Discussion:
CE is a non-atherosclerotic cause of AMI that can present as either
STEMI or NSTEMI. CE accounts for 4% to 13% of acute MI cases, as
observed in angiographic and autopsy studies. The first description of
CE-related MI dates back to 1856 by Rudolf Virchow. The primary causes
of CE include atrial fibrillation (AF), cardiomyopathy, and malignancy;
however, 26.3% of cases have no discernible source8,9.
CE can theoretically arise from three primary sources. The first is
direct embolism, occurring from thrombi originating in the left atrial
appendage, left ventricle, or heart valves, often due to conditions such
as infective endocarditis or cardiac tumors. The second source is
paradoxical embolism, which occurs when venous thrombi travel into
systemic circulation through openings like a patent foramen ovale or
atrial septal defects. The third source is iatrogenic embolism, which
can result from medical procedures such as aortic valve replacements or
percutaneous coronary interventions (PCI). Although coronary arteries
are generally protected from systemic embolisms, risks like coronary air
embolism can arise during PCI, potentially leading to vessel occlusion.
Furthermore, complications such as device embolization and microthrombi
during STEMI interventions can complicate diagnosis, especially when
thrombi coexist with underlying atherosclerosis 8.
Diagnosing CE can be challenging due to its clinical presentation, which
resembles atherosclerotic acute coronary syndromes (ACS). To help
differentiate CE from atherosclerotic coronary artery disease (CAD),
Shibata et al. introduced diagnostic criteria based on clinical and
angiographic findings, classifying CE as either “definite” or
“probable” (Table 1). In CE cases, coronary artery stenosis is
typically minimal, aiding in distinguishing it from atherosclerotic
causes. Imaging techniques such as angiography, transthoracic
echocardiography (TTE), transesophageal echocardiography (TEE), and
magnetic resonance imaging (MRI) are essential for identifying embolic
sources, with AF being the most commonly implicated risk factor4,9.
Coronary arteries are generally more protected from embolic events than
other vascular systems due to several factors, including their smaller
diameter, higher vascular resistance, and the anatomical positioning of
the aortic valve and sinus of Valsalva, which reduce the likelihood of
embolization during systole 4. However, in patients
with AF, dilated cardiomyopathy, or prosthetic heart valves, emboli can
lodge in the coronary arteries, causing CE 10.
Notably, CE preferentially affects the left coronary system, occurring
three to four times more frequently than the right, particularly in the
left anterior descending artery, due to its anatomical orientation,
which makes it more susceptible to embolization. In contrast, coronary
vasospasm is more frequently reported in the proximal right coronary
artery 1.
It is crucial to emphasize the relationship between MI and the presence
of a left intraventricular thrombus. In these instances, CE can either
serve as a cause, where MI leads to the formation of the ventricular
thrombus, or as a consequence, where CE arises from a pre-existing
ventricular thrombus 8.
Cocaine use stimulates the formation of intraventricular thrombus
through sympathetic activation, resulting in prolonged coronary
vasospasm and direct myocardial injury. Additionally, its prothrombotic
effects further elevate the risk of intracardiac thrombus formation6,11.
Left ventricular (LV) thrombus is a significant complication of LV
dysfunction, closely associated with systemic embolism, morbidity, and
mortality. Heart failure and acute MI, particularly STEMI, are common
causes of LV thrombus. Reduced ejection fraction (EF) is prevalent in
these cases, with 36% of patients having an EF <20%, 38.7%
with an EF between 20% and 30%, and 25.3% with an EF between 30% and
40%. Cases with an EF between 41% and 49% are less common (8%), as
are those with an EF ≥50% (5%) 12. The LAD artery is
the most frequently involved culprit artery, accounting for 77.8% of
cases. In contrast, RCA occlusion, as seen in our patient, is rare.
Thrombus formation is significantly related to the region with the most
severe functional impairment, often reflecting infarction or scarring.
Global LV dysfunction is present in 64.8% of cases, with regional
dysfunction commonly affecting the apex (92.7%), anterior (26.8%),
septal (26.8%), inferior (14.6%), and lateral (9.8%) regions12,13.
The combination of blood stasis, endothelial injury, and
hypercoagulability, collectively known as Virchow’s triad, is essential
for thrombus formation. In the context of acute MI, particularly
associated with cocaine use, all three components of this triad are
evident. Regional wall akinesia and dyskinesia contribute to blood
stasis; prolonged ischemia leads to subendocardial tissue injury and
inflammation; and cocaine use promotes a hypercoagulable state6,13.
Cocaine is emerging as a significant cause of MI through both coronary
vasospasm and thrombosis. It increases platelet aggregation and induces
vasoconstriction, leading to thrombus formation within the coronary
arteries. The drug’s ability to enhance norepinephrine activity
heightens sympathetic activation, resulting in coronary vasospasm that
can lead to ischemia and MI. Cocaine not only enhances thromboxane A2
production, a promoter of platelet aggregation and vasoconstriction, but
also reduces the release of prostacyclin, which normally inhibits
platelet aggregation. These imbalances promote a prothrombotic state,
while cocaine also increases platelet sensitivity to aggregating agents
such as adenosine diphosphate (ADP) and epinephrine, further heightening
platelet activity. The combination of endothelial dysfunction and
increased platelet activation raises the risk of coronary thrombosis and
MI, even in the absence of atherosclerotic disease. Additionally,
chronic cocaine use can lead to premature atherosclerosis,
cardiomyopathy, and conduction abnormalities, further elevating the risk
of MI 6(p1),14.
The combination of smoking and cocaine use, as observed in our patient,
amplifies the risk of cardiovascular events due to their combined impact
on endothelial function and thrombotic pathways. Both substances cause
endothelial injury and impair prostacyclin production, exacerbating
platelet aggregation. Smoking also increases oxidative stress and
inflammatory markers, further contributing to endothelial dysfunction6(p1),14. Additionally, chronic smokers have elevated
fibrinogen levels, which, when combined with cocaine’s effects, enhance
platelet aggregation and increase the risk of thrombus formation.
Moreover, the effects of cocaine can be exacerbated by concomitant
alcohol consumption, which may also be relevant to our patient6.
Aortic dissection is one of the cardiac manifestations that cocaine can
induce, and it should be highly suspected in patients presenting with
chest pain radiating to the back following cocaine use. In such cases, a
CT angiogram can be utilized to rule out the condition. Cocaine has
several pathophysiological effects that may increase the risk of aortic
dissection. By inhibiting catecholamine reuptake, cocaine stimulates the
autonomic nervous system, resulting in elevated heart rate and blood
pressure. Additionally, cocaine acts synergistically with alpha agonists
to induce vasoconstriction. Chronic cocaine consumption can alter the
elastic properties of the aorta, leading to decreased strain, reduced
distensibility, and increased aortic stiffness. Furthermore, the sudden
and severe elevation of blood pressure induced by cocaine produces
increased shear stress in the aorta, contributing to intimal disruption
that allows the blood column to enter the media and leads to subsequent
antegrade or retrograde propagation of the medial hematoma15.
In terms of management, coronary interventions for CE differ from those
for atherosclerotic MI. Thrombus aspiration and balloon angioplasty are
preferred approaches, often eliminating the need for stent implantation4. Aoun et al. proposed a comprehensive algorithm for
managing CE 16. In cases of small, distal CE without
hemodynamic instability, the recommended approach is anticoagulation
therapy alone. However, in the presence of high intracoronary thrombus
burden accompanied by instability, thrombus aspiration should be
prioritized. If angiography indicates CE and the coronary anatomy is
favorable, thrombectomy may be attempted. While the efficacy of
intracoronary thrombolysis or glycoprotein IIb/IIIa inhibitors has not
been established through randomized clinical trials, their use is
frequently reported in clinical cases. Notably, Popovic et al. found
that interventional procedures for CE involved significantly higher
utilization of glycoprotein IIb/IIIa inhibitors compared to non-CE cases
(73.9% vs. 37.7%), alongside a markedly lower rate of angioplasty
(45.3% vs. 95.5%) 10. In instances where thrombus
aspiration results in a TIMI flow grade of less than 2, primary stenting
may be considered. Conversely, if TIMI flow is 2 or greater following
thrombus aspiration, intravascular ultrasound or optical coherence
tomography may be employed to investigate potential plaque erosion. A
minimalistic revascularization strategy aimed at achieving TIMI flow
grade 3 is preferred, ideally without the need for stenting8.
The Penumbra CAT RX has demonstrated significant efficacy and safety in
thrombus removal in acute settings, without the heightened risk of
systemic emboli associated with manual aspiration thrombectomy. Approved
for coronary use in 2017, this device features an atraumatic catheter
combined with a sustained vacuum source, providing consistent power
aspiration throughout the procedure. Clinical outcomes reveal that after
the use of the CAT RX, 88% of patients achieved a post-procedure TIMI
flow of 3, 9% attained TIMI 2 flow, and 3% experienced TIMI 0 flow17.
In conclusion, this case underscores the critical need for heightened
awareness of coronary embolism (CE) as a potential cause of acute
myocardial infarction (AMI), particularly in younger patients with a
history of substance abuse, such as cocaine use. The interplay between
cocaine’s thrombogenic effects, the formation of a left ventricular
thrombus, and subsequent coronary artery embolism highlights the
complexities of diagnosing and managing such cases. Successful
aspiration thrombectomy in this patient not only restored coronary blood
flow but also emphasizes the importance of tailored therapeutic
approaches in managing CE, differing from conventional treatment
strategies for atherosclerotic causes. Clinicians should consider CE in
the differential diagnosis of AMI, especially in patients with risk
factors associated with thrombus formation, and remain vigilant for
potential complications arising from both substance use and
cardiovascular pathology.