Predisposing Factors for Postoperative Stroke in CABG Patients
Given the common pathogenesis of atherosclerotic coronary and carotid diseases, increasing attention has been paid by cardiovascular surgeons for detection, evaluation and treatment of carotid artery stenosis in patients undergoing Coronary Artery Bypass Graft (CABG). Coronary artery bypass is a frequent surgery with a global scope; it has been proven that the presence of carotid artery stenosis in these patients increases the risk of ischemic stroke before surgery resulting in reduced quality of life and increased mortality, as well as disability of patients and increased costs and hospitalization. In fact, preoperative strokes account for about 3% of the CABG complications. Given that cardiac surgery patients with carotid artery stenosis are at high risk for surgery-associated neurological events , therefore, the key points in facing with these patients are introduced in this pilot study, to help treat them better and with a proper prognosis. Atherosclerosis Atherosclerosis is an epidemic in most developed countries, with a less prevalence in Central and South America, Africa and Asia. Premenopausal women compared with same age men are at lower risk for atherosclerosis, but the incidence becomes equal in men and women in postmenopausal women(1). In industrialized countries, atherosclerosis often begins in the first few decades of life. So that one out of every 6 suddenly died American adolescents aged 13-19 has pathological evidence of atherosclerotic coronary arteries. Accumulation of lipoproteins, endothelial damage and inflammation are of numerous processes that contribute to the initiation and progression of atherosclerosis (2). The pathogenesis of atherosclerosis In the early stages of atherosclerosis, small particles of lipoproteins penetrate the vascular endothelium; they are oxidized there and accumulate in the tunica intima. This process is accelerated at the site of endothelial damage. The damage may arise from hypertension, hypercholesterolemia, smoking, or excessive shear forces (tangential). Lipid accumulation in the tunica intima leads to the expression of adhesion molecules on the luminal surface of endothelial cells and thereby allows them to attach the circulating monocytes ( e.g. , macrophages)(3-6). The monocytes swallow lipoproteins and changes to fat-accumulated monocytes or foam cells. Accumulation of these foam cells is the first visible evidence of atherosclerosis. Foam cells multiply and lead to continuation of local inflammation and thus degradation of endothelium through releasing proinflammatory mediators. Accumulation of fat in foam cells results in their necrosis, but fat remains at the center of the plaque. Macrophages and mast cells release enzymes such as metalloproteinases (such as collagenase and gelatinase) which degrade collagen and the proteins of extracellular matrix adjacent to the plaque. While, T cells inhibit collagen formation by vascular smooth muscle cells through secreting cytokines ( e.g. , interferon alpha)(7-8). Increased degradation and reduced formation of collagen predispose the plaque to corrosion and tear. Activated platelets also release some substances (such as thromboxane, serotonin) which stimulate vasoconstriction and expansion of thrombus. When the extent of platelet aggregation and thrombus formation in sufficient to halt blood flow (either partial or full), an acute coronary event occurs (such as unstable angina, non-ST elevation myocardial infarction [NSTEMI] or ST elevation myocardial infarction [STEMI]) (9-10). Risk factors for atherosclerosis Several risk factors have been identified for development of atherosclerosis. Unrecoverable risk factors include older age, male gender, and family history of premature atherosclerosis. Other modifiable risk factors and their treatment may reduce the risk of atherosclerosis. These factors include hyperlipidemia, hypertension, diabetes mellitus, metabolic syndrome, smoking, obesity, sedentary lifestyle, and excessive alcohol consumption. As a marker of inflammation, CRP may increase the risk of plaque rupture or contribute to clot formation. Increased serum levels of CPR, if measured by very sensitive methods, is strongly associated with risk of MI, stroke, peripheral arterial disease, and sudden death. Coronary artery calcification is also a typical manifestation of coronary atherosclerosis and is associated with the presence and severity of CAD (11). Carotid Artery The common carotid artery originates from the brachiocephalic artery at right and the aortic arch at left. The artery is divided into internal and external carotid arteries at the upper rim of the thyroid cartilage. The external carotid artery supplies the structures in neck, face, skull, tongue and cheeks. The internal carotid artery supplies the brain, eyes, forehead, and a part of the nose (11-12). Carotid Artery Stenosis Approximately 730 thousand strokes occur in the United States per year, which impose a cost of more than $ 40 million. Half of these strokes are the consequence of carotid artery atherosclerosis (3). The signs depend on the brain area involved. Many patients are asymptomatic and stenosis may be detected during an examination. The disease may present itself as loss of vision, weakness and tingling in the extremities, muffled speech, inability to articulate words, or eventually coma. In such situations, an emergency consultation with a physician is essential to avoid a real stroke. History of cerebrovascular accident, hypertension, smoking, diabetes, obesity, high cholesterol (especially LDL), age over 60, female gender, and severe coronary artery disease are the most common risk factors associated with the occurrence of carotid artery stenosis (4, 5). As mentioned, carotid artery stenosis has been highly reported in females (12) as well as in patients with rheumatoid arthritis compared with patients without rheumatoid arthritis, because cardiovascular mortality and morbidity increase in rheumatoid arthritis (13). This disease is treated based on being symptomatic or asymptomatic and may include the followings: 1. Medical procedures or medications 2. Endarterectomy: surgical removal of plaque from the vessel 3. Repair with open surgery 4. Endovascular procedures: insertion of a vascular stent (4).