Carotid angioplasty and stenting (CAS) are a widely accepted procedure due to its simplicity and noninvasiveness.1-3 However, because of anatomical closeness of the procedure to the carotid sinus, hemodynamic instability (HDI) can occur during the procedure. Many studies have been performed to determine the risk factors of HDI.4-12 Nevertheless, most of the studies failed to clearly show the relationship between calcified plaques and hemodynamic instability.

The goal of this study was to investigate the risk factors of HDI focusing on characteristics of plaque.

Thirty-nine patients (70.2±8.5 years) were examined. These patients were mostly male (n=32, 82.1%), and the majority had symptomatic lesions (n=25, 64.1%). Stenosis value was 79.4±6.6. Nineteen of the 39 patients had HDI due to hypotension or bradycardia during and after CAS. Prolonged HDI lasting over 30 min occurred in eight patients. The vital signs of transient HDI were normalized in an average of 7.8 min after development (range, 0.5-24 min). Bradycardia occurred in 19 patients, hypotension occurred in 10 patients, and both occurred in 10 patients. All bradycardia recovered well within 30 min with the use of a transcutaneous temporary cardiac pacemaker.17 All patients with hypotension were treated by intravenous fluid replacement, and eight patients received dopamine which was started at a dosage of 5 µg/kg/min. Among them, systolic pressure normalized in two patients 24 h after onset. The demographic and clinical characteristics of the 39 patients are shown in Table 1. The results revealed that calcified plaques and extensive plaque from carotid bulb to common carotid artery (CCA) were associated with HDI due to hypotension and bradycardia (p=0.001 and p=0.006, respectively). Other risk factors including age, coronary artery disease, HTN, ulceration of the plaque, maximal ATM used for ballooning, degree of diameter, and length of the stent and balloon did not differ significantly. A binary logistic regression model was used to determine the risk factors of HDI (Table 2). The presence of calcified plaque was an only significant predictable factor of HDI (OR, 8.571; 95% CI, 1.321-55.62; p=0.024)

Prolonged HDI was found in eight patients. Each prolonged HDI was caused by hypotension, despite recovery of heart beats to over 60 bpm. A calcified plaque was found in eight patients with prolonged HDI and four patients with transient HDI (p=0.005). Eccentric calcified plaques were found in eight patients with prolonged HDI and two patients with transient HDI (p=0.028) (Table 3), and most (n=8) were posterior. There were no neurological and hemodynamic complications after CAS at this institution due to proper treatment without delay.

HDI can occur during CAS due to its close location to baroreceptors. When stretch receptors located in carotid sinus are activated during inflation of balloon or deployment of stent, activation of nerve fibers to the nucleus tracts solitaries through the glossopharyngeal nerve can occur, which causes the vague nerve to stimulate the parasympathetic pathway to the cardiac nodes. The results can be lowered heart rate and reduced peripheral resistance.18,19 HDI can lead to permanent or transient adverse effects. Minor neurological problems such as transient ischemic attacks and serious complications such as acute renal failure, myocardial infarctions (MI), intra-cerebral hemorrhages, and cerebral ischemia have been reported.20,21

Many studies have been performed to reveal risk factors that contribute to the development of HDI. These HDI risk factors have been grouped into three sectors by their radiological findings, combined underlying diseases, and demographic characteristics. Radiological findings included lesions involving the carotid bulb, isolated ICA lesion near the carotid bulb, the right side of CAS, ulceration or calcification of the plaque, eccentric posterior carotid plaque, and the presence of a contra-lateral occlusion.22 Combined underlying diseases included coronary artery disease,9 major or minor strokes, DM, HTN, hyperlipidemia, and a previous history of carotid endarterectomy. Demographic characteristics involved male or female gender,11 old age,9 and the presence of symptoms.4-6,22,23 General anesthesia is also related to the development of HDI.22

Most studies have focused on finding contributory risk factors to HDI. Transient HDI can be treated well without complications. Thus, more emphasis has to be put on prolonged HDI due to its greater chance of causing complications such as cerebral infarction, renal failure, and MI. Intraprocedural hypotension has been suggested as a predictor of persistent hypotension.11,24 Nonaka, et al.12 reported that distance from carotid bifurcation to maximal stenotic lesion and eccentric type stenois on angiogram and fibrous plaque and combined calcification on ultrasonogram are related to prolonged hypotension lasting more than 3 h. However, ultrasonography is not always an exact means of revealing characteristics of plaques. Furthermore, echogenicity of plaque and calcification of plaque with ultrasonogram may be overlapped.12

The present study is different from previous studies in two aspects. First, location of plaque was categorized by including the CCA near to carotid bifurcation or only carotid bulb longitudinally. Many studies reported that lesion with carotid bulb is a risk factor for HDI. Although, a high density of baroreceptors is found in the wall of ICA just above the carotid bifurcation, baroreceptors are also located in CCA near to the carotid bifurcation.25,26 This may imply that more extensive plaque that is located from carotid bulb to CCA is vulnerable to the development of HDI. Second, calcification of plaque was described in detail by the eccentricity of the plaque. Baroreceptors are stretch receptors and their activation is affected by the rate of increasing pressure and degree of pressure. Thus, uneven pressure may be transmitted to baroreceptors and its increasing inflation rate may be different in the presence of eccentric calcified plaque during arterial distension.

The development of hypotension can be explained by decreased cardiac output due to bradycardia and venous return due to decrease in peripheral resistance. Among patients with prolonged hypotension, some characteristics of plaque were related. Eccentric calcified plaque was associated to prolonged hypotension (p=0.028) and extensive plaque that covered from CCA to carotid sinus was also related to the development of prolonged hypotension (p=0.04).

Reducing sudden and high activation of baroreceptors is a key factor in lowering the incidence of HDI and its complications. Therefore, when extensive plaque is found with eccentric calcified plaque, another strategy is needed, such as suboptimal expansion at a slow rate and preventive measures to increase venous return. Suboptimal distension of stenotic lesion was suggested in some studies. Setacci, et al.27 reported the benefit of cutting-balloon angioplasty for the treatment of highly calcified de novo stenotic lesions, and Jin, et al.28 reported good results for suboptimal pre-stent balloon angioplasty without post-stent balloon dilatation. The preventive measures for increasing venous return may be done with enough intravenous fluid administration before and during the procedure and apply of compression stocking in high risk patients.

In conclusion, HDI can occur during and after CAS, and transient HDI can be treated well with transcutaneous temporary cardiac pacemaker, fluid replacement and inotrophic agents without complication. When extensive plaque combined with eccentric calcification is found, however, more caution is required and another treatment plan is needed to prevent prolonged HDI.