Aortic valve stenosis (AS) is a common heart valve disease in the elderly population, and its pathogenesis remains an interesting area of research. The degeneration of the aortic valve leaflets gradually progresses to valve sclerosis. The advanced phase is marked by the presence of extracellular fibrosis and calcification. Turbulent, accelerated blood flow generated by the stenotic valve causes excessive damage to the aortic wall. Elevated shear stress due to AS leads to the degradation of high-molecular weight multimers of von Willebrand factor, which may involve bleeding in the mucosal tissues. Conversely, elevated shear stress has been associated with the release of thrombin and the activation of platelets, even in individuals with acquired von Willebrand syndrome. Moreover, turbulent blood flow in the aorta may activate the endothelium and promote platelet adhesion and activation on the aortic valve surface. Platelets release a wide range of mediators, including lysophosphatidic acid, which have pro-osteogenic effects in AS. All of these interactions result in blood coagulation, fibrinolysis, and the hemostatic process. This review summarizes the current knowledge on high shear stress-induced hemostatic disorders, the influence of AS on platelets and antiplatelet therapy.

Background Speckle tracking echocardiography (STE) is based on tracing of pixel groups in grayness scale for the quantitative measurement of myocardium strain and myocardium strain rate. Recent data suggest that evaluation of STE could be a tool for myocardial function assessment similar to MRI. Aim To assess the predictive value of STE for the evaluation of infarct size in patients with anterior ST-elevation myocardial infarction (STEMI). Materials and methods We enrolled 39 patients with the first anterior wall STEMI (mean age 59±10 years, 29 men). All patients were treated with a primary percutaneous coronary intervention, and the time from the symptom onset to reperfusion was 298±195 min. Left ventricular ejection fraction assessed in three-dimensional echocardiography was 47±9%. On the day of discharge, STE was performed to determine the average global value of peak longitudinal strain (GLS) of 16 myocardial segments. The average value of the peak longitudinal strain for nine segments supplied by the left anterior descending artery anterior wall global longitudinal strain was assessed separately. Infarct size was assessed 3 months after STEMI by MRI using late gadolinium enhancement, and a large infarct was defined as at least 20% left ventricle myocardium covered by the scar. Results According to the results of MRI, we defined two groups: 22 patients with a large infarct (≥20%, group A) and 17 patients with a small infarct (<20%, group B). There were no differences between both groups in the demographics and cardiovascular risk factors. There was a significant correlation between GLS and the degree of myocardium injury assessed by MRI (r=0.62, P=0.001). The correlation was higher for anterior wall global longitudinal strain (r=0.68, P=0.001). With the receiver operating characteristic curve, the cut-off point for GLS was calculated (−12.3), which defined a large infarct with 82% sensitivity and 87% specificity (area under the curve=83). For segments supplied by the left anterior descending artery, the cut-off value for the prediction of a large infarct was −11.5 (sensitivity 90%, specificity 73%, area under the curve=84). Conclusion STE seems to be a very promising tool in the prediction of infarct size in patients with anterior STEMI.

We sought to determine the frequency of left ventricular remodeling in the 6-month follow-up after anterior ST elevation myocardial infarction and the value of quantitative parameters of perfusion contrast echocardiography for prognosis of left ventricular remodeling against other established risk. A total of 60 patients with anterior ST elevation myocardial infarction treated by primary percutaneous intervention were examined. In 28 patients, thromboaspiration was performed before stent implantation with Driver catheter. Before and after successful angioplasty, perfusion in myocardial blush grade (MBG) scale was assessed. Various electrocardiogram parameters were analyzed. Resting perfusion with myocardial contrast echocardiography was performed. Logistic regression has permitted one to conclude that higher value of MBG, higher left ventricular ejection fraction at discharge, and higher value of parameter A at quantitative echocardiography in dysfunctional segments were prognostic for lack of remodeling over 6 months. The receiver operating characteristics curves for parameters of quantitative perfusion echocardiography (A, β, A×β) allowed us to conclude that value A>1.96 dB, value β>0.155 s, and value A×β>0.57 dB/s are optimal cut-off points prognostic for remodeling. Area under the curve was 0.8 for A and 0.85 for β. The best predictors of remodeling in 6 months' observation have appeared to be lower left ventricular ejection fraction at discharge, poorer perfusion assessed angiographically (MBG scale), and the rate of signal intensity increase reflecting the mean bubble velocity of the myocardium by contrast as assessed by contrast echocardiography. Quantitative perfusion angiography independently has high predictive value for the development of remodeling in long-term follow-up.

Background: The aim of the study was to describe a series of acute coronary syndrome (ACS) patients in whom anomalous origin of culprit coronary artery (AOCCA) was diagnosed. Percutaneous coronary interventions (PCI) in AOCCA are performed very infrequently. Methods: Electronic databases from three high-volume tertiary cardiac centers were retrospectively searched for the presence of AOCCA in ACS. Results: Different types of AOCCA in ACS were identified in 20 patients. The most frequent AOCCA was left circumflex coronary artery (LCx) originating from right coronary artery (RCA) or directly from the right coronary sinus (RCS), n = 13, followed by high/atypical RCA, n = 3, left coronary artery (LCA) originating from RCS (n = 3) with either RCA-AOCCA (n = 1) or left anterior descending coronary artery (LAD)-AOCCA (n = 1) or RCA originating from left sinus of Valsalva, (n = 1), LAD originating from RCA (n = 1). In 1 ST-segment elevation myocardial infarction (STEMI)-patient RCA-AOCCA cannulation was unsuccessful, in 1 non-STEMI-patient AOCCA was missed, 1 ACS- -patient was treated surgically and 1 ACS-patient was treated conservatively (both patients with non- STEMI). In the remaining patients PCI was successfully performed. Conclusions: The most frequently encountered AOCCA is LCx branching-off from RCA. AOCCA may either be difficult to cannulate and PCI aborted even in STEMI, or missed, especially when the intermediate branch from LCA is mimicking proper LCx. Background: The aim of the study was to describe a series of acute coronary syndrome (ACS) patients in whom anomalous origin of culprit coronary artery (AOCCA) was diagnosed. Percutaneous coronary interventions (PCI) in AOCCA are performed very infrequently. Methods: Electronic databases from three high-volume tertiary cardiac centers were retrospectively searched for the presence of AOCCA in ACS. Results: Different types of AOCCA in ACS were identified in 20 patients. The most frequent AOCCA was left circumflex coronary artery (LCx) originating from right coronary artery (RCA) or directly from the right coronary sinus (RCS), n = 13, followed by high/atypical RCA, n = 3, left coronary artery (LCA) originating from RCS (n = 3) with either RCA-AOCCA (n = 1) or left anterior descending coronary artery (LAD)-AOCCA (n = 1) or RCA originating from left sinus of Valsalva, (n = 1), LAD originating from RCA (n = 1). In 1 ST-segment elevation myocardial infarction (STEMI)-patient RCA-AOCCA cannulation was unsuccessful, in 1 non-STEMI-patient AOCCA was missed, 1 ACS- -patient was treated surgically and 1 ACS-patient was treated conservatively (both patients with non- STEMI). In the remaining patients PCI was successfully performed. Conclusions: The most frequently encountered AOCCA is LCx branching-off from RCA. AOCCA may either be difficult to cannulate and PCI aborted even in STEMI, or missed, especially when the intermediate branch from LCA is mimicking proper LCx.