Relationship between carotid disease on ultrasound and coronary disease on CT angiography.

OBJECTIVES: The purpose of this study was to assess the relationship between carotid artery disease by ultrasound and coronary artery disease by coronary computed tomography angiography (CTA) and to identify carotid ultrasound parameters predictive of coronary artery disease. BACKGROUND: Carotid ultrasound and CTA are noninvasive modalities used to image atherosclerosis. Studies examining the relationship between the 2 tests, however, are lacking. METHODS: We performed carotid ultrasound on predominantly nondiabetic subjects referred for CTA. Carotid intima media thickness (IMT) and plaque were assessed and compared with coronary artery calcification and the number of coronary arteries with any evidence of atherosclerosis on CTA. RESULTS: A total of 150 subjects underwent both CTA and carotid ultrasound on the same day. Carotid plaque was present in 71.3% (n = 107), whereas the presence of at least 1 coronary artery with disease on CTA was present in 57.1% (n = 84). Carotid plaque was present in 47.6% (30 of 63) of subjects with a calcium score of 0 and 88.5% (77 of 87) of subjects with a calcium score >0 (p = 0.0001). Similarly carotid plaque was present in 52.4% (33 of 63) of subjects with no CTA evidence of atherosclerosis versus 85.7% (72 of 84) of subjects with any CTA evidence of atherosclerosis (p < 0.0001). Carotid plaque, IMT ≥ 1.5 mm, or averaged mean IMT >0.75 mm were associated with a calcium score >0 (odds ratio: 5.4, p < 0.0001, 2.7, p < 0.001; 2.9, p = 0.011, respectively) and disease in at least 1 vessel on CTA (odds ratio: 2.8, p = 0.03, 2.19, p = 0.073; 2.22, p = 0.058, respectively) independent of age and sex. CONCLUSIONS: Carotid plaque and increased carotid IMT are associated with the presence and severity of coronary calcification and disease on CTA in ambulatory subjects.

The critical role of the intrinsic VSMC proliferation and death programs in injury-induced neointimal hyperplasia.

Postangioplasty and in-stent restenosis remain ominous problems in percutaneous coronary intervention where good animal models of restenosis proneness and resistance are needed. We accidentally discovered that the carotid arteries (CAs) of the Harlan and Sasco substrains of Sprague-Dawley rats display drastically different restenosis phenotypes following balloon-induced endothelial denudation. When subjected to balloon injury, Sasco CAs exhibited significantly larger neointimal mass than did Harlan CAs at both days 14 and 32, as evidenced by a higher intima-to-media ratio and a greater number of intimal cells in Sasco CAs. This was due to a greater cell proliferation and to a less vigorous apoptosis of Sasco neointima, as assessed by 5-bromo-2'-deoxyuridine and terminal deoxynucleotidyl transferase-deoxyuridine nick-end labeling staining, respectively. At a cellular level, whereas vascular smooth muscle cells (VSMCs) isolated from Sasco and Harlan CAs were identical in morphology and in propensity to migrate, Sasco VSMCs proliferated more robustly and died far less, suggesting that under the exact same microenvironment, Sasco and Harlan VSMCs respond to growth and noxious stimuli in a drastically different fashion and that Sasco's significantly more robust neointimal proliferation after vascular injury in vivo can be accounted for by these intrinsic differences in VSMCs of these substrains in vitro. Sasco and Harlan Sprague-Dawley rats as well as VSMCs from these rats will prove to be powerful tools to study genes involved in the pathogenesis of restenosis.