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Background: Multiple risk factors for coronary artery disease have been identified without answering one of the leading questions related to the extent of the involvement of the epicardial arteries. Trace elements are involved in various stages of atherosclerotic lesion formation and may play a significant role in the advancement of coronary artery disease. Methods: A total of 157 (92 (59%) men and 65 (41%) women) patients with a median age of 71 (65–75) years presenting with chronic coronary syndrome were enrolled in the prospective single-center analysis. The coronary angiography results were compared with the concentration of trace elements in scalp hair. Results: Through Spearman analysis, a positive correlation between the number of diseased coronary arteries and hair trace element concentration was found for sodium (r = 0.198, p = 0.013), vanadium (r = 0.164, p = 0.040), chromium (r = 0.242, p = 0.002), and nickel (r = 0.176, p = 0.026). A negative relationship was noted between magnesium (r = −0.237, p = 0.003) and calcium (r = −0.217, p = 0.007) and the extent of epicardial lesions. Conclusions: Scalp hair trace element analysis indicates the possible modulatory role of trace elements in advancing coronary artery disease. Since a significant correlation with one- and two-vessel but not with three-vessel disease was noted, it might be considered an "all or nothing" phenomenon. A positive correlation between the number of diseased coronary arteries and sodium, vanadium, chromium, and nickel and an inverse correlation with magnesium and calcium were noted. The presented analysis is hypothesis-generating, and further studies are necessary to corroborate the results from a clinical perspective. [ABSTRACT FROM AUTHOR]

Coronary artery aneurysm or ectasia (CAAE) is a term that includes both coronary artery ectasia (CAE) and coronary artery aneurysm (CAA), despite distinct phenotypes and definitions. This anomaly can be found in 0.15–5.3% of coronary angiography. CAE is a diffuse dilatation of the coronary artery at least 1.5 times wider than the diameter of the normal coronary artery in a patient with a length of over 20 mm or greater than one-third of the vessel. CAE can be further subdivided into diffuse and focal dilations by the number and the length of the dilated vessels. Histologically, it presents with extensive destruction of musculoelastic elements, marked degradation of collagen and elastic fibers, and disruption of the elastic lamina. Conversely, CAA is a focal lesion manifesting as focal dilatation, which can be fusiform (if the longitudinal diameter is greater than the transverse) or saccular (if the longitudinal diameter is smaller than the transverse). Giant CAA is defined as a 4-fold enlargement of the vessel diameter and is observed in only 0.02% of patients after coronary. An aneurysmal lesion can be either single or multiple. It can be either a congenital or acquired phenomenon. The pathophysiological mechanisms responsible for the formation of CAAE are not well understood. Atherosclerosis is the most common etiology of CAAE in adults, while Kawasaki disease is the most common in children. Other etiological factors include systemic connective tissue diseases, infectious diseases, vasculitis, congenital anomalies, genetic factors, and idiopathic CAA. Invasive assessment of CAAE is based on coronary angiography. Coronary computed tomography (CT) is a noninvasive method that enables accurate evaluation of aneurysm size and location. The most common complications are coronary spasm, local thrombosis, distal embolization, coronary artery rupture, and compression of adjacent structures by giant coronary aneurysms. The approach to each patient with CAAE should depend on the severity of symptoms, anatomical structure, size, and location of the aneurysm. Treatment methods should be carefully considered to avoid possible complications of CAAE. Simultaneously, we should not unnecessarily expose the patient to the risk of intervention or surgical treatment. Patients can be offered conservative or invasive treatment. However, there are still numerous controversies and ambiguities regarding the etiology, prognosis, and treatment of patients with coronary artery aneurysms. This study summarizes the current knowledge about this disease's etiology, pathogenesis, and management. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) are currently investigated as crucial regulatory factors which may serve as a potential therapeutic target. Reports on the role of miRNA in patients with coronary artery aneurysmal disease (CAAD) are limited. The present analysis aims to confirm the differences in the expression of previously preselected miRNAs in larger study groups and evaluate their usefulness as potential markers of CAAD. The study cohort included 35 consecutive patients with CAAD (Group 1), and two groups of 35 patients matched Group 1 regarding sex and age from the overall cohort of 250 patients (Group 2 and Group 3). Group 2 included patients with angiographically documented coronary artery disease (CAD), while Group 3 enrolled patients with normal coronary arteries (NCA) assessed during coronary angiography. We applied the RT-qPCR method using the custom plates for the RT-qPCR array. We confirmed that the level of five preselected circulating miRNAs was different in patients with CAAD compared to Group 2 and Group 3. We found that miR-451a and miR-328 significantly improved the CAAD prediction. In conclusion, miR-451a is a significant marker of CAAD compared to patients with CAD. In turn, miR-328-3p is a significant marker of CAAD compared to patients with NCA. [ABSTRACT FROM AUTHOR]

Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a working diagnosis and requires identification of the underlying causes to optimize treatment, improve prognosis, and prevent the recurrence of myocardial infarction. According to the literature, the prognosis of patients diagnosed with MINOCA is comparable to the group of patients with myocardial infarction (MI) and significant stenosis of the coronary arteries. Intracoronary imaging is a crucial diagnostic tool used in identifying epicardial causes of MINOCA that are not visible in coronary angiography. Optical coherence tomography (OCT) provides the highest spatial resolution, simultaneously allowing detailed visualization of plaque pathology in individuals with MINOCA and identifying the cause of MI in up to 80% of patients. Common causes of a MINOCA may include plaque disruption, spontaneous coronary artery dissection (SCAD), coronary artery spasm, and coronary thromboembolism. The optimization of pharmacological treatment in this group of patients, especially dual antiplatelet therapy and statins, improves the prognosis. Data on the indications for invasive treatment of patients with MINOCA based on OCT findings are insufficient. There is a strong need for research comparing treatment strategies, especially in high-risk lesions visualized in OCT. The main aim of this review is to demonstrate the usefulness of OCT in determining the mechanism of MINOCA. [ABSTRACT FROM AUTHOR]

Background: Whereas the efficacy and safety of intravascular lithotripsy (IVL) have been confirmed in de novo calcified coronary lesions, little is known about its utility in treating stent underexpansion. This study aimed to investigate the impact of IVL in treating stent underexpansion. Methods and Results: Consecutive patients with stent underexpansion treated with IVL entered the multicenter IVL-Dragon Registry. The procedural success (primary efficacy endpoint) was defined as a relative stent expansion >80%. Thirty days device-oriented composite endpoint (DOCE) (defined as a composite of cardiac death, target lesion revascularization, or target vessel myocardial infarction) was the secondary endpoint. A total of 62 patients were enrolled. The primary efficacy endpoint was achieved in 72.6% of patients. Both stent underexpansion 58.5% (47.5–69.7) vs. 11.4% (5.8–20.7), p < 0.001, and the stenotic area 82.6% (72.4–90.8) vs. 21.5% (11.1–37.2), p < 0.001, measured by quantitative coronary angiography improved significantly after IVL. Intravascular imaging confirmed increased stent expansion following IVL from 37.5% (16.0–66.0) to 86.0% (69.2–90.7), p < 0.001, by optical coherence tomography and from 57.0% (31.5–77.2) to 89.0% (85.0–92.0), p = 0.002, by intravascular ultrasound. Secondary endpoint occurred in one (1.6%) patient caused by cardiac death. There was no target lesion revascularization or target vessel myocardial infarction during the 30-day follow-up. Conclusions: In this real-life, largest-to-date analysis of IVL use to manage underexpanded stent, IVL proved to be an effective and safe method for facilitating stent expansion and increasing luminal gain. [ABSTRACT FROM AUTHOR]

Introduction: Inflammation and angiogenesis disturbances are considered as factors contributing to the development of coronary artery ectasias (CAE). Endocan (endothelial cell-specific molecule-1 -- ESM-1) regulates both inflammatory and angiogenetic processes. However, there are no data about the correlation between endocan level and the severity of CAE measured with total volume of coronary artery dilation. Aim: To assess whether the severity of the inflammatory process measured as endocan concentration correlates with the total volume of CAE. Material and methods: We selected prospectively a total of 43 consecutive patients with coronary artery ectasia from 2240 patients who underwent coronary angiography in our center. Determination of endocan was performed by using the Human Endothelial cell-specific Molecule 1 (ECSM1/ENDOCAN) ELISA Kit. 3D QCA (three-dimensional quantitative coronary angiography) was used for coronary lesion and aneurysm quantification. The total volume of dilation was defined as the volume of all aneurysms and ectasias of coronary arteries in 1 patient. Results: The mean volume of all aneurysms in 1 patient was 677 ±878.7 mm3. The total aneurysm volume was positively strongly correlated with endocan concentration (Pearson correlation coefficient: 0.811; 2-tailed p < 0.001). Conclusions: Endocan is a potential marker of vascular wall damage mainly as a result of inflammation in the course of atherosclerosis, but also vascular remodeling as a result of a disturbance of pro- and anti-angiogenic processes. Endocan level reflects the intensity of the above processes and therefore correlates with the severity of CAE, measured as the total volume of dilation. [ABSTRACT FROM AUTHOR]