Skip to content

Advertisement

  • Poster presentation
  • Open Access

The involvement of the aorta by cardiac magnetic resonance in the inflammatory process of acute coronary syndrome

  • 1,
  • 1,
  • 2,
  • 2,
  • 2,
  • 2,
  • 2,
  • 2,
  • 2,
  • 2 and
  • 2
Journal of Cardiovascular Magnetic Resonance200911 (Suppl 1) :P256

https://doi.org/10.1186/1532-429X-11-S1-P256

  • Published:

Keywords

  • Emergency Department
  • Chest Pain
  • Acute Coronary Syndrome
  • Cardiac Magnetic Resonance
  • Aortic Wall

Introduction

In patients presenting with acute coronary syndrome (ACS), it has been shown that multiple coronary arteries are involved during the inflammatory process. Growing literature has also revealed that carotid and aortic vessels maybe involved in the inflammatory cascade of ACS.

Purpose

To assess the involvement of the aorta during ACS by cardiac magnetic resonance (CMR).

Methods

We prospectively evaluated 78 patients who presented to the emergency department (ED) with chest pain and were classified as either: 1) ACS: if they had positive Troponin levels and typical chest pain or 2) Non-cardiac chest pain: if they had negative Troponins and a normal stress test or catheterization. We compared these 2 groups to a control group of 45 asymptomatic diabetic patients. The descending aortic wall area (AWA) and aortic wall thickness (AWT) were measured using a double inversion recovery T-2 weighted spin echo sequence by CMR with computer software analysis. See Table 1.
Table 1

Clinical and aortic wall characteristics of the study population

Characteristics

Acute coronary syndrome n = 27

Non-cardiac chest pain (ED) n = 51

Asymptomatic diabetes (Control group) n = 45

p-value

Age (yrs)

60.3 ± 11.4

53.6 ± 10.7

59.9 ± 8

 

Gender (female)

52.2%

47%

44.5%

 

BMI

29.19

19.85

14.10

 

Past medical history:

    

   Smoker

43.5%

13.7%

11.1%

 

   Hypertension

78.2%

49%

75.5%

 

   Diabetes Type 2

21.7%

17.7%

100%

 

   Hyperlipidemia

30.4%

37.3%

73.3%

 

Family history of:

    

   CAD

34.8%

39.2%

33.3%

 

   Angina

91.3%

53%

0

 

   MI

4.3%

0

0

 

   Coronary angiography

4.3%

5.9%

0

 

Claudication

34.8%

0

6.7%

 

Renal disease

8.7%

3.9%

0

 

CVA/TIA

13%

7.8%

6.7%

 

Blood tests:

    

   Troponin

1.37 ± 2.1

NA

NA

 

   CKMB

61.9 ± 71.1

NA

NA

 

   Creatinine

1.1 ± 0.33

1.1 ± 0.9

1.09 ± 0.8

 

   LDL

109 ± 46.2

104 ± 36.6

107.8 ± 36.3

 

   HDL

47 ± 11.8

47.5 ± 16.2

50.04 ± 11.8

 

   Triglycerides

149.8 ± 101.7

149.7 ± 76.2

212.5 ± 143

 

   Total cholesterol

181.8 ± 51.3

183.9 ± 43

198.25 ± 41

 

   CRP

2.16 ± 1.8

0.51 ± 0.6

0.61 ± 0.9

 

Medications:

    

   Aspirin

21.8%

33.3%

62.2%

 

   Plavix

0

0

0

 

   Beta blockers

4.3%

17.6%

20%

 

   ACEI

34.8%

23.5%

55.5%

 

   ARB

0

0

17.8%

 

   Statin

43.4%

27.5%

53.5%

 

   Diuretics

26.1%

13.7%

-

 

Aortic wall characteristics:

    

   Wall thickness (mm)

    

Mean

3.173 ± 0.2

2.576 ± 0.1

2.305 ± 0.13

 

Min-Max

2.0–5.4

1.1–4.0

1.2–4.2

<0.001

   Wall area (mm2)

    

Mean

2.114 ± 0.2

1.526 ± 0.06

1.382 ± 0.06

 

Min-Max

1.17–4.3

0.77–2.7

0.70–1.99

<0.001

   Lumen area (mm2)

    

Mean

4.501 ± 0.248

4.3076 ± 0.136

4.006 ± 0.136

 

Min-Max

2.36–8.22

2.69–8.2

1.58–7.22

0.136

Data are mean (SD) or n (percentage).

Results

The AWA and AWT were significantly greater in patients who presented to the ED with ACS (AWA-mean 2.28 ± 0.78 mm2; AWT-mean 3.30 ± 0.88 mm) then both patients presenting with non-cardiac CP (AWA-mean 1.52 ± 0.39 mm2, p < 0.01; AWT-mean 2.53 ± 0.64 mm, p < 0.01) and the controls (AWA-mean 1.39 ± 0.36 mm2, p < 0.01; AWT-mean 2.36 ± 0.80 mm, p < 0.01). There was no significant difference in the patients with non-cardiac CP compared to the controls.

Conclusion

Aortic wall may be involved in the inflammatory process of patients presenting with ACS.

Authors’ Affiliations

(1)
New York Methodist Hospital, Brooklyn, NY, USA
(2)
Duke Univ Medical Center, Durham, NC, USA

Copyright

© Bhumireddy et al; licensee BioMed Central Ltd. 2009

This article is published under license to BioMed Central Ltd.

Advertisement