Floating aortic arch thrombus involving the left common carotid artery complicated with ischemic stroke associated with cocaine use.

BACKGROUND: Floating aortic thrombi (FLOAT) are rare, with very few cases attributed to cocaine use. We report a new case of FLOAT involving the left common carotid artery due to cocaine use, for the first time, complicated with acute ischemic stroke.
METHODS: We present in detail our case report, and then, a literature search in PubMed and Scopus was performed up to March 20, 2022, to review the reported cases of aortic thrombus associated with cocaine use.
RESULTS: A 39-year-old man with a history of smoking and daily cocaine use was admitted to our stroke unit for acute left-hemispheric symptoms due to carotid-Sylvian occlusion. CT angiography of the supra-aortic trunks showed FLOAT involving the left common carotid artery. The thrombus was removed successfully by endovascular thrombectomy with recanalization of carotid-Sylvian occlusion. Our literature search yielded seven reported cases of aortic thrombus due to cocaine use revealed by lower limb ischemia (3 patients), renal infarction (1 patient), abdominal pain (1 patient), bowel ischemia (1 patient), and lower limb ischemia with renal infarction (1 patient).
CONCLUSION: Aortic thrombus should be suspected in patients without overt cardiovascular risk factors but with a recent history of cocaine use who presents with acute ischemic stroke.

Introduction

Floating aortic thrombi (FLOAT) are rare and mainly diagnosed after an embolic event such as acute lower limb ischemia, renal infarction, and bowel ischemia [1-3]. FLOAT are mainly secondary to atherosclerotic disease of the aortic wall [2]. However, a very few cases of FLOAT have been attributed to cocaine use. Here, we report a new case of FLOAT involving the left common carotid artery (CCA) due to cocaine use, for the first time, complicated with acute ischemic stroke (AIS).

Methods

We present in detail our case report. Besides, we performed a systematic literature review (SLR) of the reported cases of aortic thrombus due to cocaine use.

The present study was a routine care study, and approval by an ethics committee was not required. The patient provided written informed consent to publish all the information contained in this study.

Results

Current case report

A 39-year-old man with a history of smoking and daily cocaine use was admitted to our stroke unit for acute speech disorders and right-sided weakness. Neurological examination at 473 min (7.88 h) from symptom onset to arrival found complete right-sided hemiplegia, right homonymous lateral hemianopsia, deviation of the head and eyes to the left-sided, and severe global aphasia with a LAST (Language Screening Test) of 0/15 and an NIHSS (National Institutes of Health Stroke Scale) of 21.

The 1.5 T cerebral MRI, performed at 493 min (8.2 h) from symptom onset to imaging or 20 min from arrival to imaging, showed AIS of left middle cerebral artery territory due to carotid-Sylvian occlusion with slight visibility of ischemic lesions on the lenticular caudate (Fig. 1a, b, c, d, e, f). The 80-bar computed tomography angiography (CTA) showed a FLOAT involving the left CCA (Fig. 1g, h).

Fig. 1

a, b Diffusion-weighted MR showing ischemic stroke of left middle cerebral artery territory. c, d, e Fluid-attenuated inversion recovery showing slow flows in the left hemispheric sulci with slight visibility of ischemic stroke on the lenticular caudate. f Time-of-flight MR angiography showing left carotid-Sylvian occlusion. g, h CT angiography showing floating aortic arch thrombus involving the left common carotid artery

Intravenous thrombolysis was not performed first because of the FLOAT with a high risk of fragmentation and distal embolization, and second, the slight visibility of ischemic lesions on the lenticular caudate with risk of hemorrhagic transformation. The FLOAT was removed successfully by endovascular thrombectomy with recanalization (TICI 3) of carotid-Sylvian occlusion 600 min (10 h) after the symptom onset or 107 min (1.8 h) after imaging.

Cardiac exploration (echocardiography and cardiac telemetry on 4 days) was normal. Antinuclear antibodies, anti-double-stranded DNA, antiphospholipid, and antineutrophil cytoplasmic antibodies were all negative. PCR COVID-19 test was negative. The search for metabolites of cocaine in urine was strongly positive. The diagnosis of AIS revealing FLOAT involving the left CCA due to cocaine intake was retained.

The patient improved partially, and upon discharge from the hospital on the 17th day, he had complete right-sided hemiplegia, right homonymous lateral hemianopsia, and severe aphasia without comprehension disorders with a LAST of 8/15 and an NIHSS of 17.

Systematic literature review

We performed a literature search in PubMed and Scopus up to March 20, 2022, using the combination of the following keywords: “Aorta” OR “Aortic” and “Thrombosis” OR “Thrombus” and “Cocaine.” We found seven reported cases of aortic thrombus due to cocaine use [3-8], and their baseline characteristics are presented in Table 1. Six of the seven patients were cocaine users, while the 7th patient was exposed to cocaine in utero. The clinical presentation included acute lower limb ischemia, renal infarction, abdominal pain, bowel ischemia with peritonitis by mid-jejunal perforation, and acute lower limb ischemia associated with renal infarction. The therapeutic strategy was essentially surgical thrombectomy.

Table 1

Systematic literature review of reported cases of aortic thrombus associated with cocaine use

Year	First author	Country	Sex/Age (years)	Past medical history	Clinical presentation	Diagnostic tool	Location	Treatment
2017	Poon et al. [3]	England	M/41	Cocaine use, Goodpasture syndrome, heavy smoking	Bowel ischemia with mid-jejunal perforation and peritonitis	CTA	Ascending aorta	ST
2013	Paulin Vera et al. [4]	Spain	M/35	Current smoking; cocaine use	Acute lower limb ischemia	CTA	Subrenal aorta	Revascularization surgery, aortobifemoral bypass Dacron graft, anticoagulation with LMWH and antiplatelet therapy
2004	Zhou et al. [5]	U.S.A	M/26	Cocaine Intranasal inhalation	Acute lower limb ischemia	CTA	–	ST
2003	Mochizuki et al. [6]	U.S.A	-	Cocaine use	Renal infarction	–	–	–
1999	Webber et al	U.S.A	M/34	Smoking crack cocaine	Acute lower limb ischemia, renal infarction	Aortography	Subdiaphragm abdominal aorta	ST
1999	Webber et al. [7]	U.S.A	F/39	Smoking crack cocaine	Abdominal pain	Aortography	Sub-diaphragm abdominal aorta	ST, anticoagulation with heparin sodium
1996	Wardle et al. [8]	England	F/Newborn	Cocaine use in the mother throughout pregnancy	Respiratory distress, absent femoral pulses	Intraoperative diagnosis	Ascending aorta	ST

F indicates female, M male, USA United States of America, CTA computed tomography angiography, ST surgical thrombectomy, LMWH low-molecular-weight heparin

Discussion

We report the first case of FLOAT involving the left CCA due to cocaine use complicated with AIS in a young Caucasian. An exhaustive diagnostic workup has been carried out and permitted to rule out other causes.

Cocaine is a potent vasoconstrictor due to its sympathomimetic action, which is susceptible to inducing vasospasm of small and medium caliber arteries causing AIS or myocardial infarction [9, 10]. However, the exact pathophysiologic mechanism by which cocaine causes thrombosis formation in the large arteries such as the aorta, iliac arteries, or carotid arteries remains uncertain. A study demonstrated that cocaine exposure could induce platelet activation, platelet alpha granule release, and the formation of platelet-containing microaggregates [11]. That is possible because cocaine exposure could induce alteration in endothelial antithrombotic activity by increasing the production of prostaglandins, with a disproportionate increase in thromboxane relative to prostacyclin. Another potential mechanism is that long-term cocaine exposure increases adventitial mast cells and atherosclerosis [12], favoring platelet activation and arterial thrombosis formation.

CTA of the aorta is the noninvasive diagnostic tool most used to diagnose aortic thrombus. Surgical thrombectomy was the main therapeutic strategy according to our SLR (see Table 1). In our patient, the aortic thrombus extending into the left CCA was removed successfully by endovascular thrombectomy.

Conclusion

Aortic thrombus should be suspected in patients without overt cardiovascular risk factors but with a recent history of cocaine use who presented AIS. For this purpose, it is substantial to perform a CTA of the supra-aortic trunks descending to the ascending aortic because prompt diagnosis and appropriate treatment, possibly endovascular, could avoid other embolic complications.