Mechanical Thrombectomy for Methamphetamine-Associated Cardiomyopathy with Left Ventricular Thrombus: A Case Report

Abstract

Objective: The global increase in methamphetamine abuse has increased the incidence of methamphetamine-associated cardiomyopathy (MACM), which is often complicated by left ventricular thrombosis and acute ischemic stroke. Here, we report a case of left internal carotid artery occlusion during acute heart failure treatment in a patient with MACM that led to mechanical thrombectomy.

Case Presentation: A 54-year-old man with a history of approximately 30 years of methamphetamine abuse presented with dilated cardiomyopathy complicated by a left ventricular thrombus. On the night of admission for acute heart failure management, he experienced a sudden onset of consciousness disturbance, severe aphasia, and right hemiparesis. MRI revealed mild hyperintensities in the left cerebral hemisphere cortex and lenticular nucleus on diffusion-weighted imaging, with no abnormal signals on fluid-attenuated inversion recovery. He underwent mechanical thrombectomy, achieving complete reperfusion within 150 min; however, he experienced ipsilateral cerebral hyperemia that persisted for 30 days postoperatively. By the 90th postoperative day, moderate aphasia and mild paralysis of the right upper limb remained, with a modified Rankin Scale score of 3.

Conclusion: Left ventricular thrombosis is relatively common in patients with MACM, necessitating careful consideration of the risk of cardioembolic stroke.

Introduction

Recently, the popularity, availability, and purity of methamphetamines have increased worldwide. Methamphetamine-induced sympathetic hyperactivity and direct cytotoxicity can lead to acute or chronic cardiomyopathy, known as methamphetamine-associated cardiomyopathy (MACM).¹⁾ Left ventricular (LV) thrombus occurs in 33% of patients with MACM and carries the risk of embolic complications.²⁾ We report a case of left internal carotid artery occlusion that occurred during the treatment of acute heart failure and LV thrombus associated with MACM. The patient underwent mechanical thrombectomy (MT), and persistent left cerebral hyperemia was observed 30 days postoperatively.

Case Presentation

A 54-year-old man with a 30-year history of intermittent methamphetamine abuse but no significant medical history presented with wheezing for 3 days before visiting the previous hospital. A chest X-ray revealed cardiomegaly and pleural effusion (Fig. 1A), while the electrocardiogram showed normal sinus rhythm. Echocardiography showed an apical thrombus and cardiac dysfunction, with a LV ejection fraction (LVEF) of 24.1% (Fig. 1B). The brain natriuretic peptide (BNP) level was elevated at 1119 pg/mL. He was urgently admitted and was started on intravenous furosemide and unfractionated heparin (UFH), and oral warfarin. On the night of admission, he experienced a sudden onset of consciousness disturbance and right hemiparesis. Brain MRI revealed mild hyperintensities in the left cerebral hemisphere cortex and lenticular nucleus on diffusion-weighted imaging (DWI), with no abnormal signals on FLAIR. MRA depicted occlusion of the left internal carotid artery (ICA) (Fig. 2). The DWI-Alberta Stroke Program Early Computed Tomography Score was 3. He was transferred to our hospital 100 min after his last known well (LKW) time, presenting with global aphasia, leftward conjugate deviation, and right hemiplegia, with a National Institutes of Health Stroke Scale (NIHSS) score of 25. As he was receiving intravenous UFH and oral warfarin, recombinant tissue plasminogen activator (rtPA) was withheld until coagulation status was confirmed by blood tests. Subsequent results showed a platelet count of 332000/μL, an activated partial thromboplastin time of 22.7 s, a prothrombin time-international normalized ratio (PT-INR) of 1.0, and a D-dimer level of 2.1 μg/mL.

Fig. 1 (A) Chest X-ray showing cardiomegaly and pleural effusion. (B) Echocardiography performed prior to stroke onset revealed a left ventricular thrombus.

Fig. 2 (A and B) DWI revealed hyperintensities in the left cerebral hemisphere cortex and lenticular nucleus, with no abnormal signals detected on FLAIR. (C) MRA depicted left internal carotid artery occlusion. DWI, diffusion weighted imaging

A 9-Fr long sheath (25 cm) was inserted into the right femoral artery. A 9-Fr Optimo balloon-guiding catheter (Tokai Medical Products, Aichi, Japan) was positioned in the left ICA, and angiography confirmed the occlusion of the left ICA (Fig. 3A). A coaxial system consisting of a SALVA 71 (Goodman, Aichi, Japan), a Phenom 27 (Medtronic, Minneapolis, MN, USA), and a CHIKAI 14 (Asahi Intecc, Aichi, Japan) was navigated through the occlusion site. The SALVA 71 was advanced to the proximal part of the lesion and positioned at the point where suction ceased. Upon inflating the balloon of the Optimo catheter and retrieving the SALVA 71 under continuous suction, a red thrombus was observed. Complete recanalization was achieved in a single pass using direct aspiration 26 min after puncture, corresponding to 150 min from the LKW time (Fig. 3B). Histopathological examination of the retrieved thrombus revealed that it was primarily composed of fibrin, along with erythrocytes and a relatively abundant neutrophilic infiltrate (Fig. 3C). Immediately after MT, the patient regained speech but remained confused and experienced paralysis of the right upper limb. He exhibited significant sweating and aggressive behavior, necessitating continuous sedation. This prompted a urine drug test, which returned positive for amphetamine, revealing for the first time his history of methamphetamine addiction. Echocardiography performed after MT revealed no remaining thrombus, including in the apex (Fig. 4). Ultimately, rtPA was not administered, and oral warfarin was continued alongside UFH bridging therapy until the therapeutic PT-INR was achieved. On postoperative day 4 (POD 4), DWI and FLAIR revealed clear hyperintensities in the left cerebral cortex and basal ganglia, while MRA showed increased blood flow in the left middle cerebral artery, raising the suspicion of cerebral hyperperfusion syndrome (Fig. 5). Consequently, antihypertensive therapy and antiseizure medications were initiated to reduce the risk of hemorrhagic complications and seizures. He remained unconscious and restless until POD 16 and required sedation with intravenous dexmedetomidine during this period, despite the absence of seizures or epileptic activity on electroencephalography. On POD 17, after discontinuation of sedation, he exhibited moderate aphasia and disorientation but had improved sufficiently to ambulate. However, the left cerebral hyperemia persisted on arterial spin labeling (ASL) imaging until POD 30 (Fig. 6). On POD 10, the left cerebral deep white matter showed new hyperintensity on DWI and decreased apparent diffusion coefficient, indicating delayed injury. By POD 90, his condition had improved to moderate aphasia and mild paralysis of the right upper limb, with a NIHSS score of 6 and a modified Rankin Scale score of 3. On POD 94, echocardiography revealed an improved LVEF of 53.4%, with the BNP levels reduced to 26.0 pg/mL. Cardiac CT showed no coronary artery stenosis or intracardiac thrombus, and no episodes of atrial fibrillation were observed during hospitalization. Based on these findings, MACM was diagnosed. On POD 115, FLAIR imaging showed atrophy of the left cerebral hemisphere.

Fig. 3 (A) Digital subtraction angiography showed occlusion at the top of the left internal carotid artery. (B) Successful recanalization was achieved following mechanical thrombectomy. (C) Histopathological examination of the retrieved thrombus revealed that it was primarily composed of fibrin, along with erythrocytes and a relatively abundant neutrophilic infiltrate. HE, hematoxylin and eosin staining

Fig. 4 Echocardiography after mechanical thrombectomy showed no left ventricular thrombus.

Fig. 5 (A and B) On POD 4, DWI and FLAIR revealed hyperintensities in the left cerebral cortex and basal ganglia. (C) MRA showed increased blood flow in the left middle cerebral artery. DWI, diffusion-weighted imaging; POD, postoperative day

Fig. 6 Time course of MRI. Arterial spin labeling imaging demonstrated prolonged hyperemia of the left MCA up to POD 30. On POD 10, DWI exhibited hyperintensities and decreased apparent diffusion coefficient in the left cerebral white matter. On POD 115, FLAIR revealed atrophy of the left cerebral hemisphere. ADC, apparent diffusion coefficient; ASL, arterial spin labeling; DWI, diffusion-weighted imaging; MCA, middle cerebral artery; POD, postoperative day

Discussion

Methamphetamine abuse can lead to MACM, which are characterized by acute cardiomyopathy and myocardial fibrosis resulting from a combination of sympathetic activation-induced myocardial wall stress and direct cardiomyocyte toxicity.¹⁾ In the present case, the patient had a 30-year history of intermittent methamphetamine abuse and presented with MACM. The frequency of stroke in patients with MACM remains unclear. However, one study reported that among MACM patients at initial hospitalization, 33% had LV thrombus, and 3.4% developed ischemic stroke.²⁾ Reduced LVEF, LV enlargement, and coagulation disturbances are potential causes of LV thrombus, as observed in this case. Pathological examination of the retrieved thrombus revealed fibrin predominance, consistent with the characteristics of cardioembolic stroke described in a recent meta-analysis.³⁾ The median interval from the diagnosis of LV thrombus following acute myocardial infarction to the onset of acute ischemic stroke was 20.5 days.⁴⁾ As demonstrated in the present case, cardiogenic cerebral embolism can occur even after the initiation of anticoagulant therapy, necessitating careful neurological examination. To our knowledge, this is the first report of cardioembolic stroke in a patient with MACM undergoing MT, although a previous case of amphetamine-induced cardiomyopathy has been documented.⁵⁾

Notably, our patient experienced persistent cerebral hyperemia following MT. The duration of persistent cerebral hyperemia after MT remains unclear, with persistence reported in 49% of patients at 24 h and 40% at 5 days.⁶⁾ In the present case, hyperemia persisted for 30 days, indicating a relatively prolonged duration. The generally accepted mechanism of cerebral hyperemia involves neurogenic or myogenic impairment of vascular autoregulation, and increased the blood–brain barrier (BBB) permeability may contribute to hyperemia after MT.⁷⁾ Abrupt occlusion of arteries, acute ischemic volume, and the absence of collateral circulation are considered primary contributors to increased BBB permeability in cardioembolic stroke.^8,9) In this case, methamphetamine abuse may have contributed to the cerebral hyperemia, along with the sudden onset and poor collateral circulation. This is because long-term methamphetamine abuse disrupts the BBB function through mechanisms such as methamphetamine-induced hyperthermia, oxidative stress, and neuroinflammation.¹⁰⁾ Therefore, careful attention must be paid to the prevention of cerebral hyperperfusion syndrome when performing MT in patients with a history of methamphetamine abuse.

In cerebral hyperperfusion syndrome following MT, early postoperative blood pressure lowering¹¹⁾ and minimized blood pressure variability¹²⁾ have been associated with better outcomes. A review article proposed that after optimal recanalization, systolic blood pressure should be maintained below 140 mmHg, with its variability kept within 20 mmHg.⁷⁾ In this case, antihypertensive management was performed in reference to these recommendations. Conversely, intensive blood pressure management (≤140 mmHg) after thrombectomy has been reported to lead to worse functional outcomes than conventional management (140–180 mmHg), possibly due to reduced perfusion in the oligemic area, which may exacerbate ischemic injury.¹³⁾ In this case, delayed injury to the deep white matter of the left hemisphere was observed on POD 10. Disrupted autoregulation may have led to cerebral hyperemia, while intensive blood pressure control may have further reduced cerebral perfusion, which may have exacerbated the initial ischemic injury and contributed to delayed ischemic damage. Despite the occurrence of cerebral hyperemia following thrombectomy, the presence of viable tissue may suggest that intensive blood pressure lowering should be avoided. Single-photon emission CT may be useful for distinguishing viable from nonviable tissue after recanalization.¹⁴⁾ Although it should be noted that ASL imaging, as used in this case, tends to overestimate cerebral blood flow compared to other modalities, it remains useful due to its noninvasiveness and convenience for monitoring cerebral perfusion over time.⁹⁾

Conclusion

LV thrombosis frequently occurs in patients with MACM, warranting close attention to the potential risk of cardioembolic stroke.

Disclosure Statement

The authors declare that they have no conflicts of interest.

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