Journal of Vascular Medicine & Surgery

Takayasu Arteritis Clinical Considerations for Increased Vascular Damage

Joseph Henry^* Department of General Surgery, Tel- Aviv Sourasky Medical Center, Tel- Aviv, Israel
^*Correspondence: Joseph Henry, Department of General Surgery, Tel- Aviv Sourasky Medical Center, Tel- Aviv, Israel, Email:

Received: 27-Oct-2023, Manuscript No. JVMS-23-24129; Editor assigned: 30-Oct-2023, Pre QC No. JVMS-23-24129 (PQ); Reviewed: 15-Nov-2023, QC No. JVMS-23-24129; Revised: 22-Nov-2023, Manuscript No. JVMS-23-24129 (R); Published: 29-Nov-2023, DOI: 10.35248/2329-6925.23.11.545

Description

The aorta and its branches are the primary organs affected by the uncommon chronic idiopathic inflammatory vascular disease known as Takayasu Arteritis (TA). Vascular stenosis or occlusion, dilation or aneurysm, and vascular wall thickening are signs of vascular damage in these involved vessels. These conditions can result in ischemia of vital organs like the heart, brain, and kidneys, or aneurysmal rupture, which poses a serious risk to the survival and quality of life of TA patients. Currently, the main goal of treatment for TA is to reduce disease activity. However, some patients have silent vascular advancement, which essentially manifests as Exacerbated Vascular Damage (EVD), even though they show very little clinical evidence of disease activity. Additionally, a high mortality rate is promised by the vascular development. The general features of AVD in TA are still unknown. Poor prognoses (such as disability and mortality) in TA patients are primarily caused by AVD. To improve therapy goals and outcomes, it is essential to identify AVD risk factors. There is a discrepancy between disease activity and AVD since male sex, elevated C-Reactive Protein (CRP), and carotidynia have been found to be risk factors for TA recurrence rather than vascular problems. According to another study, smoking and being Caucasian are associated with death in TA patients. However, at this time, it is still unclear which variables could contribute to or predict AVD in TA. In addition to being crucial for assessing the state of the disease and modifying treatment plans to enhance results, dynamic and direct monitoring of vascular development during therapy is also essential for promptly identifying AVD and its predictive factors. Vascular alterations in TA can be tracked using a variety of imaging techniques. An earlier investigation demonstrated that, when contrast-enhancing drugs are present, ultrasonography may accurately depict alterations in the arterial wall and lumen as well as disease activity. Although angiographic changes have been used as significant indices in many reports to assess the effectiveness of therapy, the general conditions of vascular progression are still unknown. About one-third of TA patients experienced AVD, with a median follow-up of 14 months, according to the current study. In the original lesions, aggravated vascular stenosis was the most common type of AVD, whereas new lesions were comparatively less common. The most susceptible regions were the limb arteries, though the damage caused by lesions in these arteries is probably not as great as that caused by lesions in critical arteries controlling vital organs like the heart, brain, or kidneys, which may raise the risk of fatal cerebrovascular events and serious adverse events. Further investigation is needed as hemodynamics such as sheer press and turbulent flow may be a critical factor contributing to increased vascular findings, given the differences in vascular structure and locations between limb arteries and arteries supplying vital organs. For the time being, however, end-organ perfusion should be the basis for the therapeutic approach selection. In patients with TA, assessing and treating inflammation is crucial. Consistent with earlier findings, ESR and CRP increased in the active disease status along with SUVmax in PET-CT. AVD was not predicted by baseline inflammatory markers such as ESR, IL-6, C3, and IL-8. Six months of treatment led to a significant improvement in disease remission, suggesting that successful and proactive measures to control inflammation and disease activity are essential for TA patients. It's interesting to note that angiographic aggravation was linked to C4 and CRP. There is a strong correlation between autoimmune diseases, particularly vasculitis, and the complement system. Complement elements like C3 and complement 4-binding protein can be utilized as biomarkers in TA to track the progression of the disease. According to the current study, C4 was associated with a higher risk of progression in vascular imaging, suggesting a potential role for complement activation in the etiology of TA. Despite not being a stand-alone risk factor-possibly because of the small sample size or C4's restricted role in complement activation-it plays a crucial role in causing vascular deterioration and merits more research.