Editorial Comment—Hypotension After Carotid Revascularization
Carotid artery stenosis typically involves accumulation of hard calcified atheroma at the common carotid artery bifurcation with involvement of the origin of the internal carotid artery. Anatomically, this location is in close proximity to the area where the carotid baroreceptors are located. The function of these receptors is to sense the tension exerted on the arterial wall and provide feedback control to blood pressure regulation centers.
In patients with carotid artery stenosis requiring revascularization, the mere presence of calcified atheroma in this specific arterial location has chronically “sensitized” the carotid baroreceptors to very small changes in carotid artery tension. (The thicker and more calcified the wall, the more rapid and efficient pressure/energy transmission it allows.) Therefore, external manipulation of this area during surgery, as well as the transmission of the luminal distention through the arterial wall during balloon inflation and stent expansion, can produce a hypotensive response. This phenomenon varies with (1) the intensity of manipulation or distention of the artery and (2) plaque burden and plaque composition (thickness and calcification).
Development of significant hypotension has been linked with neurological complications after carotid stent procedures.1,2 “Persistent profound hypotension” was defined as a >40 mm Hg decrease in arterial pressure without evidence of hypovolemia, with a systolic pressure <90 mm Hg at the end of the procedure and lasting at least 1 hour1; in the other study, “severe hypotension” was defined as a pressure drop of at least 50 mm Hg.2 Lower levels of hypotension were inconsequential in relation to the patient’s neurological status.
This phenomenon was “explained” by the use of aggressive balloon dilatation and the use of balloon-expandable stents.1
In this issue of Stroke, McKevitt et al attempted to address this subject in a patient population who was enrolled in the randomized trial CAVATAS of carotid angioplasty versus surgical endarterectomy.3,4 This is the first specific report of the effects of surgery on arterial blood pressure during and after carotid revascularization. Continuous (24-hour) blood pressure monitoring was employed in the subset of patients who consented to this substudy in a single center. Furthermore, long-term follow-up was available. All these advantages really provided the foundation of a very essential experimental protocol.
The findings of this study3 mainly confirmed previous observations1,2: (1) “any” pressure drop >30 mm Hg occurred in similar degrees among the various types of endovascular procedures and was very frequent (>75%); (2) aggressive angioplasty and balloon-expandable stent deployment produced persistent hypotension more frequently than the currently accepted approach of gentle dilation with self-expanding stent deployment (62% versus 27%); (3) hypotension had a trend to correlate to neurological complications (16% versus 6% for patients without hypotension).
With respect to endovascular approach versus surgery in this study,3 the endovascular approach had (1) fewer neurological complications overall (5.5% versus 10.2%), (2) more hypotension episodes defined as a blood pressure drop of at least 30 mm Hg, and (3) higher blood pressure at follow-up (mean difference of 5 mm Hg).
The above-quoted percentage comparisons were found to be not statistically significant due to very small sample size, but they are arithmetically so far apart from each other and they qualitatively concurred with recent investigation on these subjects.1,2 (Results of the SAPPHIRE Randomized Trial were presented by J. Yadav, MD, at the AHA 2002 Annual Scientific Sessions, Chicago, Ill, November 2002.)
The acute hemodynamic differences in the 2 groups are difficult to explain because a very specific protocol to aggressively treat hypotension in the surgical group was employed (with use of intravenous pressors in one third of surgical patients), whereas no such protocol existed for the angioplasty group. This biased methodology is rather surprising given that this study was specifically designed to evaluate blood pressure fluctuation during and after the procedure in both treatment arms. It seems as though 1 arm (surgery) was specifically “assisted” in avoiding and aggressively treating hypotension.
The follow-up blood pressure results are also difficult to interpret but are a very useful foundation for further investigation. The intensity of long-term antihypertensive therapy was not specifically assessed (number and dosage of medications). Thus, it is unclear whether the observed differences in blood pressure control were due to the carotid procedure or to confounders related to the outpatient management of blood pressure.
Third, the major limitation of the main randomized trial4 as well as the present substudy3 is the fact that the endovascular approach has already evolved to improved techniques that are underrepresented in the present investigational report (due to the time lapse between trial planning and presentation of results): aggressive angioplasty with provisional stenting and deployment of balloon-expandable stents with high-pressure postdilation (the CAVATAS protocol) are no longer used, and it is really surprising that such “abandoned” techniques in fact managed to achieve equal neurological complication rates to surgery in the main study3 and almost half in the present substudy!4
Hypotension: Does It Matter?
With respect to hypotension, I would summarize the “take-home” messages as follows: (1) severe or persistent hypotension correlates to adverse neurological events; (2) mild hypotension is very frequent during carotid procedures, and therefore rather nonspecific as a marker of complications; (3) aggressive treatment of hypotension during surgery did not seem to result in low neurological complications in the present study. Still, it is unclear if preventing hypotension will prevent neurological events after carotid revascularization. It is difficult to believe that hypotension itself causes a focal neurological event, but it would be easier to adopt that profound hypotension may render a potentially inconsequential (under normal hemodynamics) microembolization into a clinically detectable neurological event. In addition, hypotension can be specifically detrimental in patients with severe coronary stenosis. Finally, hypotensive response after carotid procedure may represent a confounder that characterizes high-risk patients with generalized atherosclerosis and marked arterial stiffness. Given all these possibilities, it is recommended that hypotension should be treated aggressively during carotid procedures so that it is aborted when “mild” before it becomes “severe” or “persistent” as defined above.5 Clearly, further investigation is required with respect to the long-term implication of blood pressure fluctuations during or shortly after carotid procedures.
McKevitt FM, Sivaguru A, Venables GS, et al. How the treatment of carotid artery stenosis affects blood pressure: a comparison of hemodynamic disturbances following carotid endarterectomy and endovascular treatment. Stroke. 2003; 34: 2576–2582.
Roubin GS, New G, Iyer SS, et al. Immediate and late clinical outcomes of carotid artery stenting in patients with symptomatic and asymptomatic carotid artery stenosis: a 5-year prospective analysis. Circulation. 2001; 103: 532–537.