Abstract

Background/ObjectivesPrevious studies have demonstrated that in acute coronary syndrome (ACS), plaque destabilization and vessel inflammation, represented by vessel edema, often occur simultaneously in multiple coronaries, as well as extend to the cerebrovascular system. Our aim was to determine whether the inflammatory vascular processes occurring within the coronaries during ACS extend simultaneously to the descending aorta.MethodsWe prospectively enrolled 111 patients (56 ACS patients and 55 non-ACS patients with known coronary artery disease) to undergo cardiac magnetic resonance of the thoracic aortic wall at presentation and at three-month follow-up. The primary outcome was change in aortic wall area (AWA) and maximal aortic wall thickness (AWT) from baseline to three-month follow-up. Secondary outcomes were baseline and follow-up differences in AWA and AWT, and changes in C-reactive protein (CRP).ResultsThere was a significant reduction in mean AWA (p = 0.01) and AWT (p = 0.01) between index and follow up scans in ACS group, with no significant changes in non ACS group (both p>0.1) and no difference between ACS and non-ACS groups (p = 0.22). There was no significant difference in AWA and AWT at baseline (p>0.36) and follow-up (p>0.2) between groups. There was a significant reduction in CRP in both groups (p<0.01), with higher reduction in ACS patients (p<0.01)ConclusionsThere was a reduction in aortic wall size, aortic wall area, and aortic wall thickness in patients presenting with ACS, and no change in non-ACS patients. There were no interval between-group differences in these measurements. We observed a reduction in C-reactive protein in both groups, with higher reduction noted in ACS patients.

Highlights

  • Acute coronary syndrome (ACS) accounts for nearly half of cardiovascular disease morbidity and mortality worldwide and is usually the direct result of atherosclerotic plaque instability [1, 2]

  • There was a reduction in aortic wall size, aortic wall area, and aortic wall thickness in patients presenting with ACS, and no change in non-ACS patients

  • We observed a reduction in C-reactive protein in both groups, with higher reduction noted in ACS patients

Read more

Summary

Introduction

Acute coronary syndrome (ACS) accounts for nearly half of cardiovascular disease morbidity and mortality worldwide and is usually the direct result of atherosclerotic plaque instability [1, 2]. Beyond the coronary system, it is postulated that large vessel arterial systems are simultaneously involved in the inflammatory process of ACS. In both animal and human models, increased numbers of unstable plaques were noted on carotid evaluations during ACS, translating, in some cases, to co-incident ischemic strokes [8, 9]. A prior cardiac magnetic resonance (CMR) study has demonstrated a greater thoracic aortic wall thickness, as a surrogate measure of inflammatory mural edema, in patients presenting with ACS compared to diabetic patients without ACS [11, 12]

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call