Advertisement

The aorta wall of patients presenting to the emergency department with acute myocardial infarction by cardiac magnetic resonance

      Abstract

      Background

      Inflammation has been shown to be a major component in the pathophysiology of acute coronary syndrome (ACS). In patients presenting with acute myocardial infarction (AMI), a critical component of the ACS spectrum, multiple coronary arteries are involved during this inflammatory process. In addition to the coronary vasculature, the inflammatory cascade has also been shown to affect the carotid arteries and possibly the aorta.

      Purpose

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

      Methods

      We prospectively evaluated the aortic wall by CMR in 123 patients. 78 patients were enrolled from the emergency department (ED), who presented with chest pain and were classified as either: (1) AMI: elevated troponin levels and typical chest pain or (2) non-cardiac chest pain (CP): negative troponins and a normal stress test or normal cardiac catheterization. We compared these 2 groups to a group of 45 asymptomatic diabetic patients. The descending thoracic aortic wall area (AWA) and maximal aortic wall thickness (AWT) were measured using a double inversion recovery T-2 weighted, ECG-gated, spin echo sequence by CMR.

      Results

      Patients with AMI were older, more likely to smoke, had a higher incidence of claudication, and had higher CRP levels. The AWA and maximal AWT were greater in patients who presented to the ED with ACS (2.11 ± 0.17 mm2, and 3.17 ± 0.19 mm, respectively) than both patients presenting with non-cardiac CP (1.52 ± 0.58 mm2, p < 0.001; and 2.57 ± 0.10 mm, p < 0.001) and the diabetic patients (1.38 ± 0.58 mm2, p < 0.001; and 2.30 ± 0.131 mm, p < 0.001). The difference in the aortic wall characteristics remained significant after correcting for body mass index, hyperlipidemia, statins and C-reactive protein. There was no difference in maximal AWT or AWA between patients with non-cardiac CP and patients with diabetes.

      Conclusion

      Patients with AMI have a significantly greater maximal aortic wall thickness and area compared to patients with non-cardiac CP. Longitudinal studies are needed to assess whether this increase is due to inflammation or a higher atherosclerotic burden.

      Abbreviations:

      ACS (acute coronary syndrome), NSTEMI (non-ST-segment elevation myocardial infarction), CAD (coronary artery disease), DM (diabetes mellitus), ED (emergency department), CMR (cardiac magnetic resonance), AWA (aortic wall area), AWT (aortic wall thickness)

      Keywords

      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to Atherosclerosis
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect

      References

      1. NHLBI data base: apps.nhlbi.nih.gov/clinicaltrials.

        • Falk E.
        • Shah P.K.
        • Fuster V.
        Coronary plaque disruption.
        Circulation. 1995; 92: 657-671
        • Libby P.
        Current concepts of the pathogenesis of the acute coronary syndrome.
        Circulation. 2001; 104: 365-372
      2. The natural history of unheralded complex coronary plaques.
        J Am Coll Cardiol Img. 1996; 28: 604-608
        • Fuster V.
        • Fayad Z.A.
        • Badimon J.J.
        Acute coronary syndromes: biology.
        Lancet. 1999; 353: SII5-SII9
        • Spagnoli L.G.
        • Bonanno E.
        • Mauriello A.
        • et al.
        Multicentric inflammation in epicardial coronary arteries of patients dying of acute myocardial infarction.
        J Am Coll Cardiol. 2002; 40: 1579-1588
        • Goldstein J.A.
        • Demetriou D.
        • Grines C.L.
        Multiple complex coronary plaques in patients with acute myocardial infarction.
        N Engl J Med. 2000; 343: 915-922
        • Guazzi M.D.
        • Bussotti M.
        • Grancini L.
        • et al.
        Evidence of multifocal activity of coronary disease in patients with acute myocardial infarction.
        Circulation. 1997; 96: 1145-1151
        • Rioufol G.
        • Finet G.
        • Ginon I.
        • et al.
        Multiple atherosclerotic plaque rupture in acute coronary syndrome: a three-vessel intravascular ultrasound study.
        Circulation. 2002; 106: 804-808
        • Goldstein J.A.
        Angiographic plaque complexity: the tip of the unstable plaque iceberg.
        J Am Coll Cardiol. 2002; 39: 1464-1467
        • Asakura M.
        • Ueda Y.
        • Yamaguchi O.
        • et al.
        Extensive development of vulnerable plaques as a pan-coronary process in patients with myocardial infarction: an angioscopic study.
        J Am Coll Cardiol. 2001; 37: 1284-1288
        • Demircan S.
        Comparison of carotid intima-media thickness in patients with stable angina pectoris versus patients with acute coronary syndrome.
        Am J Cardiol. 2005; 96: 643-644
        • Lombardo A.
        • Biasucci L.M.
        • Lanza G.A.
        • et al.
        Inflammation as a possible link between coronary and carotid plaque instability.
        Circulation. 2004; 109: 3158-3163
        • Geroulakos G.
        • O’Gorman D.
        • Kalodiki E.
        • Sheridon D.
        • Nikolaides A.
        The carotid intima-media thickness as a marker of the presence of severe symptomatic coronary artery disease.
        Eur Heart J. 1994; 15: 781-785
        • Ismaeil Magdy F.
        Aortic plaque on transesophageal echocardiography as a marker for coronary artery disease.
        Ann Saudi Med. 2000; 20
      3. European Carotid Surgery Trial (ECST).
        Lancet. 1998 May; : 351
        • Schwartz G.G.
        • Olsson A.G.
        • Ezekowitz M.D.
        • et al.
        Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACLE study: a randomized controlled trial.
        JAMA. 2001; 285: 1711-1718
        • Fuster V.
        • Weinberger J.
        • Kohler T.
        • Glagov S.
        • Imperato A.
        • Goldstone J.
        Pathology: clinical correlation of carotid, aortic and peripheral vascular disease.
        in: Fuster V. Syndromes of atherosclerosis. Futura Publishing Co., New York, NY1999: 269-277
        • Fazio G.
        • Redberg R.F.
        • Winslow T.
        • Schiller N.B.
        Transesophageal echocardiogram-detected atherosclerotic aortic plaque is a marker for coronary artery disease.
        J Am Coll Cardiol. 1993; 21: 144-150
        • Graaff EricVan De
        Early coronary revascularization diminishes the risk of ischemic stroke with acute myocardial infarction.
        Stroke. 2006; 37: 2546
        • Fayad Z.A.
        • Nahar T.
        • Fallon J.T.
        • et al.
        Invivo magnetic resonance evaluation of atherosclerotic plaques in the human thoracic aorta: a comparison with tranesophageal echocardiography.
        Circulation. 2000; 101: 2503-2509
        • Helft G.
        • Worthley S.G.
        • Fuster V.
        • et al.
        Atherosclerotic aortic component quantification by noninvasive magnetic resonance imaging: an in vivo study in rabbits.
        J Am Coll Cardiol. 2001; 37: 1149-1154
        • Hiroaki Taniguchi M.D.
        • Yukihiko M.
        • Fayad Z.A.
        • et al.
        In vivo magnetic resonance evaluation of associations between aortic atherosclerosis and both risk factors and coronary artery disease in patients referred for coronary angiography.
        Am Heart J. 2004; 148: 137-143
        • Li A.E.
        • Kamel I.
        • Rando F.
        • et al.
        Using MRI to assess aortic wall thickness in the multiethnic study of atherosclerosis: distribution by race, sex, and age.
        AJR. 2004; 182: 593-597
        • Kristian T.
        • Joseph S. Alpert
        • Harvey D. White
        Universal definition of myocardial infarction joint ESC/ACCF/AHA/WHF task force for the redefinition of myocardial infarction.
        Eur Heart J. 2007; 28: 2525-2538
        • Yuan C.
        • Beach K.W.
        • Smith Jr., L.H.
        • et al.
        Measurement of atherosclerotic carotid plaque size in vivo using high resolution magnetic resonance imaging.
        Circulation. 1998; 98: 2666-2671
        • Corti R.
        • Fuster V.
        • Badimon J.J.
        • et al.
        New understanding of atherosclerosis (clinically and experimentally) with evolving MRI technology in vivo.
        Ann NY Acad Sci. 2001; 947: 181-195
        • Corti R.
        • Fayad Z.A.
        • Fuster V.
        • et al.
        Effects of lipid lowering by simvastatin on human atherosclerotic lesions: a longitudinal study by high-resolution, non-invasive magnetic resonance imaging.
        Circulation. 2001; 104: 249-252
        • Tribouilloy C.
        • Feng Schen W.
        • Peltier M.
        • Lesbre J.
        Noninvasive prediction of coronary artery disease by transesophageal echocardiographic detection of thoracic aortic plaque in valvular heart disease.
        Am J Cardiol. 1994;
        • Jesse W.
        • Salman A.
        A new noninvasive technique for imaging atherosclerotic plaque in the aortic arch of stroke patients by transcutaneous real-time B-mode ultrasonography.
        Stroke. 1998; 29: 673-676
        • Wardlaw J.M.
        • Chappell F.M.
        • Best J.J.
        • et al.
        Non-invasive imaging compared with intra-arterial angiography in the diagnosis of symptomatic carotid stenosis: a meta-analysis.
        Lancet. 2006; 367: 1503-1512
        • Gottsegen J.M.
        • Coplan N.L.
        The atherosclerotic aortic arch: considerations in diagnostic imaging.
        Prev Cardiol. 2008; 11: 162-167
        • Konstadt S.N.
        • Reich D.L.
        • Quintana C.
        • Levy M.
        The ascending aorta: how much does transesophageal echocardiography see?.
        Anesth Analg. 1994 February; 78: 240-244
        • Kaneko E.
        • Yuan C.
        • Skinner M.P.
        • Raines E.W.
        • Ross R.
        Serial magnetic resonance imaging of experimental atherosclerosis allows visualization of lesion characteristics and lesion progression in vivo.
        Ann NY Acad Sci. 1997 Apr 15; 811 (discussion 252–4): 245-252
        • Yonemura A.
        • Momiyama Y.
        • Fayad Z.A.
        • et al.
        Effect of lipid-lowering therapy with atorvastatin on atherosclerotic aortic plaques detected by noninvasive magnetic resonance imaging.
        J Am Coll Cardiol. 2005; 45: 733-742
        • Zhao X.Q.
        • Yuan C.
        • Hatsukami T.S.
        • et al.
        Effects of prolonged intensive lipid-lowering therapy on the characteristics of carotid atherosclerotic plaques in vivo by MRI: a case–control study.
        AHA. 2001; 21: 1623-1629
        • Biasucci L.M.
        • D’Onofrio G.
        • Liuzzo G.
        • et al.
        Intracellular neutrophil myeloperoxidase is reduced in unstable angina and myocardial infarction, but its reduction is not related to ischemia.
        J Am Coll Cardiol. 1996; 27: 611-616
        • Dinerman J.L.
        • Mehta J.L.
        • Saldeen T.G.
        • et al.
        Increased neutrophil elastase release in unstable angina pectoris and acute myocardial infarction.
        J Am Cardiol. 1990; 15: 1559-1563
        • Buffon A.
        • Biasucci L.M.
        • Liuzzo G.
        • et al.
        Widespread coronary inflammation in unstable angina.
        N Engl J Med. 2002; 347: 5-12
        • Liuzzo G.
        • Biasucci L.M.
        • Gallimore J.R.
        • et al.
        Prognostic value of C-reactive protein and plasma amyloid A protein in severe unstable angina.
        N Engl J Med. 1994; 331: 417-424
        • Neumann F.J.
        • Ott I.
        • Gawaz M.
        • et al.
        Cardiac release of cytokines and inflammatory response in acute myocardial infarction.
        Circulation. 1995; 92: 748-755