APPROACHES TO MORPHOMETRIC EVALUATION OF CARDIAC REMODELING AFTER MYOCARDIAL INFARCTION

Along with the functional, morphological methods at the forefront in evaluating the effectiveness of impacts that weaken the severity of irreversible ischemic damage to the myocardium. Histological examination using hematoxylin-eosin and classical connective tissue staining — are routine methods in the assessment of myocardial remodeling after infarction. However, due to the limited use criteria for macroscopic evaluation, the possibility of these methods are not fully disclosed.

This article describes the main approaches to the evaluation of macroscopic parameters of the scar size and heart remodeling, a comparative analysis of known criteria for morphometric evaluation of the native heart and the hearts with advanced of post-infarction chronic heart failure.

For assessment of scar size used parameters such as percentage (%) of scar area with respect to left ventricle area, scar length in % of epiand endocardial ventricular circumference, left ventricular wall thickness in the scar area. Intensity of remodeling was assessed by measuring the thickness of the interventricular septum, calculating of the LV dilation index (%) with and without consideration the LV wall thickness and index of hypertrophy.

Comparative analysis of the informativeness of different parameters can be recommended for morphometric assessment of the transmural scar size and LVremodeling, scar length as a percentage of epiand endocardial circumference of the LV, LV dilatation index (%) excluding the thickness of the ventricular wall and hypertrophy index as the main criteria for assessment.

1. Roger VL. Epidemiology of myocardial infarction. Med Clin North Am. 2007; 91(4): 537-ix.

2. Takagawa J, Zhang Y, Wong ML et al. Myocardial infarct size measurement in the mouse chronic infarction model: comparison of areaand length-based approaches. J Appl Physiol. 2007; 102(6): 2104-2111.

3. Karpov AA, Dracheva AV, Pituchina NN et al. Rat model of post-infarct heart failure by left coronary artery occlusion: technical aspects, functional and morphological assessment. Biomedicina=Biomedicine. 2014; 1(3): 32-48. In Russian. [Карпов АА, Драчева АВ, Питухина НН и соавт. Моделирование постинфарктной сердечной недостаточности путем окклюзии левой коронарной артерии у крыс: Техника и методы морфофункциональной оценки. Биомедицина. 2014; 1(3): 32-48].

4. Karpov AA, Uspenskaya YK, Minasian SM et al. The effect of bone marrowand adipose tissue-derived mesenchymal stem cell transplantation on myocardial remodelling in the rat model of ischaemic heart failure. Int J Exp Pathol. 2013; 94(3): 169-177.

5. Merkulov GA. Pathology techniques. Leningrad: Megiz, 1961. p.343. In Russian. [Меркулов ГА. Курс патологогистологической техники. Л.: Медгиз, 1961. с. 343].

6. Fatkhudinov T, Bolshakova G, Arutyunyan I et al. Bone marrow-derived multipotent stromal cells promote myocardial fibrosis and reverse remodeling of the left ventricle. Stem Cells Int. 2015; 2015: 746873.

7. Alhaddad IA, Tkaczevski L, Siddiqui F et al. Aspirin enhances the benefits of late reperfusion on infarct shape. A possible mechanism of the beneficial effects of aspirin on survival after acute myocardial infarction. Circulation. 1995; 91(11): 2819-2823.

8. Shao ZQ, Takaji K, Katayama Y et al. Effects of intramyocardial administration of slow-release basic fibroblast growth factor on angiogenesis and ventricular remodeling in a rat infarct model. Circ J. 2006; 70(4): 471-477.

9. Hochman JS, Choo H. Limitation of myocardial infarct expansion by reperfusion independent of myocardial salvage. Circulation. 1987; 75(1): 299-306.

10. Jain M, Liao R, Podesser BK et al. Influence of gender on the response to hemodynamic overload after myocardial infarction. Am J Physiol Heart Circ Physiol. 2002; 283(6): 2544-2550.

11. Fishbein MC, Lei LQ, Rubin SA. Long-term propranolol administration alters myocyte and ventricular geometry in rat hearts with and without infarction. Circulation. 1988; 78(2): 369-375.

12. Villarreal FJ, Hong D, Omens J. Nicotine-modified postinfarction left ventricular remodeling. Am J Physiol. 1999; 276(3): 1103-1106.

13. Bauersachs J, Galuppo P, Fraccarollo D et al. Improvement of left ventricular remodeling and function by hydroxymethylglutaryl coenzyme a reductase inhibition with cerivastatin in rats with heart failure after myocardial infarction. Circulation. 2001; 104(9): 982-985.

14. Levit RD, Landazuri N, Phelps EA et al. Cellular encapsulation enhances cardiac repair. J Am Heart Assoc. 2013; 2(5): e000367.

15. Dmitriev YV, Karpov AA, Dracheva AV et al. Cardioproteсtive Effects of Necrostatin-7 in the Rat Model of Permanent Coronary Occlusion. Ross Fiziol Zh Im I M Sechenova= Neuroscience and Behavioral Physiology — Sechenov Physiology Journal. 2015; 101(4): 408-414. In Russian. [Дмитриев Ю.В., Карпов А.А., Драчева А.В., Минасян С.М., Чефу С.Г., Васина Л.В., Демченко Е.А., Галагудза М.М. Кардиопротективные эффекты некростатина-7 на модели хронического инфаркта миокарда у крыс. Российский Физиологический Журнал имени И.М. Сеченова. 2015; 101(4): 408-414].

16. Virag JI, Murry CE. Myofibroblast and endothelial cell proliferation during murine myocardial infarct repair. Am J Pathol. 2003; 163(6): 2433-2434

17. Paiva SA, Matsubara LS, Matsubara BB et al. Retinoic acid supplementation attenuates ventricular remodeling after myocardial infarction in rats. J Nutr. 2005; 135(10): 2326-2328.

18. Pfeffer MA, Pfeffer JM, Steinberg C et al. Survival after an experimental myocardial infarction: beneficial effects of long-term therapy with captopril. Circulation. 1985; 72(2): 406-412.