Abstract

Is Emilin-1 a molecular link contributing to the extension of thoracic aortic aneurysm dissection and increasing the magnitude of the associated hypertension

Highlights

  • Patients with acute aortic dissection, the dominant condition in acute aortic syndromes, have a high mortality [1]

  • Recent data from proteomic analysis of thoracic aortic dissection suggests a new possible molecular mechanism that may lead to increases in both the extent of a TAD and the associated hypertension

  • Proteomic analysis of aortic tissues from patients with aortic dissection and hypertension found that emilin-1 was down-regulated by approximately 2.3 fold compared to age and sex matched controls [6]

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Summary

Introduction

Patients with acute aortic dissection, the dominant condition in acute aortic syndromes, have a high mortality [1]. Refractory hypertension or high blood pressure which is difficult to control or treat, is a major component of acute aortic syndromes. Hypertension is a significant independent predictor of in-hospital mortality in acute aortic syndromes after considering other factors in multivariate analysis [5].

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