The relationship between atherosclerotic coronary artery and carotid disease is an intuitive association well supported by clinical data. These two regions of the vasculature are closely approximated and share important similarities in structure and embryological origin. Within a given individual, these vascular beds share a common genetic background and are subject to virtually the same environment throughout the individual’s lifetime. It is therefore no surprise that the finding of coronary artery disease virtually assures that there is some degree of carotid pathology and vice versa. From the standpoint of the cardiothoracic surgeon, this means that up to 22 percent of candidates for coronary artery bypass surgery will have significant carotid disease.¹ This number is likely to increase as the population continues to age and coronary artery bypass grafting (CABG) is extended to more elderly patients.

Although the importance of combined coronary and carotid disease is straightforward, its treatment is complex and controversial. Historically, the procedures to address each condition were developed separately and have been evaluated using different metrics. Traditionally, the clinical benefits of CABG were measured as reductions in the rates of myocardial infarction (MI), reintervention, and mortality rates whereas those of carotid endarterectomy (CEA) have been measured as reductions in stroke and mortality. Each procedure is associated with complications that the other is intended to prevent; MI and stroke are well-recognized complications of both CEA and CABG, respectively. Furthermore, one must consider that although carotid disease is often present in coronary bypass patients, the majority of these patients experience no symptoms from their cerebrovascular disease (CVD). In deciding which procedure(s) is appropriate for each subpopulation, one must bear in mind its impact on all endpoints (e.g., MI, stroke, death) weighed against the likelihood of all complications. Lastly, less invasive procedures such as “off-pump” CABG and carotid stenting have become more widespread in recent years, adding a further layer of complexity to surgical treatment options. This chapter guides cardiothoracic surgeons through the challenges of identifying and managing carotid disease in coronary bypass patients and reviews the evidence for and against current treatment options.

Stroke is one of the most prevalent and debilitating complications of coronary artery bypass surgery and one that frequently negates the benefits of coronary revascularization. Clinically speaking, perioperative stroke is defined as an acute neurologic event secondary to circulatory impairment lasting more than 24 hours and occurring within a specified period of time following surgery. Nearly all centers define stroke in this manner and most obtain radiologic imaging [i.e., computed tomography (CT) or magnetic resonance imaging (MRI)] to delineate the distribution and extent of cerebral injury after a perioperative stroke. Although there is variability in the definition of perioperative stroke (e.g., 14 vs 28 days), most strokes present within the first 3 days after coronary bypass surgery. Over the past 2 decades, the incidence of perioperative stroke in the general CABG population has remained fairly constant, ranging from 2.1 to 5.2 percent.^2,3 A variety of risk factors have been identified for perioperative stroke in CABG patients (Table 30-1) and several closely related mechanisms have been proposed (Table 30-2), the most important of which are arterial emboli and cerebral hypoperfusion. It is theoretically possible for carotid lesions to affect strokes by either of these mechanisms in the postoperative period, incurring emboli though plaque rupture, thrombosis, or diminished arterial flow. However, since the carotid arteries are not surgically manipulated during CABG and carotid thrombi are rarely seen on imaging, it has been postulated that carotid stenosis and/or occlusion cause strokes primarily via cerebral hypoperfusion during low cardiac output states (e.g., while on cardiopulmonary bypass or in the early postoperative period).

In a large meta-analysis, Naylor et al. concluded that less than half of CABG patients who suffered perioperative strokes had significant carotid disease, defined as either significant stenosis or occlusion.⁴ Naylor et al. also demonstrated that the degree of carotid disease was statistically associated with increasingly high rates of perioperative stroke in CABG patients, which ranged from 3 percent in patients with mild disease up to 7 to 11 percent in patients with carotid occlusion. An extensive retrospective study from our practice at The Johns Hopkins Hospital yielded similar results.⁵ However, carotid disease is a fairly specific risk factor for aortic arch atherosclerosis,⁶ which is widely believed to be the most important source of arterial emboli in CABG-related strokes. As a result, although the finding of carotid disease clearly increases the risk of perioperative stroke in CABG, it remains unclear whether the link between carotid disease and perioperative stroke is truly causal, since carotid disease alone has never been proven to be an independent risk factor for perioperative stroke while controlling for aortic atherosclerosis. At the same time, there are reports of individuals in whom the finding of preoperative stenosis preceded a “watershed” stroke in the distribution of a stenotic carotid artery.⁷ In summary, carotid disease is associated with an increased stroke risk in CABG patients, but less than half of CABG-related strokes occur in patients with carotid disease and it is likely that only a subset of these strokes are due to carotid stenosis per se rather than related conditions.

Although the effect of carotid disease on perioperative stroke risk in CABG remains uncertain, its effect on long-term stroke risk is well documented. Carotid disease is thought to cause between 20 and 30 percent of strokes.⁸ With regard to long-term stroke risk, the natural history of carotid disease in CABG patients is presumably similar to that of nonsurgical patients in large prospective studies of carotid stenosis, such as the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and Asymptomatic Carotid Atherosclerosis Study (ACAS).^9,10 No large, prospective, controlled trials to date have specifically addressed the impact of carotid stenosis and/or occlusion or their related therapies on the long-term rates of stroke free survival in CABG patients. A final point to consider is that there is likely a small degree of mechanistic overlap between “long-term” and “perioperative” strokes; there are bound to be CABG patients with carotid stenosis who, by chance, suffer strokes due to carotid plaque rupture unrelated to the operation itself, within the perioperative period.

It has long been known that vascular lesions outside the coronary vascular bed can be “index lesions” of MI. Indeed, MI is a well-documented complication of several commonly performed peripheral vascular interventions, such as aortic or infrainguinal procedures. The mechanism is thought to be embolic, as fragments of plaque from the diseased vascular bed are mobilized during surgical manipulation and become lodged in already-stenosed coronary arteries. Nonfatal and fatal MIs remain devastating postoperative complications of CEA, although the incidence of MI in ACAS was less than 1 percent.¹¹ These numbers seem surprisingly low when one considers that up to 50 percent of patients with carotid disease have some degree of coronary artery disease. Of course, MI rates are likely to be somewhat higher in CABG patients who, by definition, have severe coronary artery disease.

Previous studies have reported an incidence of carotid disease in CABG patients ranging from 2 to 22 percent.⁵ This range is rather wide because the definition of “significant” carotid disease varies between centers. For example, even ACAS and NASCET stratified their respective cohorts using different numerical thresholds. Specifically, ACAS defined 60 percent luminal stenosis as significant whereas NASCET initially employed a 70-percent threshold that was later changed to 50 percent.^9,10 After ACAS showed a significant but underwhelming clinical benefit for CEA using the 60 percent threshold, numerous follow-up studies have used greater degrees of carotid stenosis as thresholds to trigger surgical intervention. The ambiguity of the term “significant stenosis” is equally apparent in studies of carotid disease in CABG populations, where thresholds have routinely ranged from 50 to 80 percent luminal narrowing.

Regardless of the threshold one chooses to define significant carotid disease, there are several ways to identify and quantify carotid lesions. Ideally, the process begins by including questions in the history designed to identify patients at high risk for carotid disease. Because the etiologies of carotid and coronary artery disease are so similar, it is best to focus on the risk factors that have been validated in previous studies of carotid disease within CABG populations (Table 30-3). On physical examination, the most important finding is the presence of a carotid bruit. Although a carotid bruit is not pathognomonic for carotid stenosis, at our center nearly 40 percent of CABG patients with a bruit had carotid stenosis in excess of 70 percent as measured by carotid duplex ultrasound.⁵ In addition, any exam findings indicative of CVD (e.g., focal neurologic deficits) or peripheral vascular disease (e.g., weak distal extremity pulses, popliteal bruits) also greatly increase the likelihood of carotid disease.