Peroxisome Proliferator-Activated Receptor Gamma(PPAR-gamma) Agonist Improves Endothelial Function in Diabetic Patients with Metabolic Syndrome: Pivotal Role of NOx and Inflammation

BACKGROUND AND OBJECTIVES: Nitric oxide (NO) is thought to have antiatherosclerotic properties. On the other hand, NO activity is reduced in patients with metabolic syndrome, and endothelial dysfunction is an important early sign of atherosclerosis in patients with metabolic syndrome. The aim of this study was to investigate the effect of pioglitazone on the endothelial function in terms of the plasma NOx (combined nitrate/nitrite), the circulating inflammatory markers and the autonomic nervous system. SUBJECTS AND METHODS: We randomized 40 subjects with metabolic syndrome, and they were assigned to receive 15 mg of pioglitazone per day (the PIO group, n=21) during 12 weeks or they were placed in the placebo group (the PLA group, n=19). We estimate the endothelial function by performing vascular ultrasound. The plasma NOx levels, the levels of the inflammatory markers and the GRK2 levels were measured. RESULTS: After 12 weeks of therapy, flow mediated dilation (FMD) was improved in the PIO group (from 6.7+/-6% to 11.7+/-5%, respectively: p<0.05), but not in the PLA group. The level of plasma NOx was increased in the PIO group (from 67.7+/-30 nmol/dL to 92.9+/-41 nmol/dL, respectively: p<0.001), but not in the PLA group. The plasma levels of hsCRP and IL-6 dropped significantly (from 2.6+/-2.3 mg/L to 1.2+/-1.3 mg/L and 1.7+/-2.1 pg/mL to 0.7+/-0.5 pg/mL, respectively: p<0.05) in the PIO group, but not in the PLA group. The levels of GRK2 (the PLA group from 0.0061+/-0.0023 ng to 0.0075+/-0.0031 ng, and the PIO group from 0.0024+/-0.002 ng to 0.0015+/-0.001 ng, p=ns) didn't dropped significantly. CONCLUSION: Administration of PPAR-gamma agonist in patients suffering with metabolic syndrome improves their endothelial function, enhances the production of NOx and reduces the proinflammatory markers, but this is not related to sympathetic regulation. PPAR-gamma agonist may be able to modulate the progression of atherosclerosis.

A Case of Left Ventricular Pseudoaneurysm Extending to Lateral Side of Left Atrium after Myocardial Infarction

Left ventricular pseudoaneurysm is a rare but fatal complication of acute myocardial infarction. It occurs as a consequence of rupture of the ventricular free wall and is confined by a portion of pericardium. The pseudoaneurysm extended to lateral side of the left atrium is rare. We report a case of left ventricular pseudoaneurysm extended to lateral side of the left atrium in a 83-year-old man.

Carotid artery remodeling in patients with acute coronary syndrome and chronic stable angina / 대한내과학회지

BACKGROUND: Acute adaptive vascular remodeling occurs in active and unstable inflammatory plaques. It has been suggested that the adaptive coronary vascular remodeling, in patients with acute coronary syndrome (ACS), may be systemic and may show similar vascular remodeling in the carotid arteries. We investigated the ultrasonographic features of the common carotid artery (CCA) to determine whether the arterial expansive remodeling found in the coronary artery occurs in the carotid arteries of patients with ACS. METHODS: We measured lumen diameter (LD), interadventitial diameter (IAD) and intima media thickness (IMT) using a B-mode ultrasound in both common carotid arteries in patients with ACS (N=74) and chronic stable angina (CSA) (N=31). Positive remodeling was arbitrarily defined as an IMTmax >1 mm and IAD >8 mm and negative remodeling as an IMTmax >1 mm and IAD <7 mm. Other values were defined as "no remodeling" RESULTS: There were no significant differences in LD IAD and maximal IMT of the right CCA and the left CCA in comparisons between the ACS and the CSA patient groups. There were no differences for number of cases with no remodeling or differences in positive and negative remodeling in the right common carotid artery and left common carotid artery in comparisons between the ACS and CSA patient groups. . Presence of plaque in both common carotid arteries showed similar frequency in the ACS and CSA patient groups. The characteristics of carotid artery plaques were not different in the two groups. The remodeling index (IAD/LD) was correlated with IMTmax (right CCA r=0.797, p<0.001; left CCA r=0.860, p<0.001). CONCLUSIONS: The common carotid arterial structure of ACS patients was not different from that of CSA patients. Therefore, these results suggest that the expansive arterial remodeling, due to coronary inflammatory plaques, appears to take place locally rather than systemically.