Cerebral hemodynamic effects of early blood pressure lowering after TIA and stroke in patients with carotid stenosis

Background: Effects of early blood pressure (BP) lowering on cerebral perfusion in patients with moderate/severe occlusive carotid disease after transient ischemic attack (TIA) and non-disabling stroke are uncertain. Aims: We aimed to evaluate the changes in transcranial Doppler (TCD) indices in patients undergoing blood pressure lowering soon after TIA/non-disabling stroke. Methods: Consecutive eligible patients (1 November 2011 to 30 October 2018) attending a rapid-access clinic with TIA/non-disabling stroke underwent telemetric home blood pressure monitoring (HBPM) for 1 month and middle cerebral artery velocities measurements ipsilateral to carotid stenosis on TCD ultrasound in the acute setting and at 1 month. Hypertensive patients (HBPM ⩾ 135/85) underwent intensive BP-lowering guided by HBPM unless they had bilateral severe occlusive disease (⩾ 70%). Changes in BP and TCD parameters were compared in patients with extracranial moderate/severe carotid stenosis (between 50% and occlusion) versus those with no or mild (< 50%) stenosis. Results: Of 764 patients with repeated TCD measures, 42 had moderate/severe extracranial carotid stenosis without bilateral severe occlusive disease. HBPM was reduced from baseline to 1 month in hypertensive patients both with versus without moderate/severe carotid stenosis (−12.44/15.99 vs −13.2/12.2 mmHg, respectively, p-difference = 0.82), and changes in TCD velocities (4.69/14.94 vs 2.69/13.86 cm/s, respectively, p-difference = 0.52 for peak systolic velocity and 0.33/7.06 vs 1.75/6.84 cm/s, p-difference = 0.34 for end-diastolic velocity) were also similar, with no evidence of greater hemodynamic compromise in patients with stenosis/occlusion. Conclusion: There was no evidence of worsening of TCD hemodynamic indices in patients with moderate/severe occlusive carotid disease treated with BP-lowering soon after TIA/non-disabling stroke, suggesting that antihypertensive treatment in this group of patients is safe in the acute setting of TIA clinics.

Asymptomatic Carotid Disease and Cognitive Impairment: What Is the Evidence?

The development of cognitive dysfunction and dementia is a complex, multifactorial process. One of the contributors to various types of cognitive dysfunction is carotid atherosclerosis which can frequently be seen in asymptomatic individuals. There are a number of different manifestations of asymptomatic carotid atherosclerosis including arterial stiffness, carotid intima-media thickening, flow-limiting stenosis, and complex, atherosclerotic plaque. Each of these forms of atherosclerosis may contribute to cerebral parenchymal damage, contributing to cognitive dysfunction. In this review article, we will discuss each of these forms of carotid atherosclerosis, present the potential mechanistic underpinnings behind an association, and then review the scientific evidence supporting potential associations to cognitive dysfunction and dementia.

Carotid Artery Stenting

Purpose of The ReviewTo examine current understanding of diverse etiologies of extracranial carotid disease, including clinical and imaging manifestations as well as treatment approaches.Recent FindingsIncreasing availability of advanced cerebrovascular imaging modalities continues to elucidate atherosclerotic and nonatherosclerotic carotid steno-occlusive disease as a common culprit of cerebral ischemia. Individualized treatment strategies targeting each etiologic subset would optimize preventive measures and minimize recurrence of cerebral ischemia.SummaryIschemic stroke is a prominent cause of mortality and long-term disability worldwide. The magnified effect of carotid disease warrants constant and close inspection.

P.065 Physician Approaches to Anti-thrombotic Therapies for Acutely Symptomatic Carotid Stenosis: Insights from the Hot Carotid Qualitative Study

Background: Whereas the beneficial effect of antiplatelet therapy for recurrent stroke prevention is well-established, uncertainties remain regarding the optimal anti-thrombotic regimen for acutely symptomatic carotid stenosis (“hot carotid”), particularly as patients await revascularization. We sought to explore the approaches of stroke physicians to peri-procedural anti-thrombotic management of patients with “hot carotids”. Methods: We conducted semi-structured interviews regarding “hot carotid” management with purposive sampling of 20 stroke physicians from 14 centres in North America, Europe, Asia, and Australia. We identified key themes using conventional qualitative content analysis. Results: Important themes revealed from our discussion included limitations of existing clinical trial evidence, competing surgeon versus neurologist/internist preferences, and single vs dual antiplatelet therapy (DAPT) while awaiting revascularization. Areas of uncertainty included the management of stroke while on aspirin, implications of non-stenotic features of carotid disease (intraluminal thrombus, plaque morphology), the role of newer anti-platelet agents or anticoagulants, platelet aggregation testing, and how soon to start DAPT. Conclusions: Our qualitative analysis revealed themes that were important to stakeholders in stroke care. Teams designing international trials will have to accommodate identified variations in anti-thrombotic practice patterns and take into consideration areas of uncertainty, such as newer anti-thrombotic agents, and the implication of non-stenotic features of carotid disease.