Ong 2011

International Journal of Cardiology 151 (2011) e32–e34
Contents lists available at ScienceDirect
International Journal of Cardiology

j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / i j c a r d
Letter to the Editor
Coronary artery spasm as a cause for myocardial infarction in patients with systemic
inflammatory disease
Peter Ong a,⁎, Anastasios Athanasiadis a, Mark Dominik Alscher b, Peter Fritz c, Heiko Mahrholdt a,
Udo Sechtem a,1, Juan-Carlos Kaski d,1
a
Department of Cardiology, Robert-Bosch-Krankenhaus, Stuttgart, Germany
b
Department of Nephrology, Robert-Bosch-Krankenhaus, Stuttgart, Germany
c
Department of Pathology, Robert-Bosch-Krankenhaus, Stuttgart, Germany
d
Cardiovascular Sciences Research Centre, St George's University of London, United Kingdom
a r t i c l e i n f o line-testing for coronary spasm, which triggered sub-occlusive

coronary artery spasm of both, the mid segment of the left anterior
Article history: descending (LAD) coronary artery and the distal segment of the right
Received 17 March 2011
coronary artery (RCA) (Fig. 2G–J). Coronary spasm was associated
Accepted 19 March 2011
Available online 20 April 2011 with ischemic ECG changes.
A 70-year-old woman with a diagnosis of rheumatoid arthritis and
Keywords: SLE (positive ANA as well as SS-A/Ro-antibodies) was admitted with a
Coronary artery spasm sudden onset of left-sided chest pain at rest lasting N30 min. She was
Myocardial infarction
receiving treatment with prednisolone (2.5 mg/d) and azathioprin
Systemic inflammatory disease
(50 mg, 3x/d) for her chronic immunological disease and valsartan
160 mg/d for hypertension. The 12-lead ECG on admission showed
sinus rhythm and ST-segment depression in leads II, III, aVF and V4-V6
(Fig. 3A+B). Cardiac troponin I levels were raised (0.94 μg/L). A
diagnosis of non-ST-segment-elevation myocardial infarction
(NSTEMI) was made. LV angiography, carried out a few hours later,
Albeit infrequently, acute myocardial infarction (AMI) has been showed normal left ventricular ejection fraction (76%) without
reported to occur in the absence of obstructive coronary artery disease regional wall motion abnormalities (Fig. 3C+D). Coronary arteriog-
in patients with chronic inflammatory diseases (SID) such as systemic raphy showed left coronary artery irregularities (≤30% diameter
lupus erythematosus (SLE), rheumatoid arthritis and myositis. Little is reduction) and ectatic segments in both the LAD (mid segment) and
known about the pathogenic mechanisms of AMI in such patients.
Here we report two cases of non ST-segment myocardial infarction
(NSTEMI) without atheromatous coronary obstructions in patients
with SID, caused by coronary artery spasm.
A 51-year-old woman with biopsy-proven polymyositis (Fig. 1),
receiving treatment with oral prednisolone (2.5 mg/d) and cyclospor-
ine-A (200 mg/d) presented to our emergency room with non ST-
segment myocardial infarction (NSTEMI). She was receiving treatment
with metoprolol 95 mg/d and simvastatin 20 mg/d for hypertension
and hypercholesterolemia, respectively.
The 12-lead ECG at hospital admission showed sinus rhythm and
ST-segment depression in leads II, III and aVF (Fig. 2A+B) and
troponin I concentrations were increased (0.52 μg/L). Angiography,
carried out on day one after hospital admission, showed mildly
impaired left ventricular ejection fraction (47%) and inferior wall
hypokinesia (Fig. 2C+D). There were no significant atheromatous
coronary obstructions (Fig. 2E+F). The patient underwent acetylcho-
⁎ Corresponding author at: Robert-Bosch-Krankenhaus, Auerbachstrasse 110, 70376

Stuttgart, Germany. Tel.: + 49 711 8101 3456; fax: + 49 711 8101 3795.
E-mail address: Peter.Ong@rbk.de (P. Ong). Fig. 1. Case 1: Histopathologic diagnosis of Polymyositis (biopsy of left lower leg
1
U Sechtem and JC Kaski contributed equally to this work. muscle). Typical cell infiltrates are indicated by the white arrows.
0167-5273/$ – see front matter © 2011 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ijcard.2011.03.043
P. Ong et al. / International Journal of Cardiology 151 (2011) e32–e34 e33
A C D G H
B E F I J
Fig. 2. A+B: Case 1: ECG on admission showing ST-segment depression in leads II, III and aVF. C+D: Case 1: Ventriculogram shows inferior LV hypokinesia (white arrow). E+F: Case
1: Coronary angiography of right coronary artery (RCA, E) and left coronary artery (LCA, F) showing no significant flow limiting stenosis. G–J: Case 1: RCA and LCA after intracoronary
acetylcholine provocation (G+H) and the same arteries after intracoronary nitroglycerine administration (I+J). Occlusive spasm can be seen in the mid-LAD (H, after administration
of 100 μg ACH) and the distal part of the right coronary artery (G, after administration of 80 μg ACH) (white arrows).
circumflex (proximal segment) coronary arteries. However, no culprit These findings suggest that coronary artery spasm might offer a
lesion was found (Fig. 3E+F). The patient underwent acetylcholine- plausible explanation for the occurrence of the acute coronary syndrome
testing for coronary spasm, which reproduced the patient's typical in both patients [1]. In patients with SID the chronic inflammatory status
chest pain and showed focal severe narrowing in the mid LAD, as well characteristic of the condition can lead to endothelial dysfunction via
as a focal coronary artery spasm of the proximal LCX, both at the side several inflammatory pathways, which can contribute to the abnormal
of minor plaques (Fig. 3G+H). The RCA was not assessed as the vasomotor response, as seen in our cases [2]. Elevated CRP concentrations
findings in the LCA required administration of glyceryltrinitrate. have been shown to induce significant expression of adhesion molecules
A C D G
B E F H
Fig. 3. A+B: Case 2: 12-lead resting ECG showing ST-segment depression in leads II, III, aVF and V4-6. C+D: Case 2: Ventriculogram with normal LV function without any regional
wall motion abnormalities. E+F: Case 2: Coronary angiography of right coronary artery (RCA, E) and left coronary artery (LCA, F) revealed ectatic segments and plaques ≤30% in the
mid LAD and proximal LCX but no flow limiting stenosis. G+H: Case 2: LCA after 100 μg acetylcholine (G) and after intracoronary nitroglycerine administration (H). Severe focal
narrowing in the mid LAD and focal coronary spasm of the proximal LCX was observed, both at the side of minor plaques (white arrows).
e34 P. Ong et al. / International Journal of Cardiology 151 (2011) e32–e34
(e.g. ICAM-1, VCAM-1 and e-selectin) by human endothelial cells, which Acknowledgement
can, in turn, lead to endothelial injury [3]. In addition, it has been
described that CD4+CD28null T cells can be expanded in patients with SID The authors of this manuscript have certified that they comply
leading to endothelial damage and early atherosclerosis either via direct with the Principles of Ethical Publishing in the International Journal of
cytolytic effects on endothelial cells or indirectly through macrophage Cardiology (Shewan and Coats 2010;144:1-2).
activation [4]. These processes can lead to an imbalance in vascular
homeostasis with excessive release of endothelin-1 and a reduction in
nitric oxide production [5], making the epicardial coronary arteries more References
prone to vasospasm.
[1] Ong P, Athanasiadis A, Hill S, Vogelsberg H, Voehringer M, Sechtem U. Coronary
To the best of our knowledge this is the first report of coronary artery spasm as a frequent cause of acute coronary syndrome: the CASPAR
artery spasm as a mechanism for myocardial infarction (NSTEMI) in (Coronary Artery Spasm in Patients With Acute Coronary Syndrome) study. J Am
the presence of unobstructed coronary arteries in a patient with Coll Cardiol 2008;52:523–7.
[2] Sherer Y, Shoenfeld Y. Mechanisms of disease: atherosclerosis in autoimmune
biopsy-proven polymyositis and another patient with rheumatoid diseases. Nat Clin Pract Rheumatol 2006;2:99–106.
arthritis/systemic lupus erythematosus. Treatment strategies includ- [3] Pasceri V, Willerson JT, Yeh ET. Direct proinflammatory effect of C-reactive protein
ing not only anti-inflammatory therapy but perhaps also calcium on human endothelial cells. Circulation 2000;102:2165–8.
[4] Dumitriu IE, Araguás ET, Baboonian C, Kaski JC. CD4+ CD28 null T cells in coronary
channel blockers to prevent vasospastic episodes should be devised artery disease: when helpers become killers. Cardiovasc Res 2009;81:11–9.
and tested in ad hoc trials. Our cases indicate that patients with SID [5] Nguyen A, Thorin-Trescases N, Thorin E. Working under pressure: coronary arteries
presenting with an acute coronary syndrome despite unobstructed and the endothelin system. Am J Physiol Regul Integr Comp Physiol 2010;298:
R1188–94.
coronary arteries should be investigated with tests for vasospasm i.e.
intracoronary provocation with acetylcholine, to establish the correct
diagnosis.

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International Journal of Cardiology 151 (2011) e32–e34

Contents lists available at ScienceDirect

International Journal of Cardiology

Letter to the Editor

a r t i c l e i n f o line-testing for coronary spasm, which triggered sub-occlusive

⁎ Corresponding author at: Robert-Bosch-Krankenhaus, Auerbachstrasse 110, 70376

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