Management of Concomitant Carotid and Coronary Arterial Disease



Management of Concomitant Carotid and Coronary Arterial Disease



Virendra I. Patel, Cary W. Akins and Richard P. Cambria


The management of patients with coexistent carotid and coronary artery disease (CAD) depends upon the circumstances of clinical presentation. Most surgeons would agree that symptomatic carotid stenosis requires prompt, if not urgent, surgical therapy based on presentation. In such patients, concurrent CAD should be managed with maximal medical therapy in the perioperative setting. A more controversial issue is the management of patients who require coronary artery bypass grafting (CABG) and who have asymptomatic carotid artery occlusive disease. The management of such patients varies widely, and there is no consensus among practitioners regarding optimal management.


Of the potential causes of perioperative stroke after cardiac surgery, carotid stenosis is the one situation that may be eliminated before the cardiac procedure. Because carotid stenosis is a significant risk factor for perioperative stroke, the need to define carotid disease before coronary artery grafting becomes obvious. The logical extension that surgical correction of carotid stenosis can decrease the risk of stroke has been the basis of our approach for many years. The reported safety of the combined operative approach as well as level I evidence supporting this approach is key to its continued application.



Cardiac Risk Stratification Prior to Carotid Endarterectomy


An assessment of CAD before vascular reconstruction has several purposes. These include preventing perioperative cardiac ischemic complication and assessing long-term prognosis because natural history implicates CAD as the principal cause of late mortality in patients following carotid endarterectomy (CEA). Several studies have highlighted the prevalence of CAD and its short- and long-term implications for patients treated with CEA. Hertzer and colleagues performed routine preoperative coronary angiography in 506 carotid endarterectomy patients and found that the severity of coronary artery disease was normal in 7%, mild to moderate in 28%, advanced and compensated in 30%, severe and correctable in 28%, and inoperable in 7%.


Mackey and colleagues found that 53% of patients undergoing CEA had evidence of CAD by clinical history or electrocardiographic studies. CEA patients with clinical CAD had an operative mortality of 1.5% and a rate of myocardial infarction (MI) of 4.3% compared with 0% mortality and 0.5% MI rates in patients without CAD. They reported the 5- and 10-year survival rates of patients with CAD to be 68.6% and 44.9%, respectively, versus 86.4% and 72.3% for patients without CAD.


Urbinati and colleagues found that 25% of 106 patients undergoing CEA had significant defects on thallium exercise testing. They noted 7-year freedom from cardiac events after CEA was 51% for patients with silent myocardial ischemia versus 98% for patients with normal stress tests. In our own’ cohort of more than 2000 CEA patients (1990–1999), the rate of perioperative MI was 1.2%, and 10-year actuarial survival was 45%. Among variables associated with increased late mortality, concomitant CAD (odds ratio [OR] 1.4; p = .0002) figured prominently.


Improved perioperative care and adjunctive medical therapy have substantially lowered the risk of coronary ischemic events complicating CEA. Recent American College of Cardiology and American Heart Association (ACC/AHA) guidelines on perioperative cardiovascular evaluation for noncardiac surgery designated CEA as a low- to intermediate-risk procedure. The guidelines suggest that in the absence of active coronary ischemia, clinical profiling based on cardiovascular risk factors and functional capacity is the mainstay of cardiac risk stratification for such procedures. Patients undergoing noncardiac surgery in the absence of active coronary ischemia are best treated with continuance of β-blockers, statins, and aspirin and might benefit from perioperative use of these medications if they are not already taking them. Indeed, Perler and coworkers have reported the favorable role of statin therapy with respect to postoperative stroke (three fold reduction) and cardiovascular mortality (five fold reduction) following CEA.



Causes of Stroke Following Coronary Revascularization


Next to operative mortality, permanent stroke is the most dreaded complication following coronary revascularization because of the devastating consequences to the patient as well as the increased cost of hospitalization and post-hospital care. Major reported risk factors associated with stroke following coronary revascularization include age, ascending aortic atherosclerosis, long cardiopulmonary bypass time, perioperative hypotension, and preexisting cerebrovascular disease. Intracranial hemorrhage can lead to neurologic injury following cardiopulmonary bypass, but this a rare event, despite the degree of anticoagulation necessary for cardiopulmonary bypass.


Neurologic injury can also result from inadequate perfusion pressure on cardiopulmonary bypass, and adequate perfusion is especially important in the presence of carotid stenosis or occlusion. Some investigators have shown a linear relationship between the degree of carotid stenosis and the risk of perioperative stroke; in such analyses, patients with total internal carotid artery (ICA) occlusion are typically the subgroup at highest risk for stroke. Yet carotid revascularization is not possible in the circumstance of total ICA occlusion. When there is occlusion of carotid or intracerebral arteries, brain blood flow depends on collateral circulation, which, in turn, depends on perfusion pressure.


Atheroemboli or thromboemboli remain the most common causes of stroke following CABG. Intracardiac emboli emanate from mural thrombus associated with MI, valvular disease, arrhythmias, surgical suture lines, or, in rare instances, trapped air. Cannulation of the ascending aorta for bypass, aortic cross-clamp application, and intra aortic cardioplegia delivery devices can dislodge existing atherosclerotic material from the aorta. Thus, numerous investigators have identified aortic atherosclerosis as a risk factor for perioperative stroke. Use of preoperative computed tomography angiography (CTA) or intraoperative echocardiography to identify and avoid aortic atherosclerosis during clamping and cannulation has resulted in a reduced stroke risk.



Relationship of Carotid Stenosis to Perioperative Stroke


Virtually all studies have emphasized that the patient’s age is the single highest risk variable for the presence of carotid artery disease in patients undergoing CABG. In 1986, Gardner and colleagues found the risk of stroke to be a direct function of the patient’s age. Patients younger than 45 years had a stroke rate of 0.2%, which rose to 3.0% for patients in their 60s and to 8.0% for patients older than 75 years. At our institution, the mean age of CABG patients rose from 56 years in 1980 to older than 67 years in 2007. In 1980 only 6% of patients were 70 years or older, whereas by 2007 more than 41% were 70 years or older, and 10% were 80 years or older.


Berens and colleagues, using routine carotid artery scanning in 1087 cardiac surgery candidates 65 years or older (91% with coronary disease), found that 186 (17.0%) had a greater than 50% carotid stenosis and 65 (5.9%) had a greater than 80% carotid stenosis. Predictors of carotid artery disease were female gender, peripheral vascular disease, history of transient ischemic attacks (TIAs) or stroke, smoking history, and left main CAD. D’Agostino and coworkers, using noninvasive testing in 1279 CABG candidates, found that 262 (20.5%) had greater than 50% stenosis in at least one carotid artery and 23 (1.8%) had bilateral stenoses greater than 80%. Significant multivariable predictors of carotid disease were age, diabetes, female sex, left main CAD, prior stroke, peripheral vascular disease, and smoking.


The presence of carotid stenosis in patients referred for CABG has been shown to significantly increase the risk of postoperative stroke. Brener and colleagues studied 4047 cardiac surgical patients and found a 9.2% rate of stroke or transient ischemic attack in patients with asymptomatic carotid stenosis, significantly greater than the 1.3% rate in patients with no carotid stenosis. Faggioli and colleagues in 1990 reported that routine carotid noninvasive testing in CABG patients with no ischemic neurologic symptoms yielded an odds ratio for stroke of 9.9 with greater than 75% carotid stenosis. In patients older than 60 years with greater than 75% carotid stenosis, the stroke rate was 15%, versus 0.6% for patients of the same age with no carotid disease. Using routine carotid duplex scanning for cardiac surgical patients 65 years of age or older, Berens and colleagues found that the risk of stroke was 2.5% for carotid stenoses greater than 50%, 7.6% for carotid stenoses greater than 50%, 10.9% for carotid stenoses greater than 80%, and 10.9% for unilateral carotid artery occlusion. Thus, adequate evidence exists that significant carotid artery stenosis is an important incremental risk factor for the development of perioperative neurologic injury following CABG.

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Aug 25, 2016 | Posted by in CARDIOLOGY | Comments Off on Management of Concomitant Carotid and Coronary Arterial Disease

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