The inflammatory response in patients with acute myocardial infarction with st segment elevation during the development of adaptive and pathological remodeling of the myocardium: Summary of the doctoral thesis in Medical Science: 321.03 - Cardiology

Abstract

Actuality. ST-elevation acute myocardial infarction (STEMI) is the most severe form of myocardial infarction associated with increased morbidity and mortality. Primary mechanical revascularization of the myocardium by coronary angioplasty in patients with STEMI performed in the first 12 hours after the onset of infarction has become the therapeutic option of choice, leading according to data from various meta-analyzes, to the decrease of in hospital mortality and in time distance mortality, as well [1,2]. However, STEMI remains a current and intricate problem of cardiology, dictated by the unstable clinical evolution in the post-infarction period caused by exacerbation of heart failure and the high incidence of major cardiovascular events (MACE), such as repeated acute myocardial infarction (MI), unstable angina, arrhythmias or stroke. The results of several studies demonstrate the evolution of MACE over a post-infarction period of 1-10 years at rates of 4.2-51% [3,4]. One of the determining factors of post-infarction MACE risk in patients with STEMI is the quality of post-infarction myocardial remodeling. The remodeling involves a set of structural and geometric changes of the heart, which are triggered by cardiomyocyte necrosis and end on average after 4-6 months from the time of revascularization [5,6]. LV dilatation at the end of post-infarction remodeling of the myocardium is the echocardiographic predictor of the pathological pattern of remodeling and is manifested by an increase of > 20% in indices, which characterizes the phenomenon of dilation, compared to admission parameters: end-diastolic volume and end-diastolic pressure of LV [7,8]. Assessment of the factors that contribute the development of PMR or AMR is important for the reinforcement of the algorithm for the postinfarction prognosis predictors in patients with STEMI favorable in the optimization of longterm therapeutic management [9]. The hypothesis of the study is based on the evidence of the presence of the inflammatory response triggered by myocardial necrosis in the first hours after the onset of ischemic injury. Inflammation defines the extension of the necrotic area. On the other hand, inflammation triggers and governs the process of removing dead cells by phagocytosis, as well as the repair of damaged myocardium by stimulating collagen synthesis through the action of cytokines (primarily interleukins and growth factors) and activation of cardiomyocyte hypertrophy genes [10, 11]. Although the role of inflammation is certified in the genesis of coronary heart disease and heart failure, as well as in the pathogenesis of ischemia-reperfusion impact [12], studies evaluating the link between the inflammatory response and the pattern of post-myocardial remodeling in patients with STEMI with the purpose of assessing the ratio between the dynamic of pro- and antiinflammatory markers especially in the acute phase of infarction were not realized. At the same time, the correlation between the type of change of inflammatory markers in the acute phase and the markers of fibrillar collagen type III and type I turnover at the distance of 1- and 3-months post-infarction were not determined. Although the pathogenesis of post-infarction HF is studied over several decades, some conceptual issues such as: the mechanism of compensation and decompensation of the heart in hemodynamic effort, the impact of ischemia-reperfusion, the peculiarities of myocardial inotropism to the action of neuroendocrine factors and the coronary phenomenon, the plausibility of the functional benefit in attenuating the inflammatory response and / or potentiating the action of anti-inflammatory markers, remain unclear. 5 Some answers can be found through experimental research, using in vitro isolated heart perfusion models, which allow the reproduction of different types of effort with volume, resistance, or ischemic impact. More other, particularities of the functional benefit of the inflammatory response modulation, based on the principles of anti-cytokine treatment, could be studied. [...]