Serum cystatin C is associated with early stage coronary atherosclerotic plaque morphology on multidetector computed tomography.

OBJECTIVE: Cystatin C, a novel marker of kidney function, has been reported to be a predictor of adverse cardiovascular outcomes in patients without established chronic kidney disease. However, the relationship between serum cystatin C concentrations and early stage coronary atherosclerotic plaque morphology among patients with preserved kidney function has not been fully evaluated. METHODS AND RESULTS: 405 outpatients with early coronary artery disease with estimated glomerular filtration rate (eGFR) ≥ 60ml/min/1.73m(2) and <50% stenosis on 64-slice CT coronary angiography were enrolled. Subjects were categorized into quartiles by serum cystatin C (quartile I: ≤ 0.88mg/L - quartile IV: ≥ 1.16mg/L). Plaques in coronary segments were categorized as calcified or noncalcified. Multiple linear regression analysis revealed that lower eGFR, higher age, increasing numbers of noncalcified and calcified plaques, lower high-density lipoprotein cholesterol, and female gender were statistically significant predictors of increased cystatin C concentrations. The risk for presence of noncalcified plaques increased significantly with increasing quartiles of cystatin C. Compared with those in the lowest quartile, patients in each subsequent quartile were at steadily increased risk of having noncalcified plaque (quartile IV: OR 5.6; 95% CI 2.3-13.9, p-value <0.001). Both number of segments with calcified plaque and Agatston score were highly correlated with cystatin C concentrations (both p<0.001), but when adjusted for segments with noncalcified plaque and other risk factors, calcified plaque segments were no longer independently predictive. CONCLUSION: Higher serum cystatin C concentrations were correlated with early stage coronary atherosclerotic plaques among patients without established chronic kidney dysfunction. Noncalcified plaques increased with serum cystatin C concentrations, an association independent of eGFR and other cardiovascular risk factors.

Idiopathic pulmonary vein thrombosis complicated with old myocardial infarction detected by multidetector row computed tomography.

Pulmonary vein thrombosis is rarely detected in patients with cancer, lung lobectomy, trauma and so on. We report the case of idiopathic pulmonary vein thrombosis complicated with coronary heart disease. A-57-year-old man with suspected coronary heart disease underwent computed tomography coronary angiography. He did not show any sign of malignancy in lung or other organs. Multi-detector row computed tomography demonstrated 3-dimensional images for the thrombi in bilateral lower pulmonary veins besides an old anterior myocardial infarction. Previously, few reports have described the detection of pulmonary vein thrombosis, however, multi-detector row computed tomography was thought to be useful for detecting and evaluating pulmonary vein thrombosis.

Periodontal ligament cells under mechanical stress induce osteoclastogenesis by receptor activator of nuclear factor kappaB ligand up-regulation via prostaglandin E2 synthesis.

Previously, we discovered that periodontal ligament (PDL) cells not only support osteoclastogenesis through cell-to-cell contact, but also inhibit the formation of tartrate-resistant acid phosphatase-positive (TRAP+) multinucleated cells by a producing soluble factor(s). Furthermore, PDL cells express both receptor activator of nuclear factor kappaB ligand (RANKL) and osteoprotegerin (OPG) messenger RNA (mRNA). Clinically, "ankylosed teeth," which lack periodontal ligament, cannot be moved with orthodontic tooth treatment. From this, we hypothesized that PDL cells under mechanical stress should play a pivotal role in osteoclast formation during orthodontic tooth movement. This study examined how mechanical stress affects the osteoclastogenesis-supporting activity of PDL cells. PDL cells were compressed continuously and then cocultured with peripheral blood mononuclear cells (PBMCs) for 4 weeks. PDL cells under mechanical stress up-regulated osteoclastogenesis from PBMCs. Furthermore, the expression of RANKL mRNA and protein in PDL cells increased with compressive force in parallel with the change in the number of osteoclasts. In addition, cyclo-oxygenase 2 (COX-2) mRNA expression was induced by compressive force, and indomethacin inhibited the RANKL up-regulation resulting from compressive force. PDL cells under compressive force exhibited significantly increased prostaglandin E2 (PGE2) production in comparison with control PDL cells. Exogenous PGE2 treatment increased RANKL mRNA expression in PDL cells. Interestingly, OPG expression remained constant throughout compressive force or PGE2 treatment. In conclusion, compressive force up-regulated RANKL expression in PDL cells. Furthermore, RANKL up-regulation in mechanically stressed PDL cells was dependent on PGE2.