Aim. To analyze the effect of intramyocardial haemorrhage (IMH) on the structural and functional echocardiographic parameters of myocardium in patients with primary ST-segment elevation myocardial infarction (STEMI).Material and methods. The study included 60 patients with primary STEMI reperfused within 12 hours after symptom onset. On the second day after the event, all subjects underwent gadolinium-enhanced cardiac magnetic resonance imaging (MRI). IMH was visualized as T2-weighted hypointense areas. Subsequently, all patients underwent the standard echocardiography on the 7th day after MI.Results. IMH was revealed in 31 patients (51,6%). In 22 patients (70,9%), IMH was accompanied by microvascular obstruction (MVO). In the remaining 9 patients (29%), an isolated IMH phenomenon was visualized. Lower values of left ventricular ejection fraction (LVEF) and LV volume parameters were associated with a combination of MVO and IMH. At the same time, the indices of volumetric characteristics and LVEF in isolated IMH were the same as in the group without IMH and MVO. It was demonstrated that the IMH occupies 1% (1-3%) of the LV myocardium. Correlation analysis showed a moderate inverse correlation between the IMH area and LV contractile function: the larger the area, the lower the LVEF (R=-0,35; p=0,007).Conclusions. The analysis of the influence of different IMH phenotypes on the structural and functional echocardiographic parameters of myocardium in the short-term period after STEMI has shown that the combination of IMH with MVO and isolated IMH have different effects on LV contractile function. The combination of IMH with MVO is a predictor of a decrease in LVEF and increase of end-systolic volume (ESV), while an isolated IMH does not affect these parameters. Correlations between the IMH area and a decrease in LVEF, as well as an increase in ESV, have been demonstrated.

At a time of a wide use of coronary reperfusion for treatment of acute myocardial infarction, the microvascular phenomena significantly affecting the postinfarction state of the myocardium have been discovered. These phenomena include microvascular obstruction with a clinical presentation in the form of the no-reflow phenomenon and intramyocardial hemorrhage that strongly aggravate cardiac damage. The aim of this review was to analyze accumulated data on the prevalence, pathophysiology, diagnostic modalities, and approaches for prevention and treatment of microvascular injury.

By researches it is proved that the phenomenon of no-reflow is an independent predictor of remodeling of the left ventricle at the moment. Particular importance in formation of this phenomenon is the fragmentation of a thrombus with distal embolization of small vessels, which often arise as a complication of the percutaneous coronary intervention during the destruction of a thrombus. Attempts to prevent the development of microvascular obstruction led to the creation of delayed stenting.The Purpose:assessing the efficacy and safety of deferred stent implantation in patients with ST-segment elevation myocardial infarction and massive coronary thrombosis.Material and Methods.12 patients with STEMI are included in a research. In the course of emergency coronary angiography was performed a massive thrombosis of the infarct-related coronary artery was observed with TIMI 2–3 blood flow. The emergency stenting wasn’t carried out to these patients, but continued anti-thrombotic therapy within 24 hours. After one day, repeated the coronary angiography was performed and, according to the indications, performed stenting of residual stenosis.Results.Development of the phenomenon of no-reflow, deaths and coronary events due to reocclusion of the infarctrelated coronary artery at all patients wasn’t observed. Also, all patients had a positive angiographic result in the form of regurgitation of the thrombus as a result of repeated the coronary angiography.Conclusion.Two-stage revascularization with delayed-on-day stenting with massive thrombosis of the infarct-related coronary artery in patients with acute myocardial infarction combined with aggressive antithrombotic therapy may be use in clinical practice to reduce the risk of developing the no-reflow phenomenon.

The emergence of new COVID-19 infection aggravated the existing issues and gave rise to new challenges associated with the impact of viruses on the atherosclerotic process and development of cardiovascular complications. Atherosclerosis is a multifactorial disease and its progression is largely determined by dyslipidemia and chronic low-grade systemic vascular inflammation. There are a number of viruses known to be involved in maintaining the inflammatory state through the prolonged viral persistence and replication in the macrophages whose plasticity changes due to the infection. The viruses can trigger the pro-atherogenic cytokine response through the diverse macrophage-dependent mechanisms. There is lack of data regarding impact of viral infections on the monocyte/macrophage plasticity and possible control of inflammation in atherogenesis. It is still unclear whether the relationships between the viral diseases and atherosclerosis are causal or merely associative. In this review, we summarize and critically analyze the current state of knowledge regarding the virus-related mechanisms promoting atherosclerosis.