Kawagoe, Takuji

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hJournal of Cardiology Cases 9 (2014) 168–169
Contents lists available at www.sciencedirect.com
Journal  of  Cardiology  Cases
j ourna l h omepa ge: www.elsev ier .com/ locate / j ccaseditorial
ditorial:  Spontaneous  coronary  artery  dissection  in  pregnancyeywords:
pontaneous coronary artery dissection
regnancy
cute coronary syndrome
Spontaneous coronary artery dissection (SCAD) is a rare cause
f acute coronary syndrome or sudden cardiac death. The clinical
resentation of SCAD depends on the extent and the ﬂow-limiting
everity of the coronary dissection, and ranges from asymptomatic
o unstable angina, acute myocardial infarction, and ventricular
rrhythmias to sudden cardiac death [1].
The incidence of SCAD in angiographic series varies widely from
.07% up to 1.1% for patients who are referred for coronary angiog-
aphy. The mean age at presentation is 30–45 years (range 30–70
ears) and more than 70% of SCAD cases are women [2,3]. One third
f all SCAD cases in women occur in the peripartum period, of which
ne third occur in late pregnancy and two thirds in the early post-
artum period. The peak incidence is within the ﬁrst 2 weeks after
elivery [1].
In a population-based study of more than 12 million deliver-
es in the USA, the incidence of acute myocardial infarction was
.2 per 100 000 deliveries [4]. The prevalence of pregnancy-related
cute myocardial infarction in Japan seems lower than in Western
ountries [5]. Evaluation of coronary artery morphology (angio-
raphically or at autopsy) revealed a dissection only in 27% of the
atients, whereas a coronary stenosis due to atherosclerosis was
bserved in 40%. Coronary dissection was the primary cause of
nfarction in the peripartum period (50%) and was found more com-
only in postpartum compared with antepartum cases (34% vs.
1%) [6].
The pathogenesis of SCAD in the peripartum period is still
nclear. Hemodynamic factors together with arterial wall changes
elated to pregnancy, a lytic action of proteases released from
osinophils, and intimal tears are the main hypotheses presented
o explain the pathophysiology involved. First, changes in the con-
entrations of sex hormones are thought to alter the normal arterial
all architecture, resulting in an increased susceptibility to sponta-
eous dissection. The changes in the vascular wall include smooth
uscle cell proliferation, impaired collagen synthesis, and alter-
tions in the protein and acid mucopolysaccharide content of the
edia. Also, total blood volume and cardiac output are increased
DOI of original article: http://dx.doi.org/10.1016/j.jccase.2013.10.005.
878-5409/$ – see front matter © 2014 Japanese College of Cardiology. Published by Else
ttp://dx.doi.org/10.1016/j.jccase.2013.11.005during pregnancy. This may  lead to augmented shear forces on
the luminal surface and an increased wall stress in pregnancy and
particularly during labor. These changes predispose the coronary
arteries to the development of intramural dissections [1]. Second,
a periadventitial inﬁltrate composed of eosinophilic granulocytes
involving the vasa vasorum has been observed in patients with
SCAD. The inﬁltrate of eosinophils that can be observed in dissected
coronary arteries could be a systemic manifestation of this process.
Eosinophil granules contain lytic enzymes including collagenase,
major basic protein, and other substances that have a cytotoxic
effect. It was  postulated that spontaneous dissection could result
from the breakdown of media-adventitial wall layers by the sub-
stances released by activated eosinophils [1,7]. Third, since an
intimal tear is found only infrequently at autopsy, disruption of
the vasa vasorum leading to intramedial hemorrhage and subse-
quent dissection without an intimal tear also has been proposed as
a possible mechanism in this subset of patients with SCAD [1,8].
Whenever a young patient without major coronary risk factors
or a woman in the postpartum period presents with acute coro-
nary syndrome or sudden death, the possibility of a SCAD should
be suspected and an urgent coronary angiography considered [1].
There is no speciﬁc guideline on how to manage patients with SCAD.
Treatment options for SCAD include medical therapy, percutaneous
coronary intervention (PCI), or coronary artery bypass graft surgery
(CABG). When there is no evidence of ongoing ischemia or hemody-
namic instability, SCAD can be managed successfully with medical
treatment alone. If a pronounced dissection persists in a major ves-
sel after prolonged medical treatment, or in SCAD causing marked
epicardial coronary ﬂow impairment and/or ongoing ischemia, PCI
or CABG should be considered [1]. Initial conservative manage-
ment and CABG were associated with an uncomplicated in-hospital
course, whereas PCI was complicated by technical failure in 35%. In
this regard, PCI was  associated with elevated rates of technical fail-
ure relating to passage of coronary wire into the false lumen of
the dissected vessel or loss of coronary ﬂow through propagation
of dissection and displacement of intramural hematoma by stent
placement [9].
In this issue of the Journal of Cardiology Cases, Ryshten et al.
present a thought-provoking case report of a postpartum woman
with SCAD-related acute myocardial infarction who survived car-
diac shock by excellent PCI [10].References
[1] Vrints CJ. Spontaneous coronary artery dissection. Heart 2010;96:801–8.
vier Ltd. All rights reserved.
iology
[
E-mail address:
kawataku@city-hosp.naka.hiroshima.jp
11 November 2013Editorial / Journal of Card
[2] Vanzetto B, Berger-Coz E, Barone-Rochette G, Chavanon O, Bouvaist H, Hacini
R,  Blin D, Machecourt J. Prevalence, therapeutic management and medium-
term prognosis of spontaneous coronary dissection: results from a database of
11,605 patients. Eur J Cardiothorac Surg 2009;35:250–4.
[3] Mortensen KH, Thuesen L, Kristensen IB, Christiansen EH. Spontaneous coro-
nary artery dissection: a Western Denmark Registry Study. Catheter Cardiovasc
Interv 2009;74:710–7.
[4] James AH, Jamison MG,  Biswas MS,  Brancazio LR, Swamy GK, Myers ER. Acute
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[5] Satoh H, Sano M,  Suwa K, Saotome M,  Urushida T, Katoh H, Hayashi H.
Pregnancy-related acute myocardial infarction in Japan. Circ J 2013;77:725–33.
[6] Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy. J
Am Coll Cardiol 2008;52:171–81.
[7] Borczuk AC. Review and hypothesis: the eosinophil and peripartum heart dis-
ease (myocarditis and coronary artery dissection) coincidence or pathogenetic
signiﬁcance? Cardiovasc Res 1997;33:527–32.
[8] Thayer JO, Healy RW,  Maggs PR. Spontaneous coronary artery dissection. Ann
Thorac Surg 1987;44:97–102.
[9] Tweet MS,  Hayes SN, Pitta SR, Simari RD, Lerman A, Lemon RJ, Gersh
BJ,  Khambatta S, Best PJM, Rihal CS, Gulati R. Clinical features, manage-
ment, and prognosis of spontaneous coronary artery dissection. Circulation
2012;126:579–88. Cases 9 (2014) 168–169 169
10] Ryshten N, Janssens L, Ector B. Acute myocardial infarction due to sponta-
neous postpartum multi-vessel coronary artery dissection. J Cardiol Cases
2014;9:80–3.
Takuji Kawagoe (MD, PhD, FJCC) ∗
Department of Cardiology, Hiroshima City Hospital,
7-33 Moto-machi, Naka-ku, Hiroshima 730-8518,
Japan
∗ Tel.: +81 82 221 2291; fax: +81 82 223 1447.


Editorial: Spontaneous coronary artery dissection in pregnancy 

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Editorial: Spontaneous coronary artery dissection in pregnancy

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