Asymptomatic carotid bifurcation stenosis with noise

Asymptomatic Carotid Stenosis with Bruit ("Noise") Overview

The precise etiology (cause) and origin of a carotid bruit – a "whooshing" sound heard with a stethoscope over the carotid artery bifurcation in the neck – remain subjects of discussion, especially when it occurs in the presence of atherosclerotic lesions that have not yet caused symptoms like a transient ischemic attack (TIA) or stroke (i.e., asymptomatic stenosis) [1, 2]. Historically, many published studies investigating this phenomenon, often based on small patient groups, had limitations in accurately determining the exact location and severity (degree) of the underlying carotid bifurcation stenosis responsible for the bruit [1].

Studies examining patients with asymptomatic carotid stenosis and an audible cervical bruit, particularly those focusing on outcomes after vascular surgery, often share similar methodological limitations from the past [1]. It is generally accepted that patients with a cervical bruit have an increased overall risk of cardiovascular disease, subsequent stroke (not necessarily related to the bruit itself), and mortality [1, 4]. Importantly, a stroke, when it occurs in these patients, may not necessarily originate from the vascular territory supplied by the stenotic artery causing the bruit (it could be from the other carotid artery, the heart, or elsewhere) [1, 4]. Therefore, the mere presence of an asymptomatic carotid bruit is not, by itself, a universal indication for carotid artery intervention (like surgery or stenting) [1, 5].

However, specific subgroups are at higher risk. Patients identified as having severe stenosis specifically at the proximal internal carotid artery (often defined by imaging as a residual lumen ≤ 1.5 mm), which may result in reduced distal cerebral blood flow, face an increased risk of subsequent thrombotic occlusion (complete blockage) of the artery [1, 6].

Although these patients with severe stenosis may experience reduced blood flow distal to the lesion, they often remain asymptomatic initially [1]. This is frequently due to adequate collateral blood flow compensating via the Circle of Willis, particularly through the ipsilateral (same side) anterior communicating artery or posterior communicating artery, supplying the middle and anterior cerebral artery territories [1, 7]. Therefore, even with severe stenosis, a stroke (cerebral infarction), when it occurs, might develop later due to arterio-arterial embolism (fragments breaking off the plaque) rather than purely low flow [1, 6]. The characteristics of the bruit associated with stenosis at the proximal internal carotid artery can sometimes offer clues: when high-pitched and prolonged, extending into diastole (the heart's resting phase), it often suggests significant stenosis [1, 2]. As the stenosis progresses towards complete occlusion, reducing cerebral blood flow further, the turbulent flow diminishes, causing the bruit to lessen and eventually disappear when the artery fully occludes [1, 2].

Modern non-invasive carotid artery studies are essential for identifying and quantifying significant stenosis [5]. These include B-mode ultrasound (visualizing the plaque), Doppler ultrasound (USDG) to measure blood flow velocities distal to the stenosis, quantitative spectral analysis of the bruit itself (less common now), and historically, techniques like oculoplethysmography for determining relative eye artery pressures (rarely used today) [1, 8]. Carotid Duplex ultrasound, combining B-mode and Doppler, is the primary screening and surveillance tool [5, 8].

Regarding treatment, large randomized controlled trials (like ACAS [9] and ACST [10]) have compared outcomes for carotid endarterectomy (surgical removal of plaque) plus medical therapy versus medical therapy alone (including antiplatelet agents like aspirin, statins, and blood pressure control) in patients with significant asymptomatic carotid stenosis. While these trials showed a modest benefit for surgery in reducing long-term stroke risk for carefully selected patients with high-grade stenosis (typically >60-70% depending on the trial and measurement method) treated at centers with low complication rates, the absolute risk reduction is small, meaning many patients undergo surgery without deriving benefit [5, 9, 10]. Therefore, treatment decisions must be highly individualized [5]. Antiplatelet agents (like aspirin) and optimal medical management (statins, BP control, lifestyle changes) are fundamental for all patients [5, 11]. If significant, progressive stenosis is documented via serial imaging (Doppler ultrasound, CT angiography, or MR angiography), particularly if the residual arterial lumen narrows to ≤ 1.5 mm (indicating very severe stenosis), surgical intervention (endarterectomy) or possibly carotid artery stenting may be considered in appropriate candidates after careful risk/benefit discussion [1, 5, 12].

The procedural complication rate (stroke or death) for asymptomatic carotid endarterectomy should ideally be very low (e.g., ≤ 2-3% as per trial standards) for the potential benefits to outweigh the risks [5, 9, 10]. Similarly, carotid stenting also carries procedural risks [12, 13]. Despite trial data, there remains ongoing debate and a need for personalized assessment regarding the superiority of intervention over modern optimal medical management alone for many patients with asymptomatic carotid stenosis, emphasizing the need for shared decision-making between physician and patient [5, 13].