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Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
Online ISSN 1827-1839
Irace C., Pujia A., Motti C. *, Massimo F., Gnasso A.
From the University of Catanzaro, Department of Clinical and Experimental Medicine, Atherosclerosis Centre, Catanzaro, Italy
* Department of Internal Medicine, “Tor Vergata” University, Rome, Italy
Objective. To evaluate the presence of carotid plaque and/or stenosis in patients with different phenotype of hyperlipidaemia.
Experimental design. Case-control study.
Setting. Outpatients metabolic clinic.
Patients. Sixty type IIa, 50 type IIb and 40 type IV hyperlipidaemic subjects were compared with 50 normolipidaemic controls, matched for sex and age.
Interventions. Blood lipid analysis for phenotype classification was performed after two months of diet. Blood pressure was measured by a zero-random sphygmomanometer. CHD risk factors, smoking habit, previous and ongoing drug therapy were assessed by a self-administered questionnaire. Echo-Doppler examination of the extracranial arteries (common, internal and external carotid artery and bulb) was done by a Multigon Angioview 600 provided with a 7.5 MHz probe for B-mode and 5 MHz for pulsed Doppler. Subjects were classified as having carotid atherosclerosis when a plaque and/or a stenosis was found in at least one of the examined segments and as normal when no atherosclerotic lesions were detected.
Results. There were more hypertensives among type IV subjects whereas the prevalence of smokers and diabetics was similar in all four groups. The prevalence of carotid atherosclerosis was higher in type IIb and IIa subjects than in controls (58% and 38% respectively vs 14%, p<0.01) while in type IV subjects it was comparable to that of controls (25%).
Conclusions. The present findings show that hypercholesterolaemia and mixed hyperlipidaemia are frequently associated with carotid atherosclerosis, whereas hypertriglyceridaemia is not. The role of hypertriglyceridaemia in the development of atherosclerosis seems mediated by mechanisms other than plaque formation.