Dilatation of common carotid artery is strongly associated with cerebral ischemic stroke with or without the presence of carotid atherosclerosis
Background: Dilatation of common carotid artery (CCA) was related to age, sex, and body height in population studies. It was also considered a compensatory mechanism to carotid atherosclerotic stenosis. The present study examined the risk of CCA dilatation associated with ischemic stroke (IS) and its relations to carotid atherosclerosis, hypertension, hyperglycemia, fibrinogen, cholesterol, HDL-cholesterol (HDL-C), smoking, and alcohol consumption. Methods: A case-control study was carried on 251 first-ever IS patients (age≥40) excluding previous history of myocardial infarction and cancer and 242 non-stroke outpatients. Intraluminal diameter of middle portion of CCA, and plaque thickness in CCA, bulb, internal and external carotid arteries were measured. Information on hypertension and diabetes status and data of life-styles such as smoking and alcohol consumption were collected. Levels of fibrinogen, factor VIIIc, cholesterol, HDL-C and glucose were obtained. Results: CCA dilatation was a strong factor for IS (OR=4.13, P=0.0001). It was also associated with hypertension, hyperglycemia, smoking, alcohol consumption, low HDL-C, and high levels of fibrinogen, factor VIIIc, cholesterol, and plaque score. The association remained significant with or without each of the following conditions: hypertension (p=0.0001, p=0.0007), hyperglycemia (p=0.0446, p=0.0001), elevated fibrinogen (p=0.0104, p=0.0001) or factor VIIIc (p=0.2458, p=0.0001), hypercholesterolemia (p=0.0238, p=0.0001), decreased HDL-C (p=0.0012, p=0.0001) and presence of plaque score (p=0.0263, p=0.0003). Adjusting above risk factors, odds ratios of elevated diameter could associated with IS, before (OR=2.21, P=0.0066) and after (OR=6.63, p=0.0055) excluding subjects with plaque. Conclusion: Dilatation of CCA is a strong risk factor for IS. The fact the association remained significant without ultrasonic evidence of carotid plaque indicates that IS in Chinese involved a mechanism of active vasculopathy, not just a passive compensatory process to extracranial atherosclerosis.