(Stroke. 1999;30:2086-2093.)
© 1999 American Heart Association, Inc.
Original Contribution |
Frequency and Determinants of Postprocedural Hemodynamic Instability After Carotid Angioplasty and Stenting
From the Department of Neurosurgery and Toshiba Stroke Research Center, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY.
Correspondence to Adnan I. Qureshi, MD, SUNYAB Department of Neurosurgery, 3 Gates Circle, Buffalo, NY 14209-1194.
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Abstract |
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Background and Purpose—Hemodynamic instability can occur acutely after carotid angioplasty and stent placement (CAS). We performed this study to determine the frequency of hemodynamic instability in a series of patients who underwent CAS and to analyze factors associated with development of postprocedural hemodynamic events.
Methods—We reviewed medical records and angiograms in a series of 51 patients (mean age 68.3±8.9 years) who underwent CAS for symptomatic (n=29) or asymptomatic (n=22) carotid artery stenosis. Any episodes of hypotension (systolic blood pressure <90 mm Hg), hypertension (systolic blood pressure >160 mm Hg), or bradycardia (heart rate <60 bpm) that occurred in the acute postprocedural period were recorded. The effect of demographic, clinical, intraprocedural, and angiographic factors on subsequent development of hemodynamic instability was analyzed by logistic regression.
Results—The frequency of postprocedural hemodynamic complications in our patient series was as follows: hypotension, 22.4%; hypertension, 38.8%; and bradycardia, 27.5%. Intraprocedural hypotension (odds ratio [OR] 14.6, P=0.024) and history of myocardial infarction (OR 14.1, P=0.04) independently predicted postprocedural hypotension. Postprocedural hypertension was predicted by intraprocedural hypertension (OR 7.6, P=0.01) and previous ipsilateral carotid endarterectomy (OR 7.6, P=0.02). Postprocedural bradycardia was associated with intraprocedural hypotension (OR 74, P=0.001) and intraprocedural bradycardia (OR 12, P=0.008). All events had resolved at the conclusion of the intensive care unit monitoring period (mean 25.7 hours, range 18 to 43 hours).
Conclusions—Postprocedural hemodynamic instability is frequent after CAS and supports the need for monitoring in settings suited to expeditious management of cardiovascular emergencies. Patients who have evidence of hemodynamic instability during the procedure are at highest risk.
Key Words: angioplasty • carotid artery • hypotension • stents
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Hemodynamic instability consisting of hypertension, hypotension, or bradycardia after carotid endarterectomy (CEA) is well recognized.1 2 3 4 5 6 7 Acute hypertension is attributed to transient dysfunction of adventitial baroreceptors in the endarterectomized carotid artery segments, although metabolic factors such as renin and vasopressin have also been implicated.3 5 7 Bradycardia, sometimes associated with hypotension, is also reported to occur frequently in the early postoperative period.7 Presumably, bradycardia and hypotension are related to increased activity from the carotid sinus nerve or carotid baroreceptors due to increased compliance and stretch in the arterial wall after removal of atheromatous plaque.1 6 Recently, carotid angioplasty and stent placement (CAS) has been introduced as an alternative to CEA for the treatment of carotid artery stenosis.8 9 10 11 Although CAS involves extensive manipulation in the vicinity of both the adventitial baroreceptors and the carotid sinus, the frequency and predisposing factors of hemodynamic instability in the postprocedural period have not been investigated.
We performed this study to determine the frequency and characteristics of hemodynamic instability in the acute postprocedural period after CAS. We also evaluated the effect of factors related to both the patient's medical condition and the procedure itself on postprocedural hemodynamic status.
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Subjects and Methods |
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We reviewed the medical records and angiograms of patients who underwent CAS from September 1997 through October 1998. Patients were identified by a registry maintained by the Department of Neurosurgery. Only those patients who underwent angioplasty for carotid artery stenosis were included. Patients with stenosis related to dissection or radiation therapy were not included.
A written informed consent was obtained from each patient. The study was approved by the local institutional review committee.
Protocol for Angioplasty and Stent Placement
Patients were started on aspirin (325 mg/d) and ticlopidine (250
mg BID) or clopidogrel (75 mg/d) 72 hours before the procedure. On the
day of the procedure, each patient was evaluated by a physician from
the endovascular team, and a complete physical examination was
documented, including measurements of heart rate, respiratory rate, and
blood pressure. Each patient was given dexamethasone (10
mg) and nimodipine (60 mg) orally on the morning of the procedure for
potential neuroprotective effect. Patients taking hypertensive
medications received their morning doses; additional doses were
withheld until after the procedure.
Heart and respiratory rates were monitored continuously throughout the procedure. Blood pressure was measured at 5-minute intervals at the start of the procedure and every minute during balloon inflations and stent placement. The blood pressure was measured in 1 arm (usually the left) by an automated-cuff-inflation sphygmomanometer (Omnicare 24, Hewlett Packard). The same arm was used consistently throughout the procedure and during the postoperative period.
Baseline angiography was performed, and the lumen diameters of the
stenotic and adjacent arterial segments were
measured. The angioplasty was performed with a large-lumen guide
catheter, a flexible guidewire, and a balloon catheter. An
intravenous heparin bolus (5000 to 7500 U) was given to
achieve an activated clotting time of 
300 seconds. If there
was evidence of thrombosis or ulceration in the stenotic
segment, urokinase (150 000 to 250 000 U) was infused through a
microcatheter (around the guidewire) proximal to the lesion before
introduction of the balloon.12 A 6F to 9F guide catheter
(2 to 3 mm in diameter) was advanced through the sheath into the
common carotid artery. The flexible, angulated-tip guidewire (0.14 to
0.18 inches in diameter) was advanced through the guide catheter,
navigated across the stenosis, and positioned in the distal
arterial segment. With the guidewire across the
stenosis, the deflated balloon catheter was advanced over the
wire and positioned at the stenosis. The positions of the
guidewire and balloon catheter were inspected periodically under
fluoroscopy. Intravenous atropine was given for prophylaxis
in some patients at the physician's discretion before inflation of
balloon. Intravenous atropine was given either as a 0.5-
(n=6), 1.0- (n=10), or 1.5-mg (n=2) dose. The balloon was inflated for
a period lasting from a few seconds to 1 minute at 6 to 12 atm with a
mixture of saline and contrast material used to fluoroscopically
visualize the inflation. If the stenosis was adequately
dilated, the balloon catheter was removed. If the dilation was
inadequate, the balloon catheter was replaced by a larger one. After
predilatation, a stent was placed across the dilated segment over the
guidewire by use of a stent-delivery system. The size and type of stent
selected were determined by both baseline and predilatation
angiographic evaluations. After stent placement, a second dilatation
was performed to anchor the stent in normal vessel by full expansion
with a larger balloon catheter. A final angiogram was obtained to
confirm that the final dilation of the stenotic segment was
adequate and no local complications such as dissection had occurred.
Intracranial vessels were also imaged to avoid undetected compromise of
intracranial circulation by thromboembolic events.
The patient was transferred to the neurointensive care unit for overnight observation. Heart rate and respiratory rate were monitored continuously. Blood pressure was monitored every 15 minutes by use of an automated-cuff-inflation sphygmomanometer (model 56, Hewlett Packard). Neurological evaluations were performed every 2 hours and more frequently if the patient's condition was deteriorating. Postprocedural hypotension was treated with intravenous infusion of dopamine titrated to maintain systolic blood pressure greater than 100 mm Hg. Postprocedural hypertension was treated with intravenous labetalol or hydralazine to reduce systolic blood pressure to preprocedural values. Postprocedural sinus bradycardia was treated with intravenous atropine (0.5 to 1.0 mg), and bradycardia due to second- or third-degree atrioventricular block was treated with transvenous pacemaker.
Data Collection
Records Review
From the medical records review, the following information
was collected for each patient: age; sex; race; current smoking status
or alcohol use; history of angina pectoris, myocardial infarction (MI),
coronary artery disease (including previous bypass or
angioplasty), hypertension, diabetes mellitus,
hyperlipidemia, cardiac dysrhythmia, valvular
heart disease, cardiac failure, peripheral vascular
disease, renal insufficiency, pulmonary disease, or CEA; and
medications used before admission (including antiplatelet agents).
Any clinical symptoms were noted for documentation of
symptomatic ipsilateral or contralateral carotid artery
disease. The following procedural details were collected: diameter of
largest balloon used and diameter and type of stent placed.
Blood pressure, heart rate, and respiratory rate measurements obtained before, during, and after the procedure were recorded. Any episodes of bradycardia (defined as heart rate <60 bpm), hypotension (defined as systolic blood pressure <90 mm Hg), and hypertension (defined as systolic blood pressure >160 mm Hg), as well as medications used to treat these conditions, were recorded. Although recordings were made more frequently, blood pressure, heart rate, and respiratory rate values (for purposes of analysis) were collected at 30-minute intervals during the procedure and at 2-hour intervals for 18 to 43 hours (mean 25.7 hours) afterward. The lengths of stay in the hospital and in the intensive care unit were recorded for each patient.
Evaluation of Angiograms
Digital subtraction angiography images were collected
retrospectively from the digital tape storage system of our angiography
unit (Toshiba Medical Systems). Ipsilateral and contralateral
diagnostic images of the extracranial carotid arteries and
the intracranial circulation, as well as images of the stented artery,
were obtained. The extracranial carotid artery images were transferred
to a computer workstation running NIH Image software
(http://rsb.info.nih.gov/nih-image/) for subsequent measurements. After
adjustments for magnification were made, diameters of the
stenosis, the distal internal carotid artery (ICA), and the
stented lesion were measured. All measurements were made on lateral
views. The measurements were performed in user-defined regions of
interest (ROIs) after adjustment for image scale. NIH Image measurement
functionality was used (rulers that were applied manually after the
ROIs were magnified 4-fold). The degree of stenosis was
calculated according to the primary NASCET method, ie, diameter of
stenosis/distal ICA diameter.13 This method was
chosen to ensure comparability with other studies.14
Extension of the lesion was classified according to involvement of the
common carotid artery, the medial or lateral wall of the carotid bulb,
the external carotid artery, and/or the distal ICA. Similarly, it was
recorded whether the stent covered the common carotid artery, the
bulb, and/or the ICA. Each of these angiographic features was further
analyzed as a dichotomized variable.
Statistical Analysis
The effects of 43 variables collected from patient charts
and 11 variables obtained from angiographic images were evaluated
for each of the following outcomes: postprocedural hypotension,
postprocedural hypertension, and postprocedural bradycardia. Stepwise
logistic regression was used to analyze these relationships
with an entry criteria of P<0.1. A P value of
<0.05 was considered significant. The effects of continuous
variables, such as age or the degree of stenosis, were
entered as linear factors after they were tested for nonlinearity by
use of the Box-Tidwell transformation.15 Interactions
among the effects variables were tested for significant
contribution to the logistic-regression model (P<0.1). All
possible interaction terms were nonsignificant and were therefore
excluded from the model.
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Results |
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Fifty-four consecutive patients were initially included in the study. Three patients were excluded because angiographic material was not available. For the remaining 51 patients (18 women, 33 men; mean age 68.3 years), descriptive characteristics are given in Table 1
,
2, and
3. The mean degree of
stenosis on the treated side was 69±19% (Table 3). The
severity of stenosis ranged from 50% to 97.5% in all but 1
patient. One patient had a measured stenosis of 42.5% despite
high-grade stenosis because the stenosis extended up to
the petrous portion, therefore affecting the distal reference point. In
45 patients, the contralateral ICA showed stenoses of varying
degrees (complete occlusion in 6 cases). Stenoses in 42
patients were treated with Wall stents (Schneider), in 1 patient with a
GFX stent (Arterial Vascular Engineering), and in 4
patients with Integra stents (SCIMED Boston Scientific). In procedures
in 4 patients treated early in our series, Palmaz stents (Johnson &
Johnson) were used. The mean intensive care unit and hospital stays
after angioplasty and stent placement were 2.2±2.5 and 4.2±3.5 days,
respectively.
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Postprocedural Hypotension
Postprocedural hypotension was observed in 13 cases. Two of these
patients were excluded from additional analysis because the
hypotensive event followed postoperative antihypertensive treatment. Of
the 49 patients included, the frequency of postoperative hypotension
was 22.4% (n=11). The period of blood pressure instability (end point
defined by the latest reading <90 mm Hg with intermittent higher
readings) lasted for 4 to 27 hours (mean 14.8 hours). Eight of 11
(72.7%) hypotensive patients required dopamine treatment (Table 2). In the remainder, hypotension resolved spontaneously.
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When all mean arterial pressure (MAP) readings for each patient were averaged over the entire monitoring period, these values ranged from 55.7 to 95.6 mm Hg (mean 72.5 mm Hg) in the hypotensive group. This compares with 70.5 to 104.3 mm Hg (mean 85.4 mm Hg) in the nonhypotensive group. These differences in minimal (P<0.001), maximal (P<0.05), and mean (P<0.01) MAP values were statistically significant. Accordingly, significant differences also were found for time-averaged systolic and diastolic blood pressures (P<0.01). No differences were found in heart or respiration rates between hypotensive and nonhypotensive patients.
In 6 (54.5%) of 11 patients experiencing postprocedural hypotensive
episodes, hypotension was also present intraoperatively. In
contrast, only 2 (5.3%) of 38 nonhypotensive patients had
intraprocedural hypotension (Pearson 
2
P<0.001). Postprocedural bradycardia was significantly more
frequent in hypotensive than in nonhypotensive patients (64% versus
18.4%; Pearson 2 P<0.01).
However, the changes in blood pressures and heart rate were not
associated in time. Patient age was a predictor for postprocedural
hypotension: the mean age of hypotensive patients was 74.1 years versus
66.7 years in the nonhypotensive group (2-sided t test with
unequal variances P<0.005). The incidence of hypotension
was highest in patients between 70 and 75 years of age (38.5%). In
patients older than 75 years, the incidence decreased slightly
(30.0%). A history of MI was often found in the hypotensive group
(54.5% versus 21.1% in the remaining patients; Pearson
2 P<0.05). Carotid
stenosis was less frequently symptomatic in
hypotensive patients than in nonhypotensive patients (27.3% versus
63.2%; Pearson 2 P<0.05). An
additional variable associated with postoperative hypotension was
the change in vessel diameter after stenting, as described by the ratio
of the diameter of the unstented stenotic segment divided by
that of the stented stenotic segment. Greater diameter changes
were protective for hypotension, ie, the greater the change in
diameter, the lower the incidence of hypotension (2-sided t
test with unequal variances P<0.05).
After the influence of each variable was tested separately, a
logistic regression model with hypotension as the dependent
variable was constructed. The final model consisted of the
following independent variables: age, previous MI,
symptomatic carotid stenosis (ipsilateral), and
intraprocedural hypotension (Table 4).
The strongest predictor was intraprocedural hypotension, followed by MI
history. The overall predictability of the model was 91.8%.
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Postprocedural Hypertension
Compared with postprocedural hypotension, postprocedural
hypertension was observed more frequently. Of 21 cases of hypertension
during the monitoring period, 2 were excluded from additional
analysis because the respective patients had hypertension after
vasopressive treatment for hypotension. Therefore, the frequency of
hypertension in our series was 38.8%. All 19 patients had a history of
hypertension at baseline. Four of the 19 patients had systolic
blood pressure >160 mm Hg before the procedure. Nine of 19
hypertensive patients required intravenous antihypertensive
therapy in the postprocedural period. Two patients had both
hypertension and hypotension during the monitoring period. Because
these patients received neither vasopressive nor antihypertensive
medication, it is assumed that both events were procedure
related.
Univariate testing revealed the following significant
predictors of postprocedural hypertension: sex (female risk>male risk,
P<0.05), history of hypertension (P<0.05),
intraprocedural hypertension (P<0.01), previous ipsilateral
CEA (P<0.01), and preprocedural diastolic blood
pressures (each P<0.05). The preprocedural
diastolic blood pressure was 85.5±13.1 and 76.0±10.9
mm Hg in patients with and without postprocedural hypertension,
respectively. In the multivariate model, the
variables ipsilateral CEA, intraprocedural hypertension, and
preprocedural diastolic blood pressure remained in the
final model (Table 5). The strongest
predictor was ipsilateral CEA, followed by intraprocedural
hypertension. The overall predictability of the model was 80.9%.
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Postprocedural Bradycardia
Postprocedural bradycardia occurred in 14 (27.5%) of 51 patients
in our series. Bradycardia was noted in 7 patients with postprocedural
hypotension and in 4 with postprocedural hypertension. One patient who
had postprocedural hypotension and hypertension also experienced
postprocedural bradycardia. During the procedure, 7 of the 14 patients
were given atropine, and 1 patient required transvenous pacing after
bradycardia developed.
In univariate analyses, significant predictors of
bradycardia were claudication (protective, P<0.05),
intraprocedural hypotension (P<0.01), and intraprocedural
bradycardia (P<0.05). The final model included
intraprocedural hypotension and intraoperative bradycardia as
independent variables (Table 6). Both
variables had a high predictive power. The overall predictability
of the model was 83.7%. When prophylactic use of atropine
was added to the model, atropine use was independently associated with
higher risk of postprocedural bradycardia (OR 32.7, 95% CI 3.2 to
340.5). Both intraprocedural hypotension and intraoperative bradycardia
remained significant in this model as well.
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Temporal Relationship Between Postprocedural and Intraprocedural
Hemodynamic Instability
The majority of postprocedural events were temporally separate
from the intraprocedural hemodynamic events. Both
postprocedural hypotension and bradycardia represented a
continuum of intraprocedural events in 2 patients and 1 patient,
respectively. Postprocedural hypertension was temporally separate and
continuous with intraprocedural hypertension in 11 and 7 patients,
respectively. Exclusion of patients in whom intraprocedural and
postprocedural events were continuous did not affect the prediction
model for either postprocedural hypotension or bradycardia. For
postprocedural hypertension, both intraprocedural hypertension and
preprocedural diastolic blood pressure remained significant
predictors. However, ipsilateral CEA lost significance in the model.
Because our results were affected minimally by exclusion of events that
continued from the intraprocedural into the postprocedural period, such
patients are not excluded in the reported analysis.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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This report suggests that sustained hemodynamic instability occurs in a significant proportion of patients in the acute period after CAS. In our patient series, postprocedural hypertension occurred in 38.8%, bradycardia in 27.5%, and hypotension in 22.4% of patients. All events were transient and had resolved at the conclusion of the intensive care unit monitoring period (mean 25.7 hours, range 18 to 43 hours). Previous studies have reported on hemodynamic complications after angioplasty and stent placement.16 17 18 19 20 21 The frequency of these complications has varied depending on patient selection and procedural technique. Most studies have focused on intraprocedural hemodynamic events. Mendelsohn et al16 observed that bradycardia or hypotension occurred during 13 (68.4%) of 19 CAS procedures studied. Vasopressive medication was required in 7 patients with sustained hemodynamic instability. Wholey et al20 observed bradycardia requiring temporary pacemaker insertion in 11 (9.6%) of 114 patients who underwent CAS. Hypotension requiring vasopressor therapy was observed in 1 patient. Yadav et al21 reported bradycardia in 71% of 107 patients who underwent elective CAS. The bradycardia persisted for a few minutes after balloon deflation. One patient required permanent pacemaker placement 3 days after carotid stenting. Waigand et al19 reported the development of a sinoatrial block in 40 of 50 patients with severe coronary artery disease during high-pressure inflation for carotid angioplasty followed by stenting. Teitelbaum et al18 performed CAS in 22 patients. All patients experienced transient bradycardia with or without asystole (lasting <30 seconds) that resolved after balloon deflation and intravenous administration of glycopyrrolate or atropine. Although the frequency of postprocedural hemodynamic instability was not mentioned, 1 patient had transient neurological deficits associated with postprocedural hypotension.
Hemodynamic complications that occur during and after CAS are probably mediated through dysfunction of adventitial baroreceptors in arterial segments that are dilated and covered with intravascular stents.17 The baroreceptors are stretch receptors located in the carotid sinus (dilated segment of the ICA at its origin from the common carotid artery).22 Impulses arising in the carotid sinus travel through the sinus and glossopharyngeal nerves to the nucleus tractus solitarius (NTS) in the caudal medulla. Stimulation of the carotid sinus inhibits sympathetic neurons in the NTS and reduces sympathetic tone to peripheral blood vessels, leading to a reduction in systemic blood pressure. In conjunction with aortic baroreceptors, the carotid sinus plays a key role in short-term adjustments of blood pressure when relatively abrupt changes in blood volume, cardiac output, or peripheral resistance occur. Impulses from the carotid sinus also initiate excitatory impulses from the NTS to the nucleus ambiguus and dorsal vagal nucleus.23 The increase in vagal activity results in a decrease in heart rate. Carotid sinus activity is dependent on arterial pressure. Below a MAP of 60 mm Hg, there are no sinus nerve impulses. Progressively increasing sinus activity is seen above 60 mm Hg, which plateaus at 200 mm Hg.22 Carotid artery baroreceptors modulate blood pressure by reciprocal changes in vagal and sympathetic neural activity. At low arterial pressures, carotid sinus impulses only invoke a sympathetic response, with no vagal response. In contrast, at high levels of MAP, the predominant response is vagal activity, with minimal sympathetic response.
We evaluated the predictors for each hemodynamic complication, ie, hypotension, hypertension, and bradycardia, to gain a better understanding of the underlying pathophysiology and to identify at-risk individuals. Postprocedural hypotension was associated with age, previous MI, ipsilateral symptomatic carotid stenosis (protective effect), and intraprocedural hypotension. The strongest predictor was intraprocedural hypotension. Mendelsohn et al16 observed that postprocedural hypotension only occurred in patients with intraprocedural hypotension. In 54.5% of our patients who had hypotensive episodes after the procedure, hypotension was already present during the procedure. However, we observed that patients without intraprocedural hypotension can develop hypotension after the procedure. History of MI was another determinant of postprocedural hypotension. Previous studies have demonstrated increased sensitivity of carotid artery baroreceptors in patients with coronary artery disease.24 25 Increased baroreceptor sensitivity in conjunction with a history of MI may have predisposed patients in the present study to postprocedural hypotension. The mechanism underlying increased responsiveness to carotid sinus stimulation is not known. Activation or sensitization of the vagal nerve by receptors located in the atrial or ventricular region or the atrioventricular node due to chronic or acute coronary ischemia has been implicated in the exaggerated carotid sinus response.25 Mendelsohn et al16 additionally observed that the occurrence of postprocedural hypotension was also related to the placement of large-sized stents. We found that postprocedural hypotension was associated with the change in vessel diameter after stenting, as described by the ratio of the diameter of the unstented stenosis divided by the diameter of the stented stenosis. Greater diameter changes were protective for hypotension, ie, the greater the change in diameter, the lower the incidence of hypotension. However, this association was not significant in multivariate analysis after adjustment for other variables. Nimodipine, which can exert a hypotensive effect, was administered hours before the procedure. However, the hypotensive effect is seen soon after administration and is not consistent with the late hypotension observed in the present study.
Postprocedural hypertension was associated with ipsilateral CEA, intraprocedural hypertension, and preprocedural diastolic blood pressure. Ipsilateral CEA was the strongest predictor. Because preprocedural diastolic blood pressure was entered as a continuous variable, no cutoff value could be identified. The preprocedural diastolic blood pressure was 85.5±13.1 and 76.0±10.9 mm Hg in patients with and without postprocedural hypertension, respectively. Carotid baroreceptor modifications were reported by Angell-James and Lumley26 and Tyden et al27 in the acute period after CEA in humans. However, these alterations are transient. Long-term changes in carotid baroreceptor function after restenosis subsequent to CEA are not well described. Dehn and Angell-James28 assessed the long-term effect of CEA on carotid sinus baroreceptor function and observed decreased baroreceptor function in a minority of patients. They attributed this diminished activity to periarterial fibrosis (reduced compliance) and operative trauma to the carotid sinus nerve and baroreceptors. Our results suggest that postendarterectomy restenosis predisposes patients to postprocedural hypertension, presumably by diminution in baroreceptor function. Theron et al11 similarly observed that bradycardia during balloon inflation in patients undergoing CAS was not observed in patients who had previously undergone CEA. Potentially confounding these observations is the unquantifiable effect of alterations in the daily antihypertensive regimens of hypertensive patients.
Intraprocedural hypotension and intraprocedural bradycardia predicted postprocedural bradycardia. Bradycardia was noted in 7 patients who experienced postprocedural hypotension. Four patients with postprocedural hypertension also had bradycardia. Although postprocedural bradycardia was significantly more frequent in hypotensive (64%) than in nonhypotensive (18.4%) patients, there was no temporal association between blood pressure and heart rate in either group. The lack of a temporal association may be attributed to concomitant administration of inotropic agents, such as dopamine, that alter the heart rate or to mediation of heart rate or blood pressure responses by separate pathways. Paradoxically, prophylactic use of atropine during the procedure was associated with a higher risk of postprocedural bradycardia. The exact reason underlying this association is unclear. Because prophylactic atropine use was based on the discretion of the physician performing the procedure, there may be bias toward use of atropine in patients considered at risk for developing bradycardia.
Our observations suggest that intraprocedural
hemodynamic instability was an important determinant of
postprocedural hemodynamic complications. Modification
of the elasticity (compliance) of the arterial wall, eg,
during angioplasty and stent placement, may alter the sensitivity of
carotid baroreceptors. Angioplasty stretches the vessel wall, resulting
in superficial splitting of the intima and atherosclerotic
plaque.8 Retraction of the intima and distention of the
media results in a permanent increase in vessel diameter. Bagshaw and
Barrer29 demonstrated in dogs that angioplasty of
nondiseased carotid arteries increases the sensitivity of carotid sinus
baroreceptors. They attributed this increased sensitivity to changes in
the mechanical properties of the carotid sinus, such as greater
compliance and increased diameter for a given MAP. We were unable to
observe any effect of diameter of largest balloon used, ratio of
largest balloon diameter to vessel diameter, or magnitude of change in
vessel lumen diameter on postprocedural hemodynamic
instability. Individual variations in sensitivity of the baroreceptors
and adaptive responses may have confounded the association between
hemodynamic instability and these mechanical factors.
Furthermore, desensitization of baroreceptors due to longstanding
hypertension may also diminish response to baroreceptor stimulation.
The stent covered the sinus region in most patients (Table 3
),
and therefore, an effective analysis of the association between
sparing of sinus and hemodynamic instability could not
be performed.
Previous investigators have suggested that baroreceptors have a short-lasting effect (minutes) on the regulation of systemic blood pressure.30 However, we observed that acute intraprocedural dysfunction was a strong predictor of protracted hemodynamic instability in the postprocedural period. Fadali and Walstad31 observed that enlargement of the canine carotid sinus diameter by angioplasty or vein-patch grafting produced decreases in blood pressure in normal and hypertensive dogs that persisted for days in the presence of normally active arterial baroreceptors at other sites. They postulated that adaptation of carotid sinus receptors to changes in mechanical properties is slow and incomplete. Bagshaw and Barrer29 supported this hypothesis by showing that carotid angioplasty resulted in steady-state increases in sinus baroreceptor stimulation and activity. However, the NTS is not capable of determining the source of accurate blood pressure information, ie, the altered carotid sinus or intact aortic and contralateral carotid baroreceptors.29 Burystyn et al32 suggested that brain-stem centers will not ignore abnormal afferent signals from the reset baroreceptors if their pulsatile nature is intact. Furthermore, aortic baroreceptors may have a higher threshold for stimulation than carotid receptors.33 Our observations suggest that modification of baroreceptor sensitivity after angioplasty does not persist indefinitely, because all hemodynamic complications had resolved within 43 hours.
The mean intensive care unit and hospital stays after angioplasty and
stent placement were 2.2±2.5 and 4.2±3.5 days, respectively. The
intensive care unit stay was 
2 days in 76% of the patients. The
hospital stay was 4 days in 66% of the patients. The stay was
prolonged in a small proportion of patients because CAS was followed by
coronary bypass surgery. Other factors contributing to
prolonged stay included the high frequency of
hemodynamic instability and concurrent medical problems
in these patients.
The phenomenon of hemodynamic instability after CAS has clinical implications. At present, this procedure has been reserved mainly for patients who are at high risk for CEA owing to preexisting coronary artery disease.8 9 Postoperative hemodynamic instability places additional stress on patients with coronary artery disease. Furthermore, preexistent cardiac rhythm abnormalities may be exacerbated in the postprocedural period. Hemodynamic instability may also increase the risk of altered perfusion and stroke in the postprocedural period. None of our patients with hypotension suffered any permanent cardiac or neurological consequences. Because of the early and aggressive use of inotropic and antihypertensive medications, the full severity and neurological consequences of these hemodynamic events are undermined in our analysis. Therefore, the potential detrimental effects of untreated hypotension or hypertension should not be underestimated despite the lack of clinical consequences in the present study. Our observation also argues against postprocedural monitoring of patients in settings not suited for intensive cardiovascular monitoring. Furthermore, same-day discharge for patients after CAS may not be adequate given the risk of hemodynamic instability.
Conclusions
The risk of hemodynamic instability after CAS
should be recognized. Intensive care unit management may facilitate the
identification of hemodynamic complications and
potentially reduce their severity. Therefore, we recommend
postprocedural monitoring of blood pressure and electrocardiographic
changes in patients undergoing CAS, particularly in those patients who
have intraoperative hemodynamic instability.
Received March 11, 1999; revision received June 24, 1999; accepted July 22, 1999.
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References |
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