Impact of Remnant Lipoprotein on Coronary Plaque Components.

AIM: Intravascular ultrasound (IVUS) is a useful modality for visualizing atherosclerotic lesions in coronary arteries, not only for the degree of arterial luminal stenosis but also for the plaque composition within the vessel walls. We aimed to determine the relationship between the clinical parameters and coronary plaque characteristics evaluated by IVUS in patients with stable angina under medical treatment. METHODS: Plaque measurements within the coronary arteries were collected by coronary angiography and iMAP-IVUS in 40 men with stable angina. The serum remnant-like cholesterol (RemL-C) was measured using homogeneous assays and serum adiponectin and omentin-1 levels were measured by enzyme-linked immunosorbent assays. RESULTS: The iMAP-IVUS analysis of the coronary arteries demonstrated that the plaque cross-sectional area (CSA) was 11.0±3.5 mm(2). Plaque CSA positively correlated with body mass index and negatively correlated with the serum adiponectin levels. Both areal and volumetric analyses of the plaque characteristics demonstrated that the serum RemL-C level was a positive determinant for %Necrosis and the negative determinant for %Fibrosis of the plaques. Neither serum high-density lipoprotein cholesterol nor low-density lipoprotein cholesterol levels correlated with the proportion of any plaque components. Additionally, the RemL-C/triglyceride ratio positively correlated with %Lipid significantly in the areal analysis. CONCLUSION: Elevation of the serum RemL-C levels in the patients with stable angina may link to coronary plaque vulnerability, which is characterized by high necrotic and low fibrotic components.

Abnormal regional left ventricular systolic and diastolic function in patients with coronary artery disease undergoing percutaneous coronary intervention: clinical significance of post-ischemic diastolic stunning.

OBJECTIVES: This study was designed to characterize both regional left ventricular (LV) systolic and diastolic function after percutaneous coronary intervention by using strain imaging (SI) derived from 2-dimensional speckle-tracking echocardiography. BACKGROUND: Ischemic insult after coronary occlusion affects not only regional LV systolic but also diastolic function. METHODS: Regional LV transverse peak strain and strain changes during the first one-third of diastole duration (strain imaging diastolic index [SI-DI]) were monitored in at-risk segments after percutaneous coronary intervention in 30 patients with coronary artery disease. The segments were divided into proximal and distal. Strain data in the at-risk segments were compared with values derived from remote nonischemic segments. RESULTS: Coronary occlusion induced a marked reduction in the systolic strain in both proximal and distal at-risk segments (from 36.9 +/- 6.0% to 12.0 +/- 3.9% and from 31.9 +/- 5.6% to 6.2 +/- 3.3%, respectively, p < 0.0001). Concomitantly, SI-DI values decreased (from 76.6 +/- 5.3% to -21.2 +/- 9.1% and from 72.5 +/- 5.9% to -48.7 +/- 20.8%, respectively, p < 0.0001). Upon reperfusion, systolic deformation parameters returned to near-normal pre-occlusion values. However, SI-DI values in the both proximal and distal at-risk segments decreased (43.2 +/- 9.5%, p < 0.01, and -17.3 +/- 11.1%, p < 0.0001, respectively) 30 min after reperfusion and were still lower (51.5 +/- 9.9%, p < 0.01) in the distal at-risk segment 24 h after reperfusion. CONCLUSIONS: SI analysis provides detailed mechanical characterization of regions with myocardial ischemic insult and can demonstrate post-ischemic diastolic stunning despite complete systolic functional recovery after reperfusion.

Human aquaporin adipose (AQPap) gene. Genomic structure, promoter analysis and functional mutation.

Aquaporin adipose (AQPap), which we identified from human adipose tissue, is a glycerol channel in adipocyte [Kishida et al. (2000) J. Biol. Chem. 275, 20896-20902]. In the current study, we determined the genomic structure of the human AQPap gene, and identified three AQPap-like genes that resembled (approximately 95%) AQPap, with little expression in human tissues. The AQPap promoter contained a putative peroxisome proliferator response element (PPRE) at -46 to -62, and a putative insulin response element (IRE) at -542/-536. Deletion of the PPRE abolished the pioglitazone-mediated induction of AQPap promoter activity in 3T3-L1 adipocytes. Deletion and single base pair substitution analysis of the IRE abolished the insulin-mediated suppression of the human AQPap gene. Analysis of AQPap sequence in human subjects revealed three missense mutations (R12C, V59L and G264V), and two silent mutations (A103A and G250G). The cRNA injection of the missense mutants into Xenopus oocytes revealed the absence of the activity to transport glycerol and water in the AQPap-G264V protein. In the subject homozygous for AQPap-G264V, exercise-induced increase in plasma glycerol was not observed in spite of the increased plasma noradrenaline. We suggest that AQPap is responsible for the increase of plasma glycerol during exercise in humans.