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Haemostasis refers to the physiological process aimed at repairing vessel injury and preventing bleeding. It involves four interlinked stages culminating in the formation of a platelet–fibrin haemostatic plug that is eventually dissolved once the vessel heals. In contrast, arterial thrombosis is a pathological condition resulting from atheroma exposure, triggering the formation of a platelet-rich thrombus that may obstruct blood flow, leading to the clinical manifestations of ischaemic cardiovascular disease. The following review will provide a comprehensive overview of the finely regulated endogenous antithrombotic mechanisms responsible for maintaining the haemostatic balance and preventing intravascular thrombosis. Thereafter, it will further detail the different stages and mechanisms governing the intricate interplay between the vessel, platelets, and the coagulation cascade in haemostasis, highlighting the most recent advances in platelet biology and function, to further elucidate the differential traits and players contributing to pathological arterial thrombus growth. The review will also delve into the impact of emerging cardiovascular risk factors on tilting the haemostatic balance towards a pro-thrombotic state, thereby increasing the patient’s vulnerability to thrombotic events. Finally, it will underscore the importance of early screening for subclinical atherosclerosis through advanced imaging technologies capable of quantifying plaque burden and metabolic activity since they may set the stage for an increased thrombotic risk. Implementing proactive interventions to halt atherosclerosis progression or inducing its regression at early stages is crucial for preserving haemostasis and reducing the likelihood of ischaemic atherothrombotic disease.
Haemostasis refers to the physiological process aimed at repairing vessel injury and preventing bleeding. It involves four interlinked stages culminating in the formation of a platelet–fibrin haemostatic plug that is eventually dissolved once the vessel heals. In contrast, arterial thrombosis is a pathological condition resulting from atheroma exposure, triggering the formation of a platelet-rich thrombus that may obstruct blood flow, leading to the clinical manifestations of ischaemic cardiovascular disease. The following review will provide a comprehensive overview of the finely regulated endogenous antithrombotic mechanisms responsible for maintaining the haemostatic balance and preventing intravascular thrombosis. Thereafter, it will further detail the different stages and mechanisms governing the intricate interplay between the vessel, platelets, and the coagulation cascade in haemostasis, highlighting the most recent advances in platelet biology and function, to further elucidate the differential traits and players contributing to pathological arterial thrombus growth. The review will also delve into the impact of emerging cardiovascular risk factors on tilting the haemostatic balance towards a pro-thrombotic state, thereby increasing the patient’s vulnerability to thrombotic events. Finally, it will underscore the importance of early screening for subclinical atherosclerosis through advanced imaging technologies capable of quantifying plaque burden and metabolic activity since they may set the stage for an increased thrombotic risk. Implementing proactive interventions to halt atherosclerosis progression or inducing its regression at early stages is crucial for preserving haemostasis and reducing the likelihood of ischaemic atherothrombotic disease.
Introduction. Defining a treatment strategy for patients with stable coronary heart disease will require the development of personalized criteria, among which the assessment of myocardial dyssynchrony is considered promising. The aim of the study was to evaluate the effect of revascularization of coronary arteries on indicators of mechanical myocardial dyssynchrony in patients with stable coronary heart disease. Materials and methods. The study included 121 patients with coronary heart disease, who were assessed for mechanical myocardial dyssynchrony before and 2 weeks after revascularization. The main group included 48 patients with myocardial dyssynchrony, and the comparison group included 73 patients without myocardial dyssynchrony. Complete occlusion and lesions of 3 coronary arteries were found more often in the group with myocardial dyssynchrony, and the main group also had a higher SYNTAX SCORE. The results. Mechanical dyssynchrony of the myocardium was found in 39% of patients with coronary heart disease. Before revascularization, a signifiant increase in SPWMD, APEI, IVMD, and a decrease in LVFT and LVET were found in the group of patients with myocardial dyssynchrony. After revascularization in the main group, in 9 patients out of 48 (18.7%), indicators of myocardial dyssynchrony returned to normal values. LVFT in the group of patients with myocardial dyssynchrony significantly increased, as well as left ventricular ejection time (LVET) (from 318.5±9.6 ms to 344.9±23.2 ms, p<0.01). Conclusions. After revascularization, the number of patients with myocardial dyssynchrony significantly decreased due to the improvement of interventricular and intraventricular dyssynchrony indicators. Key words: myocardial dyssynchrony, coronary heart disease, revascularization, coronary angiography, SYNTAX SCORE.
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