Horner JW, Evans SM, Lord EM, Koch CJ, Kitsis RN. Myocyte apoptosis during acute myocardial infarction in the mouse localizes to hypoxic regions but occurs independently of p53. J Clin Invest 100: 1363-1372, 1997.
Kajstura J, Cheng W, Reiss K, Clark WA, Sonnenblick EH, Krajewski S, Reed JC, Olivetti G, Anversa P. Apoptotic and necrotic myocyte cell deaths are independent contributing variables of infarct size in rats. Lab Invest 74: 86-107, 1996.
Gottlieb RA. Cell death pathways in acute ischemia/reperfusion injury. J Cardiovasc Pharmacol Ther 16: 233-238, 2011.
Gottlieb RA, Burleson KO, Kloner RA, Babior BM, Engler RL. Reperfusion injury induces apoptosis in rabbit cardiomyocytes. J Clin Invest 94: 1621-1628, 1994.
Sam F, Sawyer DB, Chang DL, Eberli FR, Ngoy S, Jain M, Amin J, Apstein CS, Colucci WS. Progressive left ventricular remodeling and apoptosis late after myocardial infarction in mouse heart. Am J Physiol Heart Circ Physiol 279: H422-H428, 2000.
Luo K., Long H., Xu B. Reduced apoptosis after acute myocardial infarction by simvastatin. Cell Biochem. Biophys. 2015;71:735–740. doi: 10.1007/s12013-014-0257-1. [PubMed] [CrossRef] [Google Scholar]
Hung J., Teng T.-H.K., Finn J., Knuiman M., Briffa T., Stewart S., Sanfilippo F.M., Ridout S., Hobbs M. Trends from 1996 to 2007 in incidence and mortality outcomes of heart failure after acute myocardial infarction: A population-based study of 20,812 patients with first acute myocardial infarction in Western Australia. J. Am. Heart Assoc. 2013;2:e000172. doi: 10.1161/JAHA.113.000172.
Frangogiannis NG. Pathophysiology of Myocardial Infarction. Compr Physiol. 2015 Sep 20;5(4):1841-75. doi: 10.1002/cphy.c150006. PMID: 26426469. Dézsi CA. Trimetazidine in Practice: Review of the Clinical and Experimental Evidence. Am J Ther. 2016 May-Jun;23(3):e871-9. doi: 10.1097/MJT.0000000000000180. PMID: 25756467; PMCID: PMC4856171.
Chrusciel P, Rysz J, Banach M. Defining the role of trimetazidine in the treatment of cardiovascular disorders: some insights on its role in heart failure and peripheral artery disease. Drugs. 2014 Jun;74(9):971-80. doi: 10.1007/s40265-014-0233-5. PMID: 24902800; PMCID: PMC4061463.