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Review
. 2018 Feb 27;18(1):42.
doi: 10.1186/s12872-018-0781-9.

Acute Coronary Syndrome Secondary to Allergic Coronary Vasospasm (Kounis Syndrome): A Case Series, Follow-Up and Literature Review

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Free PMC article
Review

Acute Coronary Syndrome Secondary to Allergic Coronary Vasospasm (Kounis Syndrome): A Case Series, Follow-Up and Literature Review

Jing Li et al. BMC Cardiovasc Disord. .
Free PMC article

Abstract

Background: Kounis syndrome (KS) is the concurrence of acute coronary syndrome associated with mast-cell and platelet activation in the setting of hypersensitivity and allergic or anaphylactic insults. Many drugs and environmental exposures had been reported as inducers, but various inducers and the mechanism of KS remained unknown till now. The widely used traditional Chinese medicine (TCM) as a potential sensitizer were scarcely reported to induce allergic vasospasm due to the ignorance of the linkage between traditional medicine allergy and vasospasm.

Case presentation: We described 5 rare cases of KS including unreported triggers of TCM and abortion, reported the treatment strategy and 1~4 years' follow-up results, and tried to probe into the etiology of KS. Case 1 and case 2 for the first time reported acute ST-segment elevation myocardial infarction (STEMI) caused by Chinese herbs related allergic coronary vasospasm. Case 3 reported recurrent angina following allergen contact and wheezing, indicating the internal linkage of coronary vasospasm and allergic asthma. Case 4 described a childbearing-age woman suffered refractory ischemic chest pain due to coronary vasospasm in a special period of post-abortion, the attacks suddenly disappeared when her menopause recovered. Case 5 described an isolated episode of allergic coronary vasospasm under exposure of smoking and stress, which was successfully prevented by avoiding the exposures.

Conclusion: Kounis syndrome is not rare but rarely recognized and under-diagnosed. It is necessary to recognize KS and various inducers, especially for the patients suffering refractory vasospastic cardiac attacks concentrating in special periods. Blood test of eosinophil might contribute to diagnose KS and anti-allergic agents might be helpful for controlling KS attacks.

Keywords: Anaphylaxis; Cardiac attack; Coronary vasospasm; Kounis Syndrome.

Conflict of interest statement

Ethics approval and consent to participate

Not applicable.

Consent for publication

Written informed consent was obtained from the patients for publication of the case series and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no competing interests.

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Figures

Fig. 1
Fig. 1
The first ECG demonstrated ST segment elevation of 2 mm in leads I, aVL, and ST depression in leads II, III and aVF
Fig. 2
Fig. 2
ECG at 20:30 revealed ST elevation of 3-4 mm in leads II, III, aVF, V3R~V5R with a specular changes in leads I, aVL, V4~V6
Fig. 3
Fig. 3
Coronary angiography of: Upper left: left coronary artery spasm; Lower left: left coronary artery relaxed after intracoronary nitroglycerin; Upper right: right coronary artery spasm; Lower right: right coronary artery relaxed after intracoronary nitroglycerin
Fig. 4
Fig. 4
ECG at 3:26on the ambulance revealed ST segment elevation of 4mm in leads V1~V4 and ST depression of 3 mm in leads V5 and V6
Fig. 5
Fig. 5
Tall and peaked T waves in leads V3~V6
Fig. 6
Fig. 6
ECG in the local hospital revealed ST segment elevation of 0.5 mm and peaked T wave in leads II, III and avF
Fig. 7
Fig. 7
ECG on arrival in our hospital revealed ST segment recovered to baseline in leads II, III and avF and Q wave in lead III
Fig. 8
Fig. 8
ECG showed ST segment and T wave evolution in leads II, III and avF
Fig. 9
Fig. 9
ECG on admission was normal
Fig. 10
Fig. 10
Downsloping ST segments depression of 1-3 mm in leads I, aVL, II, III, aVF, V2-V6
Fig. 11
Fig. 11
ST segment elevation for 2-3 mm in leads II, III, aVF, V5, V6 at13:40-13:42 in Holter
Fig. 12
Fig. 12
Nonsustained ventricular tachycardia at 13:42 in Holter
Fig. 13
Fig. 13
Ventricular bigeminy at 13:40 in Holter

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References

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