Sinus of Valsalva Aneurysm (SVA) is an aortic root anomaly, consisting of a lack of continuity between the aortic media and the aortic annulus, caused by a structural deficiency of muscular and elastic tissue. We present the case of a 49-year-oldman with atypical chest pain. Echocardiographic imaging described a giant unruptured aneurysm of the right sinus of Valsalva which was confirmed by cardiac computed tomography and coronary angiography. The obstruction of the right coronary artery without intravascular thrombosis and the compression of the right ventricular outflow tract with dynamic obstruction gradient represent the particularities of our case.
Inflammation of the venous wall is involved in thrombogenesis, thrombus resolution, wall remodeling and the post-thrombotic syndrome. Different mechanisms are involved in both arterial and venous thrombosis and patients with atherothrombosis hold a higher risk of venous thrombosis. Although inflammation may represent the connection between arterial and venous thrombosis, it is not yet sure if it is the cause or consequence of venous thrombosis. Consequently, the relationships between inflammation markers as indicators of the inflammatory process and clinical venous thromboembolism need to be investigatd. For example, inflammation mediators such as the pro-inflammatory cytokines interleukin 8 (IL-8), IL-6, monocyte chemotactic protein 1 (MCP-1), C Reactive Protein (CRP), vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), matrix metalloproteinases and tumor necrosis factor alpha (TNF alpha)
Atherosclerosis is a multifactorial systemic disease that affects the entire arterial tree, although some areas are more prone to lipid deposits than others. Moreover, the histopathological composition of the plaques differs, and the clinical manifestations are also different, depending on the location and structure of the atherosclerotic plaque. Some arterial systems are correlated with each other more than in that they simply share a common atherosclerotic risk. The aim of this perspective review is to discuss this heterogeneity of atherosclerotic impairment in different arterial districts and to investigate the current evidence that resulted from studies of the topographical interrelations of atherosclerosis.
Introduction: There is clear evidence of a significant reduction in all major cardiovascular adverse events (MACE) by coronary artery bypass grafting (CABG) in left main coronary artery stenosis (LMCS), but revascularization by percutaneous coronary artery intervention (PCI) shows an increasingly important role as an alternative to CABG. Several recent trials aiming to test the difference in mortality between the two types of revascularization found conflicting data. The aim of this study is to determine whether PCI is non-inferior to CABG with respect to the occurrence of MACE at 1 year in patients with significant LMCS. Material and methods: We prospectively enrolled 296 patients with chronic or acute coronary syndromes and significant LM stenosis. The angiography that recommended the revascularization procedure was used for the calculation of the Syntax II score, in order to classify the patients as low-, intermediate- or high-risk. Low- and high-risk patients were revascularized with either PCI or CABG, according to current guidelines, and were included in the subgroup S1. The second subgroup (S0) included intermediate-risk patients (Syntax II score 23–32), in whom the type of revascularization was chosen depending on the decision of the heart team or the patient preference. Patients were monitored according to the chosen mode of revascularization—PCI or CABG. LM revascularization was performed in all the patients. Clinical endpoints included cardiac death, myocardial infarction, need for revascularization and stroke. Patients were evaluated at 1 year after revascularization. Event rates were estimated using the Kaplan–Meier analysis in time to the first event. Results: At 1-year follow-up, a primary endpoint occurred in 35/95 patients in the CABG group and 37/201 in the PCI group. There were no significant differences between the 2 treatment strategies in the 1-year components of the end-point. However, a tendency to higher occurrence of cardiac death (HR = 1.48 CI (0.55–3.9), p = 0.43), necessity of repeat revascularization (HR = 1.7, CI (0.81–3.6), p = 0.16) and stroke (HR = 1.52, CI (1.15–2.93), p = 0.58) were present after CABG. Contrariwise, although without statistical significance, MI was more frequent after PCI (HR = 2, CI (0.78–5.2), p = 0.14). The Kaplan–Meier estimates in subgroups demonstrated the same tendency to higher rates for cardiac death, repeat revascularization and stroke after CABG, and higher rates of MI after PCI. Although without statistical significance, patients with an intermediate-risk showed a slightly lower risk of MACE after PCI than CABG. With the exception of dyslipidemia and gender, other cardiovascular risk factors were in favor of CABG (CKD, obesity). Conclusion: In patients with LMCS, PCI with drug-eluting stents was non-inferior to CABG with respect to the composite of cardiac death, myocardial infarction, repeat revascularization and stroke at 1 year, even in patients with intermediate Syntax II risk score.
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