Discussion

Dr Carlos Timaran (Dallas, Tex). Dr Lin and colleagues have presented an important study about a problem that is being seen more frequently by vascular surgeons as we embrace carotid angioplasty and stenting (CAS). As shown in this study, CAS may induce bradycardia and hypotension that may be associated with adverse outcomes if not resolved expeditiously. CAS-induced bradycardia is typically short lived, whereas hypotension is more persistent. Because CAS is currently reserved primarily for high-risk patients, hemodynamic changes could potentially result in significant morbidity and mortality, particularly in patients with severe cardiovascular disease. Moreover, this study has revealed that elderly patients and those with severely depressed cardiac function are at higher risk of developing CAS-induced hemodynamic depression. Based on the results of the current study, I have the following comments and questions:

First, in the multivariate logistic regression models included in your paper, age groups were analyzed rather than age as a continuous variable. This is a rather unfortunate, as most statisticians would agree that continuous variables should be maintained continuous. Did you analyze age as a continuous variable in separate models? If you did, what is the age cutoff value above which the risk of hemodynamic changes is more significant? It appears that octogenarians have the highest risk in this series. Do you believe that because of this additional risk factor, CAS should definitely be avoided in octogenarians?

Second, in this series, CAS-induced bradycardia was treated with atropine and hypotension with dopamine. The use of atropine during CAS is controversial as it has significant side effects, particularly in elderly and high-risk patients, including mental status changes and persistent tachycardia that may lead to myocardial ischemia. Dopamine, on the other hand, can also induce tachycardia and arrhythmias and its mechanism of action does not treat the physiologic changes induced by stretching the carotid sinus. Moreover, because atropine and dopamine produce tachycardia through different mechanisms, their actions could be additive even synergistic. What was the incidence of persistent hypertension or tachycardia related to the use of atropine and dopamine? What was the incidence of treatment-induced arrhythmias, angina and myocardial infections?

Third, atropine is rarely used these days as an adjunct to general anesthesia because of its serious adverse effects. Glycopyrrolate is currently the anticholinergic medication of choice because of its limited half-life. Why haven’t the authors used it instead of atropine? What do the authors think about using vasopressors with mechanisms of action that have more physiologic basis for the treatment of CAS-induced hypotension, such as ephedrine and norepinephrine.

Finally, I would like your input regarding a patient I had to treat several weeks ago. This was an 81-year-old patient with symptomatic carotid stenosis, unstable angina, 80% stenosis of the left main, and 99% stenosis of the right coronary arteries. His ejection fraction was 25%. According to your data, this patient has a high risk of adverse outcome. How would you treat this patient considering that his coronary artery disease was deemed nonreconstructable? I may consider transferring patients like this to Houston if you have the right answer.

I want to thank the authors for sending me their manuscript in advance and the association for the honor of discussing this important study and the privilege of the floor.

Dr Peter H. Lin: Regarding your first question, which deals with the statistical analyses of the age factor as a continuous variable as well as the categorical variable, we did perform analysis using age as a continuous variable and similarly discovered that increased age was associated with an increased risk of hemodynamic depression.

With that said, I think it is premature to draw a conclusion based on this study to say that carotid stenting is indeed contraindicated or avoided in elderly patients. There are many factors that can lead to the development of bradycardia or hypotension in elderly patients. One potential issue that comes to my mind is that many of these octogenarian patients are perhaps hypovolemic; particularly, many of these patients may have underlying left ventricular dysfunction, which may lower the threshold of sympathetic activation. As such, elderly patients who are dehydrated with suppressed cardiac function are more likely to develop hemodynamic depression following baroreceptor stimulation. One learning point that we can draw from our experience is that interventionalists should have a higher level of awareness when performing carotid stenting in elderly patients who might have compromised cardiac function. These patients should be appropriately hydrated during this procedure to reduce the likelihood of postprocedural hypotension or carotid sinus activation.

Your second question relates to the use of atropine and dopamine. In our practice, we only administer intravenous atropine when a patient develops bradycardia. We have found that selective atropine administration is very effective in reversing carotid-stenting-induced bradycardia. I do want to point out a technical step in our practice with regards to atropine administration. Whenever we are about to perform balloon dilation of the carotid artery or deploy a carotid stent, we have an OR nurse or nurse anesthetist read the heart rate loudly in the operating room so that everyone in the operating room can receive an audible readout of the heart rate. The decision of atropine administration is clearly communicated with everyone participating in the stenting procedures, including the surgeons, anesthesiologists, nurses, residents, and even medical students. In no instance do we have to administer additional atropine once patients leave the operating room. I do have to emphasize that we have the advantage because all carotid stenting procedures were done in the operating room with staff anesthesiology monitoring, and we have been very satisfied with added staff support in the way these patients are monitored.

With regards to your third question, we do not have experience with glycopyrrolate to treat patients with bradycardia. Additionally, we have not experience any side effects of atropine, although we fully recognize that this drug can cause hypotension, particularly in patients who are hypovolemic. With that said, our treatment approach in patients who developed post-stenting hypotension is to provide fluid resuscitation first. After a liter or so of fluid, which obviously depends on the patient’s cardiac function, we will put a central line in to monitor their intravenous pressure and follow-up by appropriate vasopressor agent administration.

With regard to your last question of an 80-year old gentleman with increased cardiac morbidities, clearly it is difficult to answer that question based on brief history. However, I do think that carotid endarterectomy under local anesthesia remains an excellent treatment option even in high-risk patients with carotid artery stenosis. I was fortunate to receive my vascular surgery fellowship training at Emory University School of Medicine where I learned the art of carotid endarterectomy under local anesthesia from surgeons such as Drs Bob Smith, Atef Salamn, Tom Dodson, and Eliot Chaikof. To this date, I continue to perform carotid endarterectomy under local anesthesia in my practice. In patients who have anatomical concern to undergo carotid stenting, we have shown in our experience that carotid endarterectomy under local anesthesia is clearly an excellent treatment option even in elderly patients. Therefore based on the scenario you provided, I would consider both options in the overall treatment strategy. The cardiac comorbidities that you had mentioned would not preclude this patient from undergoing carotid endarterectomy under local anesthesia.