Anesthetic and procedural strategy for coexisting severe aortic stenosis and carotid artery stenosis: A case report

Abstract

BACKGROUND

Aortic stenosis (AS) often coexists with carotid artery stenosis. However, clear guidelines for the optimal treatment strategy and sequencing of interventions in patients with both conditions are lacking.

CASE SUMMARY

A 79-year-old man with a history of hypertension presented with right-sided paralysis and pain. Magnetic resonance imaging revealed multiple infarctions in the left cerebral hemisphere and severe stenosis of the left carotid artery. Transthoracic echocardiography also identified coexisting severe AS. Carotid artery stenosis increases the risk of stroke during aortic valve manipulation; therefore, carotid intervention may be recommended prior to aortic valve treatment. However, perioperative hypotension and bradycardia associated with carotid intervention can precipitate circulatory collapse in patients with severe AS. After a multidisciplinary conference, the decision was made to first perform transcatheter aortic valve implantation under general anesthesia, followed by carotid endarterectomy 4 months later. Both procedures were completed successfully without complications.

CONCLUSION

Treatment strategy should be individualized, balancing perioperative risks and benefits in patients with severe AS and carotid artery stenosis.

Key Words: Aortic stenosis; Carotid artery stenosis; Transcatheter aortic valve implantation; Carotid endarterectomy; Anesthesia; Perioperative management; Case report

Core Tip: Aortic stenosis (AS) often coexists with carotid artery stenosis. The treatment strategy for patients with coexisting severe AS and carotid artery stenosis should be individualized, weighing the perioperative risks and benefits of each planned intervention.

INTRODUCTION

Aortic stenosis (AS) is the most common valvular disease in adults[1,2]. Transcatheter aortic valve implantation (TAVI) has recently emerged as a less invasive alternative to surgical aortic valve replacement (SAVR). As candidacy for intervention expands to a broader population of patients with AS[3], the presence of comorbidities plays a critical role in decision-making and perioperative management.

Carotid atherosclerosis and stenosis frequently coexist with severe AS[4]. Given that stroke is a major complication of both SAVR and TAVI, prior intervention for carotid stenosis may be beneficial. However, carotid revascularization can lead to life-threatening hemodynamic collapse in patients with AS. Although various professional societies have published guidelines for managing AS[5,6] and carotid stenosis[7] independently, no consensus exists regarding the optimal treatment strategy or sequencing of interventions for patients with both conditions.

This report presents the preoperative assessment, multidisciplinary decision-making process, and anesthetic management of a patient with concurrent severe AS and carotid artery stenosis.

CASE PRESENTATION

Chief complaints

A 79-year-old male with a body mass index of 26 kg/m² presented with paralysis of the right upper and lower limbs.

History of present illness

Numbness in the right upper and lower limbs appeared two weeks prior, and 12 days after the initial symptom onset, the numbness in the right upper limb worsened, accompanied by dysarthria and speech disturbance. He had no history of chest pain or syncope and was classified as New York Heart Association class I for heart failure.

History of past illness

The patient had a history of hypertension, treated with amlodipine.

Personal and family history

There was no personal or family history suggestive of anesthesia-related complications.

Physical examination

On presentation, his blood pressure was 128/64 mmHg, heart rate 68 bpm, and peripheral oxygen saturation 95% on room air. Although the patient was alert, he exhibited non-fluent speech and numbness in the affected limbs.

Laboratory examinations

Blood test results, including complete blood count, serum biochemistry, and coagulation parameters, were within the normal range. The plasma B-type natriuretic peptide level was 22.6 pg/mL.

Imaging examinations

Chest radiography revealed cardiomegaly with a cardiothoracic ratio of 63%. Electrocardiography (ECG) showed an incomplete right bundle branch block without evidence of left ventricular hypertrophy.

Magnetic resonance imaging revealed multiple infarctions in the left temporal, parietal, occipital, and frontal lobes, along with severe stenosis extending from the left common carotid artery (CCA) to the bifurcation of the internal carotid artery (ICA) (Figure 1). Carotid ultrasonography confirmed significant stenosis extending from the bifurcation of the left CCA to the proximal ICA, with a peak systolic flow velocity of 3.8 m/s. The degree of stenosis in the left CCA was estimated at 70% using the North American Symptomatic Carotid Endarterectomy Trial method and 90% by the area method.

Figure 1 Magnetic resonance angiography. Magnetic resonance angiography showing severe stenosis extending from the left common carotid artery to the bifurcation of the internal carotid artery. CCA: Common carotid artery; ICA: Internal carotid artery; ECA: External carotid artery; R: Right; L: Left.

Carotid endarterectomy (CEA) or carotid artery stenting (CAS) was considered for the patient. However, preoperative transthoracic echocardiography revealed severe AS, with an aortic valve cross-sectional area of 0.8 cm², peak transvalvular velocity of 4.2 m/s, and peak/mean pressure gradients of 72/45 mmHg. The left ventricular ejection fraction (EF) was preserved at 81%, with no evidence of hypertrophy. Computed tomography showed minimal aortic arch calcification. Risk stratification for cardiac surgery yielded a Society of Thoracic Surgeons morbidity/mortality risk score of 30.1% and a EuroSCORE II of 3.59%.

MULTIDISCIPLINARY EXPERT CONSULTATION

A multidisciplinary conference was convened to determine the optimal treatment sequence, and the perspectives of each specialty were explicitly discussed. From the neurosurgical standpoint, prioritizing hemodynamic stability was essential. The team emphasized that CEA carries a substantial risk of perioperative circulatory collapse due to intraoperative carotid sinus stimulation, postoperative blood pressure reduction aimed at preventing hyperperfusion syndrome, and the presence of concomitant coronary artery disease. Given that the carotid stenosis was non-urgent, the neurosurgical team advocated performing TAVI first to minimize these risks. The cardiology team acknowledged that the patient did not meet the absolute indications for TAVI; however, they agreed that TAVI could be justified, if needed, to reduce the perioperative hemodynamic burden imposed by CEA. From an anesthesiological perspective, the team concurred with the neurosurgical assessment regarding the high risk of circulatory instability during CEA and emphasized the importance of minimizing the risk of perioperative stroke during TAVI, by selecting an anesthetic strategy capable of responding flexibly to potential hemodynamic or neurological changes. Based on these multidisciplinary considerations, the team agreed to proceed with transfemoral TAVI under general anesthesia (GA) as the initial intervention and defer CEA to a later date.

FINAL DIAGNOSIS

The final diagnosis was concomitant asymptomatic severe AS, scattered cerebral infarctions in the left hemisphere, and left ICA stenosis.

TREATMENT

Upon arrival in the operating room, arterial and central venous lines were secured. GA was induced with remimazolam (5 mg), remifentanil (0.25 μg/kg/minute), and rocuronium (50 mg), followed by an endotracheal intubation. Processed regional cerebral oxygen saturation (rSO₂) and electroencephalography (EEG) were continuously monitored using INVOS^® (Medtronic, Dublin, Ireland) and BIS^® (Medtronic, Dublin, Ireland), respectively, in addition to standard monitoring modalities, including 5-lead ECG, pulse oximetry, capnography, and neuromuscular blockade monitoring. A transesophageal echocardiography probe was inserted to assess the cardiac function and detect potential intraoperative complications. Anesthesia was maintained with continuous infusions of remimazolam and remifentanil, titrated to achieve a target bispectral index value of 40-60, and appropriate EEG patterns. Norepinephrine (0.02-0.06 µg/kg/minute) was administered to maintain hemodynamic stability (Figure 2).

Figure 2 Anesthetic record for transcatheter aortic valve implantation. Regional cerebral oxygen saturation and bispectral index remained stable throughout anesthesia, with no significant decreases observed. BP: Blood pressure; HR: Heart rate; EtCO₂: End-tidal carbon dioxide; rSO₂: Regional cerebral oxygen saturation; BIS: Bispectral index; CVP: Central venous pressure.

A balloon-expandable valve (SAPIEN 3 Ultra^®, Edwards Lifesciences, Irvine, United States) was selected over a self-expanding device to minimize cerebral hypoperfusion by shortening the duration of rapid pacing during deployment. The valve was successfully deployed under rapid pacing at 180 bpm. No significant changes in rSO₂ or EEG were observed during the deployment. The procedure lasted for 105 minutes, with minimal blood loss. The patient received 1150 mL of Ringer’s solution, and the total urine output was 740 mL. Following smooth emergence from anesthesia without any neurological abnormalities, the patient was extubated in the operating room and transferred to the high-care unit as planned.

OUTCOME AND FOLLOW-UP

No TAVI-related complications or exacerbations of pre-existing neurological symptoms were observed. CEA was subsequently performed under GA without any incident 4 months later, and the patient was discharged on postoperative day 9. At both 6-month and 1-year follow-up, no new neurological abnormalities were found.

DISCUSSION

Current guidelines recommend SAVR or TAVI in both symptomatic and asymptomatic patients, depending on the severity of AS, life expectancy, and surgical risk[5,6]. Considering the presence of asymptomatic severe AS with preserved left ventricular EF, and advanced age, TAVI was considered a reasonable treatment option in this case. Extracranial carotid artery stenosis is a significant cause of stroke and mortality[8]. In patients with a recent transient ischemic attack or non-disabling ischemic stroke and ipsilateral moderate-to-severe stenosis, CEA is recommended to reduce the risk of recurrent stroke[7]. Our patient presented with moderate-to-severe left CCA stenosis and had recently experienced a stroke, warranting carotid intervention.

Although established guidelines exist for the independent management of AS[5,6] and carotid stenosis[7], evidence-based recommendations for patients with coexisting AS and carotid artery stenosis remain limited. AS has been associated with a high incidence of cardiovascular complications in patients undergoing non-cardiac surgery[9-11]. Although large-scale data on perioperative outcomes of CEA in patients with severe AS are lacking, hemodynamic depression, characterized by hypotension and bradycardia due to autonomic stimulation of the carotid sinus, is a well-documented complication of carotid surgery[12]. Hyperperfusion syndrome is another serious complication of CEA, necessitating strict blood pressure control[13]. In patients with severe AS, perioperative hypotension, whether unintended or induced, can precipitate circulatory collapse. The presence of concomitant coronary artery stenosis, as in our case, may also increase the risk of death and myocardial infarction[14].

Stroke is a potential complication of aortic valve replacement, resulting from catheter manipulation of a heavily calcified aortic valve or embolization of atheromatous plaques[15,16]. Additionally, rapid pacing and perioperative hypotension during valve deployment may result in cerebral hypoperfusion[17]. However, the association between carotid artery stenosis and stroke in patients undergoing TAVI remains controversial[4,18-20], and recent reports have suggested that unilateral carotid artery stenosis does not increase the risk of periprocedural stroke[21,22].

Several case reports have proposed different strategies for patients requiring both TAVI and carotid revascularization. Moraca et al[16] reported 16 patients who underwent concomitant interventions with CEA, followed by TAVI on the same day. Ravindra et al[23] described five patients who successfully underwent CAS before TAVI (median interval: 30 days), one of whom experienced worsening heart failure during stenting. In contrast, Gennari et al[24] and Rossi et al[25] presented cases treated with TAVI first, followed by transcarotid artery revascularization shortly thereafter. Shintoku et al[26] reported a case managed with a staged approach involving angioplasty, followed by TAVI 2 weeks later, and CAS 1 week after that[26]. No perioperative cerebrovascular events or fatal circulatory collapse were observed in these studies[16,23-26].

In our case, although the patient had a recent stroke and moderate-to-severe CCA stenosis, his neurological condition remained stable under medical management, allowing the CEA to be deferred for several months. Conversely, severe AS presented a significant obstacle to maintaining strict blood pressure control during CEA and increased the risk of circulatory collapse. After weighting the potential risks of performing CEA in the setting of concomitant AS and coronary disease, the multidisciplinary conference determined to perform TAVI prior to carotid revascularization.

Anesthetic management also required careful consideration. TAVI can be performed under either GA with endotracheal intubation or monitored anesthesia care (MAC) with sedation. GA offers several advantages, including a secured airway, controlled ventilation, enhanced preparedness for emergencies, the ability to utilize transesophageal echocardiography, and complete patient immobility without awareness. In contrast, MAC offers potential benefits, such as reduced anesthetic drug requirements, potentially less hemodynamic suppression, preservation of spontaneous negative-pressure ventilation, and afterload reduction in cases of right heart dysfunction. In our patient, controlled mechanical ventilation was preferred to prevent hypocapnia-induced reduction in cerebral blood flow. Additionally, transient cerebral ischemia because of hypotension during rapid pacing poses a risk of seizures and may necessitate emergency airway management. Before the induction of general anesthesia, arterial and central venous lines were secured to enable real-time monitoring of blood pressure and to allow prompt intervention for anesthesia-related hemodynamic instability, in order to prevent circulatory collapse associated with AS and cerebral hypoperfusion related to carotid stenosis. For anesthetic maintenance, we used remimazolam and remifentanil because of their short duration of action and low tissue accumulation, which facilitates timely postoperative neurological evaluation and allows rapid intervention in the event of complications. rSO₂ and EEG were used to detect cerebral hypoperfusion and to allow timely adjustment of parameters that affect cerebral perfusion, such as blood pressure and partial pressure of carbon dioxide. As no standardized anesthetic guidelines exist for TAVI in patients with carotid stenosis, individualized anesthetic preparation and management are required.

CONCLUSION

We encountered a patient requiring intervention for both severe AS and carotid stenosis, where treating one condition in the presence of the other poses potential complications. Given the lack of clear recommendations or clinical guidelines for managing these coexisting conditions, individualized, multidisciplinary treatment planning is essential.