Carotid Artery Angioplasty and Stent Placement: Quality Improvement Guidelines to Ensure Stroke Risk Reduction

Abstract

CERVICAL carotid atherosclerotic stenosis has been correctly surmised to be a potentially preventable cause of stroke for a half-century. For most of this time, neither the absolute risk of the condition nor the specific contributing factors were known. Not surprisingly, therefore, medical therapy was poorly understood and offered a limited armamentarium. Prior dogma maintained that medical therapy alone neither significantly affected the progression of atherosclerosis nor caused its regression. Today an extensive body of literature confirms that cervical carotid artery atherosclerosis is common, relatively easy to evaluate, a major health threat, and surgically correctable. The appropriateness of carotid endarterectomy (CEA) has been evaluated by at least seven randomized trials, and further study is warranted and ongoing. While great strides have been made in the last decade in understanding cervical carotid atherosclerotic stenosis, there are still many important unknowns concerning the clinicopathologic condition, its various manifestations, precipitating biochemical and pathophysiologic events, specific patient risk characteristics, optimal medical therapy, as well as indications for, and best methods of, surgical and interventional therapies. Perhaps one of the best examples of the evolutionary nature of knowledge in this field is the relatively new concept that the principal culpability for clinical neurologic events is not the “degree-of-stenosis” per se, but rather the pathology of the plaque and the ischemia produced by atherothrombotic emboli. This belief is universally accepted in the cardiovascular community but seems to be under-appreciated in the neuroscience community. The ultimate confirmation of this concept is the 10-fold or greater difference in risk for someone with an 80% “nonembologenic” (ie, “asymptomatic”) carotid stenosis as compared to an 80% “embologenic” (symptomatic) stenosis. For the former there is about 1% to 2% per year stroke risk from the lesion itself as compared to the latter, which has about 10% to 20% risk of stroke in the first year (1,2). Further, recent studies of newer pharmacologic agents including antiplatelet agents (such as clopidogrel) and plaque-stabilizing agents (such as HMGCoA-reductase inhibitors [“statins”] and angiotensin converting enzyme [“ACE”] inhibitors) do indeed demonstrate that the natural history of atherosclerotic plaques can be positively influenced in a way that changes the risk/benefit ratio of all therapies for not only coronary atherosclerosis but also for carotid atherosclerosis (3,4). However, none of these new medical therapies have been systematically compared to CEA or carotid artery stent placement (CAS) in controlled clinical trials aimed at evaluating the best method to reduce stroke and stroke-related morbidity and mortality. In March 2000, the American Society of Interventional and Therapeutic Neuroradiology (ASITN), the specialty organization then composed primarily of neuroradiologists and neurosurgeons most involved with cervico-cerebral angiography and cervical and intracranial endovascular intervention, published a review and analysis of the current literature on carotid atherosclerosis and its treatment (5). Since that time, continued progress has been made in further understanding the nature of carotid atherosclerosis, improving surgical techniques, advancing the pharmaceutical armamentarium, and refining a potential endovascular therapy: carotid artery angioplasty and stent placement. Three medical societies that include training in cervico-cerebral angiography as part of their ACGME defined residency programs, the ASITN, the American Society of Neuroradiology (ASNR), and the Society of Interventional Radiology (SIR), recognize the importance of carotid atherosclerosis and its appropriate management. In this issue of the Journal of Vascular and This article also appears in J Vasc Interv Radiol 2003; 14:1095–1097. From the Miami Cardiac and Vascular Institute, Miami, FL (J.J.C., G.J.B.), Department of Radiology, Reading Hospital and Medical Center, Reading PA (D.S.), and Mid-South Imaging and Therapeutics, Memphis, TN (J.D.B.). Received July 3, 2003; accepted August 6. Address correspondence to J.J.C., MCVI, 8900 Kendall Dr, Miami, FL 33176. E-mail budmancon@aol.com