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Background: Aortic aneurysms, particularly those affecting the ascending aorta, pose significant health risks due to their potential to cause life-threatening complications such as rupture and dissection. While the etiology of ascending aortic aneurysms has traditionally been associated with non-inflammatory processes, emerging evidence suggests a potential role of inflammation in their development. Methods: This study investigates the relationship between inflammatory markers and ascending aortic aneurysms, focusing on high-sensitivity C-reactive protein (hs-CRP) and the monocyte-to-HDL ratio (MHR). A total of 135 patients with ascending aortic aneurysms and 40 control subjects underwent comprehensive evaluations, including echocardiography, computed tomography imaging, and serum biomarker measurements. Results: The results indicate significantly elevated levels of hs-CRP and MHR in patients with ascending aortic aneurysms compared to the control group, suggesting a potential inflammatory component in the pathogenesis of these aneurysms. However, the precise mechanisms underlying this association remain to be elucidated. Conclusion: Despite limitations such as the cross-sectional study design and relatively small sample size, this study provides valuable insights into the potential involvement of inflammation in ascending aortic aneurysms. Further research, including longitudinal studies and histopathological analysis of aortic tissue, is warranted to confirm these findings and explore the utility of inflammatory markers as diagnostic and prognostic indicators in this patient population.
RESUMO
OBJECTIVE: Acute coronary syndromes (ACS) encompass a continuum of cardiac ischaemic events, ranging from unstable angina pectoris (UA) to ST-segment elevation myocardial infarction (STEMI). Oxidative stress may play an important role in the pathogenesis of acute coronary diseases. In the present study, we examined the associations between lipid and protein susceptibility to oxidation and total sialic acid (SA) and antioxidant status and the severity of ACS as determined by having UA, non-STEMI or STEMI. METHODS AND RESULTS: The study sample consisted of 102 patients with ACS and 45 controls. Malondialdehyde (MDA) as a marker of lipid peroxidation and protein carbonyls as a marker of protein oxidation were measured to show the susceptibility to oxidation. Antioxidant status was determined by measuring the carotenoids, vitamin C and vitamin E levels and paraoxonase and arylesterase activities. In addition to conventional lipid and lipoprotein analysis, MDA and vitamin E were quantitated by high-performance liquid chromatography. Total SA and other oxidant and antioxidant parameters were studied spectrophotometrically. As expected, patients had significantly higher total cholesterol, triacylglycerol, low-density lipoprotein cholesterol, lipoprotein (a), apolipoprotein (apo) B values and lower high-density lipoprotein cholesterol and apoAl values than controls. Our results demonstrated significant increases both in total SA levels and in indicators of oxidative stress in patients with ACS compared with the controls. However, antioxidant parameters were decreased in patients with ACS. When the patients were divided into groups with UA, non-STEMI and STEMI, respectively, total SA and oxidant parameters were significantly increased and antioxidant parameters were significantly decreased in going from UA to STEMI. CONCLUSIONS: Our study shows gradually increased lipid and protein oxidation and total SA and gradually decreased antioxidant status when the conditions advance from UA to STEMI. These results indicate that these markers may be useful both in understanding plaque destabilization and in determination of risk stratification of patients. Also, measurement of these markers may provide a noninvasive window to study atherosclerotic lesions.