S. J. Lin

Plasma matrix metalloproteinase-3 level is an independent prognostic factor in stable coronary artery disease

Backgroundu2002 Recent evidence suggests the important role of matrix metalloproteinases (MMPs) in the progression of atherosclerosis and development of clinical events. We assessed the prognostic value of different plasma MMPs in patients with stable coronary artery disease (CAD).

Hemoglobin A1c and Fructosamine for Assessing Glycemic Control in Diabetic Patients With CKD Stages 3 and 4

BACKGROUNDnHemoglobin A(1c) (HbA(1c)) and fructosamine can be used to monitor glycemic control in diabetic patients with normal kidney function, but their validity in patients with chronic kidney disease (CKD) has not been evaluated. In this study, we evaluated the correlation and accuracy of these 2 measures of glycemic control in type 2 diabetic patients with CKD stages 3-4.nnnSTUDY DESIGNnDiagnostic test study.nnnSETTING & PARTICIPANTSnType 2 diabetic patients with normal (n = 30) and abnormal kidney function (n = 30) were recruited in Taipei Veterans General Hospital, Taiwan.nnnINDEX TESTSnHbA(1c) and fructosamine.nnnREFERENCE TESTnSelf-monitoring of blood glucose levels.nnnMEASUREMENTSnBlood glucose measurements consisted of 6 preprandial, 6 postprandial, and 2 bedtime assessments in a week with a cycle of 4-week intervals for 12 weeks.nnnRESULTSnCorrelation coefficients between HbA(1c) level or fructosamine-albumin ratio and mean blood glucose levels were 0.836 and 0.645 in participants with normal kidney function and 0.813 and 0.649 in participants with CKD stages 3-4, respectively. In patients with CKD stages 3-4, mean blood glucose levels in weeks 1-12 were 21.9 mg/dL (95% CI, 11.6-32.5) higher than estimated average glucose (eAG) levels calculated from HbA(1c) levels in participants with normal kidney function. In patients with CKD stages 3-4, mean blood glucose levels in weeks 10-12 were 15.5 mg/dL (95% CI, 5.2-30.5) higher than eAG levels calculated from fructosamine levels in participants with normal kidney function, but without statistical significance when eAG calculated from fructosamine level was corrected for serum albumin level (difference of 5.6 mg/dL; 95% CI, -8.6 to 19.8).nnnLIMITATIONSnRelatively small number of participants with limited amount of blood glucose measurement data.nnnCONCLUSIONnOur data show that eAG calculated from HbA(1c) and fructosamine levels might underestimate mean blood glucose levels in patients with CKD stages 3-4. References ranges may need to be modified when interpreting results of measurements of glycemic control in type 2 diabetic patients with CKD.

Vascular stiffness in familial hypercholesterolaemia is associated with C-reactive protein and cholesterol burden

Backgroundu2002 Familial hypercholesterolaemia (FH) is characterized by very high serum cholesterol and premature coronary atherosclerosis. Arterial stiffness and atherosclerosis are two major underlying pathophysiologies of arterial disease that are predictive of future cardiovascular events. The aims of this study were to quantify atherosclerosis and arterial stiffness and to evaluate their relationship with high sensitive C‐reactive protein (hs‐CRP) and the level of exposure to high serum cholesterol in FH patients.

Effects of simvastatin withdrawal on serum matrix metalloproteinases in hypercholesterolaemic patients

Backgroundu2002 Serum matrix metalloproteinase (MMP) levels have been related to clinical outcomes in patients with coronary artery disease. Though statin treatment might reduce serum MMPs the change of levels after statin withdrawal remains obscure.

Identification and characterization of novel low-density lipoprotein receptor mutations of familial hypercholesterolaemia patients in Taiwan.

Backgroundu2002 Familial hypercholesterolaemia (FH) is an autosomal dominant disease associated with a very high risk of coronary vascular disease. The study objective was to identify patients with FH in Taiwan and characterize novel mutations.

Anti-inflammatory strategies for homocysteine-related cardiovascular disease.

Homocysteine may induce vascular damage for atherosclerosis. Vitamin/folate supplementation has been proposed to reduce the cardiovascular disease risk. Nevertheless, there is no randomized clinical trial clearly proving the efficacy of reducing the homocysteine as a means of lowering the incidence of cardiovascular disease. Homocysteine induces oxidative stress leading to endothelial dysfunction. In addition, homocysteine-induced oxidative stress favors lipid peroxidation and induces production of inflammatory factors, thus accelerating atherosclerosis. In this paper, we reviewed the available evidence concerning the association between homocysteine and cardiovascular disease, with the objective of discussing the pertinence of screening, treatment, and prevention of hyperhomocysteinemia-related cardiovascular disease. Our previous findings also indicated the significant role of mononuclear cells activation in homocysteine-induced endothelial dysfunction; treatment with statins attenuated homocysteine-induced endothelial adhesiveness, indicating the novel endothelial protection effects of statins in the presence of homocysteine. Since inflammation and oxidative stress are critical to homocysteine-induced vascular damage, the improvement of endothelial dysfunction and the inhibition of mononuclear cell activation by anti-inflammatory and/or antioxidative drugs/agents may serve as the potential therapeutic strategy for hyperhomocysteinemia-related cardiovascular disease.

Fenofibrate attenuates endothelial monocyte adhesion in chronic heart failure: an in vitro study

Backgroundu2002 Inflammation is implicated in chronic heart failure (CHF). In this study, the potential inhibitory effect of peroxisome proliferator‐activated receptor‐α (PPARα) activator fenofibrate on monocyte adhesion in CHF patients was investigated in vitro.

Interaction between glycaemic control and serum insulin-like growth factor 1 on the risk of retinopathy in type 2 diabetes.

Eur J Clin Invest 2012; 42 (4): 447–454