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C L I N I C A L V I G N E T T E A young woman with recurrent SCAD 1059 systemic inflammatory and connective tissue disorders.1,2 A comprehensive diagnostic work‑

up was performed and the diagnosis of FMD was established based on radiological findings (FIGURE 1B). The patient was discharged after 5 days.

A few hours later, the patient was readmitted with anterior ST ‑segment elevation myocardial infarction (FIGURE 1C). Emergency CA revealed a new SCAD of the middle ‑to ‑distal left anterior de‑

scending artery (with Thrombolysis in Myocar‑

dial Infarction flow grade 2/3; FIGURE 1D). The pa‑

tient received conservative treatment with in‑

travenous nitroglycerin and intravenous heparin (at the therapeutic dose) in addition to the pre‑

vious pharmacotherapy.

Cardiac magnetic resonance imaging showed transmural late gadolinium enhancement with microvascular obstruction and concomitant ede‑

ma in the left anterior descending artery terri‑

tory and a small, old infarct scar in the circum‑

flex artery territory; LVEF was 39% (FIGURE 1E and 1F; Supplementary material, Video S1).

After an interdisciplinary consultation, the patient was anticoagulated with phenprocou‑

mon for 6 months and concomitantly received aspirin (lifelong use), bisoprolol, lisinopril, ro‑

suvastatin, and pantoprazole. Besides anemia due to recurrent menorrhagia, no other clinical problems occurred during the 2‑year follow ‑up.

Follow ‑up echocardiography showed a dilated LV with slightly reduced LVEF (biplane, 45%).

Spontaneous coronary artery dissection ac‑

counts for about 1/3 of acute myocardial infarc‑

tion cases in women under 50 years of age.1,2 The prognosis following SCAD seems to be good,

as the dissection usually heals completely over a few months, although a significant recurrence A 42‑year ‑old woman was admitted to the hos‑

pital with non–ST ‑segment elevation myocardi‑

al infarction. Her medical history revealed that she suffered from 3 spontaneous abortions, mi‑

graine episodes, esophageal reflux, and asthma.

The family history was negative for cardiovas‑

cular disease.

On admission, the patient was hemodynam‑

ically stable. Electrocardiography showed sinus rhythm at a heart rate of 73 bpm, incomplete right bundle branch block, and negative T waves in leads II, III, aVF, and V4 through V6. Blood tests demonstrated elevated levels of high ‑sensitive troponin (895 ng/l; reference range <14 ng/l), creatine kinase–myocardial band (612 U/l; ref‑

erence range <170 U/l), and N ‑terminal frag‑

ment of the prohormone brain natriuretic pep‑

tide (137 ng/l; reference range <130 ng/l), yet normal levels of low ‑density lipoprotein choles‑

terol (2.5 mmol/l; reference range <3 mmol/l).

Echocardiography demonstrated a normal‑

‑sized, nonhypertrophic left ventricle (LV) with normal LV ejection fraction (biplane LVEF, 61%) and hypokinesia of the LV inferolateral, inferi‑

or midventricular, and inferior apical segments.

Coronary angiography (CA) revealed a spon‑

taneous dissection of the distal circumflex ar‑

tery (FIGURE 1A).

Due to preserved coronary perfusion and no persistent or recurrent angina, the patient was treated conservatively with dual antiplatelet therapy (aspirin for lifetime use and ticagre‑

lor for 12 months) and a β ‑blocker (bisoprolol).

The following conditions were considered as the probable causes of spontaneous coronary ar‑

tery dissection (SCAD): fibromuscular dysplasia (FMD), undefined hereditary vasculopathy, and

Correspondence to:

Robert Manka, MD,  Department of Cardiology,  University Hospital Zurich,  University of Zurich,  Raemistrasse 100,  8091 Zürich, Switzerland,  phone: +41 44 255 12 51,  email: robert.manka@usz.ch Received: May 16, 2020.

Revision accepted: July 13, 2020.

Published online: July 24, 2020.

Kardiol Pol. 2020; 78 (10): 1059-1061 doi:10.33963/KP.15526 Copyright by the Author(s), 2020

C L I N I C A L V I G N E T T E

A young woman with recurrent spontaneous coronary artery dissection

Justyna M. Sokolska1,2, Lukas M. Meier1, Erik W. Holy1, Christian Templin1, Hatem Alkadhi3, Robert Manka1,3,4 1  Department of Cardiology, University Hospital Zurich, University of Zurich, Zurich, Switzerland

2  Department of Heart Diseases, Wroclaw Medical University, Wrocław, Poland

3  Institute of Diagnostic and Interventional Radiology, University Hospital Zurich, University of Zurich, Zurich, Switzerland 4  Institute for Biomedical Engineering, University and Swiss Federal Institute of Technology in Zurich (ETH), Zurich, Switzerland

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KARDIOLOGIA POLSKA 2020; 78 (10) 1060

B

C

F

71 ms 96 ms

45 ms

21 ms 66 ms

71 ms

A

LAD

Cx

E

D

LAD

Cx

FIGURE1 A – coronary D

angiography on admission:

spontaneous dissection of the first marginal branch of  the circumflex artery  (arrows); B – extracoronary  abnormalities on computed  tomography angiography of the abdomen and pelvis: 

an ectatic celiac trunk (circle),  an aneurysm of the distal  splenic artery (red arrow),  ectasia of the left iliac  internal artery (not shown)  and a “string of beads” 

appearance of the right renal artery (arrow and  magnified picture); 

C – 12‑lead 

electrocardiogram showing  ST ‑segment elevation in all  anterior wall leads  (V1 through V5);

D – emergency coronary angiography: a new spontaneous dissection of the left anterior descending  artery (dotted arrows) and a residual dissection in  the distal circumflex artery  (arrow); E, F –cardiac magnetic resonance imaging showing transmural  late gadolinium 

enhancement in the anterior and inferior apical segments  of the left ventricle with  microvascular obstruction  (E: 2‑chamber view, dashed  line) and edema in all  midventricular segments  except the anterolateral  ones (F: T2 mapping, short‑

‑axis view)

Abbreviations: Cx, circumflex  artery; LAD, left anterior  descending artery

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C L I N I C A L V I G N E T T E A young woman with recurrent SCAD 1061 rate is observed.1,2 Conservative management

is suggested in patients with preserved flow in the coronary arteries, followed by prolonged inpatient monitoring.1-4 Pharmacotherapy and its duration in SCAD remain controversial, and the benefits from antiplatelet, anticoagulant, and statin therapies are still a matter of debate.1,4 Evaluation for underlying causes is recommend‑

ed, including screening for extracoronary arteri‑

opathy such as FMD; however, in some patients, no definitive diagnosis of the underlying cause can be made at the time of SCAD occurrence.1,2,5 SUPPLEMENTARY MATERIAL

Supplementary material is available at www.mp.pl/kardiologiapolska.

ARTICLE INFORMATION

ACKNOWLEDGMENTS SJM is a beneficiary of the Polish National Agency for  Academic Exchange (NAWA) in ‘The Iwanowska Programme’ at the Department of  Cardiology, MRI Cardiac Unit, University Hospital Zurich, Switzerland.

CONFLICT OF INTEREST None declared.

OPEN ACCESS This is an Open Access article distributed under the terms  of  the  Creative  Commons  Attribution -NonCommercial -NoDerivatives  4.0  In- ternational License (CC BY -NC -ND 4.0), allowing third parties to download ar- ticles and share them with others, provided the original work is properly cited,  not changed in any way, distributed under the same license, and used for non- commercial purposes only. For commercial use, please contact the journal office  at kardiologiapolska@ptkardio.pl.

HOW TO CITE Sokolska JM, Meier LM, Holy EW, et al. A young woman with re- current spontaneous coronary artery dissection. Kardiol Pol. 2020; 78: 1059-1061. 

doi:10.33963/KP.15526

REFERENCES

1 Adlam D, Alfonso F, Maas A, et al. European Society of Cardiology, Acute Car- diovascular Care Association, SCAD study group: a position paper on spontaneous  coronary artery dissection. Eur Heart J. 2018; 39: 3353-3368.

2 Hayes SN, Kim ESH, Saw J, et al. Spontaneous coronary artery dissection: cur- rent state of the science: a scientific statement from the American Heart Associa- tion. Circulation. 2018; 137: e523-e557.

3 Theodoropoulos KC, Hussain R, Palmer ND, et al. The use of multimodality im- aging in the diagnosis and management of spontaneous coronary artery dissec- tion and intramural hematoma. Kardiol Pol. 2020; 78: 467-469.

4 Saw J, Mancini GBJ, Humphries KH. Contemporary review on spontaneous cor- onary artery dissection. J Am Coll Cardiol. 2016; 68: 297-312.

5 Toggweiler S, Puck M, Thalhammer C, et al. Associated vascular lesions in pa- tients with spontaneous coronary artery dissection. Swiss Med Wkly. 2012; 142: 

w13538.

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