Prognostic impact of microembolic signals in arterial sources of embolism

Abstract

Sir I read with interest the review by Ritter et al. [3] regarding the prevalence and prognostic impact of microembolic signals (MES) in arterial sources of cerebral embolism. I wish to comment on some important issues related to this review. Emboli originating from an atherosclerotic stenotic plaque are considered to play an important etiological role in subsequent cerebral ischemic events [2], and the detection of MES may help in clinical decision-making, especially in patients previously considered to have asymptomatic arterial stenoses. However, this approach is still not widely accepted and appears to be looking at ‘only one side of the picture.’ Cerebral ischemic events secondary to hemodynamic disturbances (hypoperfusion) in patients with significant stenotic lesions constitute an important clinical group, and these patients can be easily evaluated with transcranial Doppler and assessment of cerebral autoregulation (CA). CA is the inherent ability of the cerebral blood vessels to maintain the blood flow over a wide range of systemic blood pressure and various provocative stimuli [6] and can be assessed by testing the vasomotor reactivity (VMR). Flow velocities obtained in real-time by TCD can reflect cerebral blood flow volume (CBFV), and the velocity changes can be proportionate to the changes in CBFV if certain parameters are known and remain constant (e.g., angle of insonation, perfusion territory, and arterial diameter) and the effect of only one stimulus is observed [5]. Evaluation of VMR to various ‘challenges’ and maneuvers may help in the prognostic assessment of patients with significant stenosis in the cervico-cranial cerebral arteries. Silverstrini et al. [4] demonstrated a significantly higher risk of subsequent cerebral ischemic events in patients with asymptomatic carotid stenosis and having impaired VMR, assessed by breath-holding index. VMR can be easily assessed by monitoring the blood flow velocities (by TCD) during voluntary breath-holding in any intracranial artery distal to the stenosis. Elevation of carbon-dioxide levels in blood during breath-holding is a strong vasodilatory stimulus and results in significant augmentation of flow velocities in the intracranial arteries. However, the arteries distal to the segment with significant stenosis tend to maintain maximal vasodilation and may not dilate further in response to hypercapnia, reflected by a blunted response in the blood flow velocities. The response may be further affected, in some cases, due to ‘intracranial steal phenomenon’ known as ‘reversed Robin Hood syndrome’ [1]. I propose that, in addition to the MES monitoring, patients with hemodynamically significant stenosis in the cervical or intracranial cerebral arteries should be evaluated for VMR by TCD. Assessment of VMR in the arterial segments distal to the atherosclerotic segment would reveal, at least to some extent, the ‘other side of the picture’ and help in better understanding of cerebral hemodynamics and the pathogenic mechanisms of cerebral ischemia in these patients. Well-designed prospective studies would, however, be needed to test the feasibility and efficacy of this approach in clinical decision-making.