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\begin{document}

\title{Acute myocardial infarction due to coronary artery embolism in atrial
fibrillation in Takotsubo cardiomyopathy patient: A case report}



\author[1]{Muhammad Hanif}%
\author[2]{Mostafa Vasigh}%
\author[2]{Muhammad Malik}%
\author[3]{Vikash Jaiswal}%
\author[4]{Abhigan  Shrestha}%
\author[2]{Hami Kozman}%
\affil[1]{SUNY The State University of New York}%
\affil[2]{SUNY Upstate Medical University}%
\affil[3]{AMA School of Medicine}%
\affil[4]{M Abdur Rahim Medical Medical College Hospital}%


\vspace{-1em}



  
  \date{June 07, 2024}


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\textbf{Introduction:}

Myocardial infarction with nonobstructive coronary artery disease
(MINOCA) is a group of conditions that share common characteristics and
is characterized by the absence of [?]50\% stenosis of coronary arteries
and without any evidence of atherosclerotic plaque rupture {[}1{]}. A
study conducted by Waller et al. reported that 4\% to 7\% of all
patients diagnosed with AMI, do not have underlying atherosclerotic
coronary disease on autopsy or angiography {[}2{]}.

Coronary artery embolism is a rare and important non-atherosclerotic
cause of acute myocardial infarction (AMI), and the first case of AMI
secondary to coronary embolism was reported in 1856 by Rudolf Virchow
and was classified initially as a precipitating factor for type-II MI,
now recognized as one of the cause of MINOCA {[}3{]}. Coronary embolism
(CE) is more frequently reported in infective endocarditis patients and
it mainly involves the left main coronary artery system due to flow
characteristics and aortic morphology {[}4, 5{]}. CE may also originate
from mural thrombus within the left-sided cardiac chambers, but it has
rarely been reported in the literature {[}6{]}. Most cases of coronary
embolism in the literature have been reported secondary to infective
endocarditis, valvular heart diseases, and atrial fibrillation
{[}7-9{]}. Here, we are reporting a case of a 74-year-old female, who
had a chronic history of atrial fibrillation on anticoagulation with
questionable compliance and was admitted with sepsis and takotasubo
cardiomyopathy and later developed AMI secondary to coronary embolism to
the left anterior descending artery.

\textbf{Case History/examination:}

A 74-year-old female with a past medical history of atrial fibrillation
on rivaroxaban with questionable compliance, type 2 diabetes, multiple
cerebrovascular accidents, and suspected paranoid schizophrenia, was
brought to the ED with altered mental status.

On examination, her pulse was 114/min, irregularly irregular, blood
pressure of 123/109 mmHg, respiratory rate of 24/min, afebrile, and was
maintaining oxygen saturation of 95\% at room air.

\textbf{Methods:}

Baseline investigations showed WBC of 14.9 and urinalysis suggestive of
UTI. Her Troponin level and proBNP were reported high (troponin 56 and
proBNP of 16, 484). Electrocardiography (EKG) revealed atrial
fibrillation with rapid ventricular response, low voltage QRS, poor R
wave progression, and non-specific T wave abnormalities. Transthoracic
echocardiography reported a mildly dilated left ventricle and new
severely reduced systolic left ventricular ejection fraction (LVEF 24\%)
with moderate diffuse~hypokinesia, akinetic left ventricular apex, and
severely hypokinetic inferolateroseptal wall, features suggestive of
Takotsubo cardiomyopathy (Figure 1). There were no LA or LV clots
detected on this echocardiogram, but this study was done without
contrast. CT head reported negative for acute intracranial abnormality
and the patient was started on IV antibiotics for treatment of sepsis in
the setting of a urinary tract infection.

Cardiology was consulted for the newly depressed EF who recommended
starting a statin, beta-blockers, and angiotensin-converting enzyme
inhibitor (ACEI) if tolerable and a pharmacologic nuclear stress test to
evaluate cardiomyopathy further.

The next day, the rapid response team (RRT) was called for hypotension
of 66/38 mmHg and chest pain. ~EKG revealed atrial fibrillation with
rapid ventricular response, right bundle branch pattern (RBBB), and ST
elevations in the anterolateral leads suggestive of acute ST-elevation
myocardial infarction (Figure no. 2).

The patient was started on inotropic support and was emergently
transferred to the cardiac catheterization laboratory.~~On coronary
catheterization, after placement of a balloon pump for hemodynamic
support, a proximal LAD lesion with 100\% occlusion and heavy thrombus
burden was discovered (Figure 3). Initially, thrombus aspiration using a
Pronto Extraction Catheter was attempted which was unsuccessful, but
after POBA (percutaneous old balloon angioplasty) of the proximal LAD
flow was restored. Post-injection revealed TIMI 3 flow in the LAD with
no further underlying LAD disease, but a new 100\% occlusion of the
proximal LCx was now detected which likely occurred due to clot
embolization during PCI to LAD (Figure 4). Again, after a trial of
unsuccessful thrombectomy using the Pronto Extraction Catheter, POBA
followed by deployment of a DES to the pLCX was performed without any
further complications.

\textsubscript{.}

A repeat transthoracic echocardiogram after PCI revealed an improvement
in LVEF from 24\% to 45\% EF. The patient was eventually weaned off the
balloon pump and pressor support after 4 days and was started on beta
blockers and angiotensin-converting enzyme inhibitors (ACEI) and
clopidogrel along with rivaroxaban and was discharged home after a week
with outpatient follow-up at the cardiology clinic.

\textbf{Conclusion and results:}

Coronary artery embolism is a rare and fatal cause of acute myocardial
infarction and has rarely been reported secondary to atrial fibrillation
in takotsubo cardiomyopathy patients. Early diagnosis and treatment play
a vital role in the prevention of short-term as well as long-term
post-myocardial infarction complications. Physicians and cardiologists
should have a low threshold for coronary artery embolism when
encountering shock patients with atrial fibrillation, as early
management prevents hazard complications.

\textbf{Discussion:}

According to angiographic and autopsy data, various causes of coronary
artery embolism have been reported in the literature {[}10{]}. Different
studies reported various causes as the most common cause of coronary
artery embolism. A study conducted by Charles et al. reported bacterial
endocarditis as the common cause of coronary embolism, while Prizel et
al. reported valvular heart diseases and cardiomyopathy as the common
risk factors for causing coronary embolism {[}11, 12{]}. However, a
recent study conducted by Popovic et al. reported atrial fibrillation as
the most common cause of coronary artery embolism, followed by dilated
cardiomyopathy and bacterial endocarditis respectively {[}13{]}.
Similarly, Shibata et al. conducted a study on new-onset MI between 2001
to 2013 and reported that 2.9\% of AMIs were due to coronary embolism,
with the most prevalent cause reported was atrial fibrillation, followed
by cardiomyopathy and valvular heart disease {[}10{]}. Very rarely,
paradoxical embolism causing acute myocardial infarction has been
reported in the literature {[}14{]}.

Atrial fibrillation patients are at increased risk of left atrium
thrombus formation, particularly in the left atrial appendage, through
Virchow's triad of blood stasis, endothelial damage, and hypercoagulable
state. These patients benefit from anticoagulation and require life-long
anticoagulation to prevent thrombus formation and associated
complications. In our case, a patient was admitted with a chronic
medical history of atrial fibrillation on anticoagulation with
questionable compliance and was admitted with sepsis and takotasubo
cardiomyopathy, and later complicated by AMI secondary to coronary
embolism to the LAD. Multiple factors played their role in developing
coronary embolism in our patients, with the most common being atrial
fibrillation with questionable compliance with anticoagulation, followed
by takotsubo cardiomyopathy. Coronary artery embolism secondary to
takotsubo cardiomyopathy has been reported in the literature {[}15{]},
and the typical apical ballooning form of takotsubo cardiomyopathy seems
to be more vulnerable to thrombus formation, which then leads to various
thromboembolic complications {[}16{]}.

\textbf{Author contribution:}

Conceptualization: Muhammad Hanif

\textsuperscript{All authors contributed equally. Supervision: Hani
Kozman}

Declaration of patient consent

Written informed consent was obtained from the patient for the
publication of this case report and

accompanying images. A copy of the written consent is available for
review by

the Editor-in-Chief of this journal on request.

Data availability: All the data are available in the manuscript.

Sources of funding

None

Ethical approval

N/A

Conflicts of Interest

There are no conflicts of interest.

Provenance and peer review

Not commissioned, externally

peer-reviewed

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12. Prizel KR, Hutchins GM, Bulkley BH. Coronary artery embolism and
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doi:10.7326/0003-4819-88-2-155

13. Popovic B, Agrinier N, Bouchahda N, et al. Coronary Embolism Among
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doi:10.1161/CIRCINTERVENTIONS.117.005587

14. Meier-Ewert HK, Labib SB, Schick EC, Gossman DE, Stix MS, Williamson
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Figure legends:

Figure No. 1: Two chambers echocardiography showing akinetic left
ventricular apex (blue arrow) and overall diffuse moderate hypokinesia,
features of takotsubo cardiomyopathy.

Figure no. 2: EKG showing right bundle branch block, ST-elevation
changes in the

anterolateral leads with reciprocal changes in inferior leads.

Figure 3: PCI showing proximal LAD lesion with 100\% occlusion (blue
arrow).

\textsubscript{Figure no. 4: PCI showing 100\% occlusion of the proximal
left circumflex artery (blue arrow)}

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