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\begin{document}

\title{The spectrum of myocardial stress: Concurrent spontaneous coronary
artery dissection and stress-induced cardiomyopathy in a patient
presenting with acute ST-segment elevation myocardial infarction.}



\author[1]{Subash Nepal}%
\author[2]{Kamala Ojha}%
\author[1]{Dana Aiello}%
\affil[1]{SUNY Upstate Medical University Hospital}%
\affil[2]{SUNY Upstate Medical University Department of Medicine}%


\vspace{-1em}



  
  \date{May 15, 2024}


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\selectlanguage{english}
\begin{abstract}
A 72-year-old lady without any conventional cardiovascular risk factors
presented to the emergency room with severe anginal chest pain. ECG
showed lateral wall ST-elevation and serial serum troponins were
elevated. Emergent cardiac catheterization showed spontaneous coronary
artery dissection involving the first diagonal artery with
angiographically normal other epicardial coronary arteries. Left
ventriculogram and echocardiogram showed a moderately reduced left
ventricular systolic function with akinetic mid to distal myocardial
segments and normal basal contraction suggestive of stress-induced
cardiomyopathy. Spontaneous coronary artery dissection presenting with
ST-elevation myocardial infarction and stress-induced cardiomyopathy is
very rare.%
\end{abstract}%



\sloppy


The spectrum of myocardial stress: Concurrent spontaneous coronary
artery dissection and stress-induced cardiomyopathy in a patient
presenting with acute ST-segment elevation myocardial infarction.

Subash Nepal\textsuperscript{a}, MD, Dana Aiello, MD, Kamala Ojha, MD.

\textsuperscript{a} Corresponding author: Subash Nepal, MD

PGY6 Cardiovascular Diseases, Upstate Medical University, Syracuse, NY

(nsubash39@gmail.com)

Dana Aiello, MD

Cardiovascular Diseases, Upstate Medical University, Syracuse, NY

(daiellomd@gmail.com)

Kamala Ojha, MD

Internal Medicine, Upstate Medical University, Syracuse, NY

(OjhaK@upstate.edu)

Conflict of interest: We have no conflict of interest to declare.

Funding source: None

Ethics approval: Our hospital does not require ethics approval or
patient consent before submitting case reports.

Abstract

A 72-year-old lady without any conventional cardiovascular risk factors
presented to the emergency room with severe anginal chest pain. ECG
showed lateral wall ST-elevation and serial serum troponins were
elevated. Emergent cardiac catheterization showed spontaneous coronary
artery dissection involving the first diagonal artery with
angiographically normal other epicardial coronary arteries. Left
ventriculogram and echocardiogram showed a moderately reduced left
ventricular systolic function with akinetic mid to distal myocardial
segments and normal basal contraction suggestive of stress-induced
cardiomyopathy. Spontaneous coronary artery dissection presenting with
ST-elevation myocardial infarction and stress-induced cardiomyopathy is
very rare.

Keywords: Spontaneous coronary artery dissection, stress-induced
cardiomyopathy, ST-elevation myocardial infarction

Introduction:

Spontaneous coronary artery dissection (SCAD) and stress-induced
cardiomyopathy (SC) are different clinicopathologic entities that
frequently present with the acute coronary syndrome (ACS) without
underlying atherosclerotic coronary artery disease. SCAD and SC commonly
present with ACS in post-menopausal women and are believed to be due to
stress-induced neurohormonal surge, exposure to female sex hormones; and
catecholaminergic toxicity leading to coronary microvascular dysfunction
and apical stunning respectively.\textsuperscript{1,2} SCAD is the most
common cause of ACS in young women without any conventional
cardiovascular risk factors, including those who are pregnant,
parturient, and on oral contraceptives.\textsuperscript{3} It is a
nontraumatic tear in the epicardial coronary artery and the spectrum
ranges from the intimal rupture to expanding intramural hematoma
obstructing the distal flow leading to ischemia. The etiology is
multifactorial and is hypothesized to be associated with exposure to
female sex hormones, environmental and emotional stressors, and
underlying fibromuscular dysplasia.\textsuperscript{4} SC is usually
preceded by physical or emotional stress. It causes a catecholaminergic
excess state, leading to hypokinesis of the cardiac apex and
hypercontractility of the base, causing classical apical ballooning. It
occurs predominantly in post-menopausal women soon after exposure to
emotional and physical stressors and presents with typical chest pain,
ST-segment changes, and troponin elevation. It is the diagnosis of
exclusion and epicardial coronary artery disease needs to be ruled out
by invasive coronary angiogram. It is generally reversible but sometimes
systolic dysfunction may persist, leading to chronic non-ischemic
cardiomyopathy. Stress causes a surge of adrenaline (Epi) from the
adrenal medulla and nor-adrenaline (NE) from cardiac nerve endings after
excitation of the medullary autonomic system. Circulating adrenal Epi
exerts stronger hormonal effects on the cardiac tissue than
NE.\textsuperscript{5} The basal myocardium is rich in sympathetic nerve
terminals and noradrenaline whereas the apex is rich in
\selectlanguage{greek}β\selectlanguage{english}\textsubscript{1}-receptors.\textsuperscript{6,7} High NE thus results
in vigorous basal contraction. However, excess Epi in the apex due to
low clearance due to sparse neural uptake leads to excitotoxicity of the
apical adrenoreceptors and intracellular Ca
\textsuperscript{2+}overload.\textsuperscript{2,8} This is compounded by
an increased afterload state created by increased Nadr surge to the
peripheral arteries leading to apical myocardial stunning which presents
as classical ``ballooning'' of the cardiac apex. \textsuperscript{5}

Although both SCAD and SC are common in post-menopausal women and are
believed to result from stress-induced neurohormonal surge, they are
rarely present concomitantly. We report a rare case of a post-menopausal
lady who presented with ST-segment elevation myocardial infarction and
was found to have SCAD of a non-culprit vessel and typical
echocardiographic features of SC.

Case report:

A 72-year-old lady with a past medical history of recurrent stage IIA
invasive ductal carcinoma of the breast, grade III, estrogen
receptor-positive status post bilateral mastectomy, radiation therapy,
chemotherapy, and adjuvant endocrine therapy with Anastrozole which was
completed a month prior to presentation and on remission presented with
anginal chest pain. The patient was hemodynamically stable, and the
cardiovascular system examination was unremarkable. ECG showed ST
segment elevation in leads I and aVL, figure 1, and serial
high-sensitivity troponins were elevated to 910 ng/L, 2000 ng/L, and
1400 ng/L. She was treated with Aspirin 324mg and Clopidogrel 600 mg and
was emergently taken to the cardiac catheterization lab. Coronary
angiogram showed type 3 spiral dissection in the first diagonal artery
and normal other major epicardial coronary arteries (Video a, Video b,
Video c, Video d, Video e, and Video f). The left ventriculogram showed
an ejection fraction of 35\%, apical akinesis, and basal hyperkinesis
suggestive of stress-induced cardiomyopathy (Video g). Transthoracic
echocardiography showed a moderately reduced ejection fraction of 35\%
with mid to distal anterior, lateral, inferior, inferoseptal,
inferolateral, and anteroseptal segments with preserved basal
contraction suggestive of stress-induced cardiomyopathy, Video h and
Video i. Her baseline echocardiography was normal. The wall motion
abnormalities along with a moderate reduction in left ventricular
systolic function were typical for stress-induced cardiomyopathy and not
explained by SCAD of the first diagonal artery (D1). This established
the fact the initiating event was SCAD of D1 which presented with acute
lateral wall STEMI and stress-induced cardiomyopathy. The patient was
medically managed with dual Antiplatelets, Metoprolol, Atorvastatin, and
Valsartan and discharged home in stable condition.

Discussion:

SCAD and stress-induced cardiomyopathy are the different manifestations
of cardiac neurohormonal stress. The first stress-induced cardiomyopathy
was first described by Iga et al\textsuperscript{9} as reversible left
ventricular dysfunction associated with pheochromocytoma. Sato et
al\textsuperscript{10} first described it as tako-tsubo-like left
ventricular dysfunction in 1990. The incidence is rising, and patients
present with typical chest pain, classical apical hypokinesis, and basal
hyperkinesis in echocardiography with elevated cardiac enzymes mimicking
acute coronary syndrome and have normal coronary angiography. These
patients are treated with beta-blockers, renin-angiotensin-aldosterone
system (RAAS) inhibitors with improvement in left ventricular ejection
fraction. First described by Pretty in 1931,\textsuperscript{11} SCAD
has been found to be increasingly associated with myocardial infarction
(MI) in premenopausal and postmenopausal women without any conventional
cardiovascular risk factors; 90 \% of SCAD patients are women who
present with ACS in their 5\textsuperscript{th} and
6\textsuperscript{th} decades of life.\textsuperscript{12} SCAD accounts
for 35\% of MIs in women \textless{}50 years and is the most common
cause of MI in pregnancy. Studies suggest SCAD accounts for less than
1\% of all MI overall and is very uncommon in
males.\textsuperscript{1,13} There are three types of SCAD, type 1:
multiple radiolucent lumens or contrast staining of the vessel wall,
type 2: diffuse stenosis with a sudden change in vessel caliber, and
type 3: focal or tubular stenosis.\textsuperscript{14} SCAD has a
predilection for the distal vessel and in terms of coronary
distribution, the left anterior descending artery is most affected, and
its diagonal and septal branches are involved in 45\%-61\% of cases,
followed by the circumflex artery and its branches in about 30\% and the
right coronary artery and its branches in abound 15\%
.\textsuperscript{15} SCAD is initially diagnosed by invasive coronary
angiography. Intracoronary imaging modalities like intravascular
ultrasound (IVUS) and optical coherence tomography (OCT) have better
spatial resolution and can be performed if a coronary angiogram is
inconclusive.\textsuperscript{14} Conservative management is recommended
as studies show spontaneous angiographic healing in 90\% of patients
within a month.\textsuperscript{16} Percutaneous coronary intervention
(PCI) can lead to an increased risk of complications. The coronary
guidewire may enter the false lumen and balloon angioplasty and stent
placement may lead to the propagation of dissection or stent
malapposition.\textsuperscript{17} PCI is only indicated for patients
with ongoing ischemia or hemodynamic instability. Coronary artery bypass
grafting is performed if PCI fails, or the patient has proximal or left
main dissection, or refractory ischemia despite conservative
management.\textsuperscript{16} These patients should be hospitalized
for 3-5 days as chances of early clinical deterioration and new
recurrent dissection are high.\textsuperscript{18} Treatment with
antiplatelets is controversial and dual antiplatelets are used for 12
months only after PCI as per the guidelines. Beta-blockers are proven to
reduce recurrence.\textsuperscript{19} Mortality is low at 1-2\% and the
incidence of recurrent SCAD and MI is about 18\%.\textsuperscript{19}The
patients frequently present to the clinic after discharge with chest
pain, due to sequelae of dissection or underlying psychologic stress,
depression, and anxiety from SCAD, hence should be closely followed up.

Conclusion

Stress-induced cardiomyopathy and SCAD are different pathophysiologic
manifestations of the same etiologic process and may present
concurrently. They masquerade as acute myocardial infarction due to
atherosclerotic coronary artery disease in their clinical presentation
and differentiation is important as treatment, outcome, and prognosis
are different. Detailed evaluation for SCAD in these patients is
important during a coronary angiogram; IVUS or OCT should be used
additionally if the angiogram is inconclusive as SCAD tends to affect
the branch vessels and distal small vessels which may be undetected with
conventional angiogram only.

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Copyright © 2023, StatPearls Publishing LLC.; 2023.

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Figure 1: ECG showing ST-elevation in leads I and aVL with reciprocal
ST-depression in leads III and aVF

Video a: Coronary angiogram LAO cranial view after left coronary artery
intubation showing type 3 dissection involving proximal first diagonal
artery (D1) and normal circumflex (Circ) and left anterior descending
coronary artery (LAD)

Video b: Coronary angiogram RAO cranial view after left coronary artery
intubation showing type 3 dissection involving D1 and normal LAD

Video c: Coronary angiogram LAO caudal view after left coronary artery
intubation showing type 3 dissection involving proximal first diagonal
artery and normal circumflex and LAD

Video d: Coronary angiogram RAO caudal view after left coronary artery
intubation showing type 3 dissection involving the first diagonal artery
and normal circumflex and LAD

Video e: Coronary angiogram LAO cranial view after right coronary artery
intubation showing a normal proximal and distal right coronary artery
(pRCA and dRCA), right posterior descending artery (RPDA) and right
posterolateral (RPL) branches

Video f: Coronary angiogram RAO cranial view after right coronary artery
intubation showing a normal proximal, mid and right coronary artery and
branches

Video g: Left ventriculogram in RAO cranial projection showing
anteroapical (A) akinesis with hypercontractile base (B)

Video h: Transthoracic echocardiography, apical two chamber view showing
akinetic mid to distal inferior and anterior walls

Video i: Transthoracic echocardiography, apical four chamber view
showing LV ejection fraction of about 35\% with akinetic mid to apical
inferoseptal, septal and lateral segments with preserved basal
contractility

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