Systemic Sclerosis

Systemic sclerosis (SSc) is a generalized connective tissue disorder characterized by fibrosis of the skin and internal organs and widespread vascular lesions. The pathogenesis of the vasculopathy is not fully understood, but a viral trigger, immune reactions to viral or environmental factors, reperfusion injury, or anti-endothelial antibodies may all be involved [1]. Also, angiogenesis is insufficient or defective [2, 3]. Most attention has been given to microvascular disease in SSc, but previous studies have suggested an increased prevalence of macrovascular disease as well [4, 5]. The development of accelerated atherosclerosis in SSc is less clear, however, an increase in carotid IMT in SSc patients has been reported [6, 7], clinically there is also little evidence for increased macrovascular complications such as stroke and myocardial infarction in SSc patients [4]. Carotid intima-media thickness (IMT) as measured by high-resolution ultrasound is a well-validated marker of subclinical atherosclerosis [8]. The study of the IMT in other rheumatic diseases on Egyptian patients showed subclinical atherosclerosis in rheumatoid arthritis [9], systemic lupus erythematosus [10], and primary osteoarthritis [11].
Earlier studies have indicated that ultrasound-detected carotid atherosclerotic lesions are associated with ischemic stroke [12, 13] and can help estimate the risk of ischemic stroke [14-16] Accordingly, both the Japanese Society of Hypertension Guidelines for the Management of Hypertension and the European Society of Hypertension/European Society of Cardiology 2003 Guidelines for the Management of Arterial Hypertension have added increased IMT and carotid artery plaques as risk factors for stroke [17,