Aim: There is a strong relationship between carotid atherosclerosis and future cardiovascular disease (CVD). This study sought to clarify the association of fatty liver and an elevated serum gamma-glutamyl transpeptidase (GGT) level with carotid atherosclerosis. Methods: We reviewed the medical records of subjects who underwent medical checkups at our institute. Carotid atherosclerosis and fatty liver were assessed using ultrasound (US), and predictors of increased carotid intima-media thickness (IMT) and carotid plaque were identified using a logistic regression model. Results: In total, 958 subjects (564 men, 394 women; median age, 59 years) were enrolled. The median value of the mean carotid IMT was 0.713 mm, and the frequency of carotid plaque was 19.5%. For the highest quartile of the mean carotid IMT (≥ 0.863 mm), a male sex, older age, hypertension (HT), dyslipidemia (DL) and type 2 diabetes mellitus (DM) were identified as independent predictors. A male sex, older age, HT and elevated serum GGT level were found to be significant predictors of the presence of carotid plaque. In addition, fatty liver correlated with the existence of carotid plaque. When the combination of the serum GGT level and presence or absence of fatty liver was included as a variable in the analysis, a male sex, older age, HT and fatty liver with a serum GGT level of ≥ 83 IU/L (90th percentile) (odds ratio 3.21, 95% confidence interval 1.27-8.12, p 0.014) were identified to be significantly associated with carotid plaque. Conclusions: This study suggests that the simultaneous presence of an elevated serum GGT level and fatty liver is highly predictive of carotid plaque.

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eft ventricular hypertrophy (LVH) is a major hazardous cardiovascular complication in patients with hypertension. 1,2 The development of LVH depends not only on the renin-angiotensin system generating angiotensin II, 3 but also on the mechanical stress, which activates the protein kinase cascade of phosphorylation in cardiac myocytes. 4 The goal of antihypertensive therapy should be prevention and regression of LVH. It is reported that angiotensin converting enzyme (ACE) inhibitors are more effective than -blockers, calcium antagonists, and diuretics in reducing left ventricular mass (LVM). 5 We therefore assessed the clinical effect of delapril hydrochloride (an ACE inhibitor) 6 from the viewpoint of echocardiographically determined cardiac function and LVH, as well as the serum concentrations of procollagen type III aminoterminal peptide (PIIIP) as reflected in the production of collagen type III. Methods Patient SelectionFifteen hypertensive patients with LVH (10 men and 5 women, mean age 77.2±7.5 years) were entered in the study. Patients were previously untreated with hypertensive drugs or had discontinued the use of these drugs for at least 4 weeks prior. Patients with hyperglycemia, liver dysfunction or pulmonary fibrosis were excluded. The 2 criteria of LVH were an interventricular septal thickness (IVST) of more than 10 mm and left ventricular posterior wall thickness (LVPWT) of more than 10 mm as measured by echocardiography. All study patients complied with these criteria. Study ProtocolAll patients were treated with an ACE inhibitor (delapril hydrochloride, 30 mg/day po) for 12 months. To evaluate the clinical effect of delapril hydrochloride, blood pressure (BP) and heart rate were measured in a supine position before administration of delapril hydrochloride and then after 6 and 12 months of administration. Blood samples were obtained from each patient. Plasma renin activity (PRA) and concentrations of serum atrial natriuretic peptide (ANP) and serum PIIIP were measured by radioimmunoassay before administration and again after 6 and 12 months of taking the drug. The normal serum concentration of PIIIP, which was 0.40±0.13 U/ml (0.25-0.70 U/ml), was obtained from 24 normal volunteers (aged 20-80 years).Jpn Circ J 1998; 62: 900 -902 (Received June 30, 1998; revised manuscript received August 20, 1998; accepted August 21, 1998

Secretion of platelet granule constituents is closely associated with the phosphorylation of a cytosol polypeptide that we called P47 of Mr 47,000 (Imaoka, T. and Haslam, R.J., J. Biol. Chem. 258, 11404, 1983), by protein kinase C. Since the identity and function remains to be known, we purified protein kinase C, unphosphorylated and phosphorylated P47 to homogeneity from human platelets. Then precise phosphorylation reaction of P47 in vitro and a biological function of P47 were studied. Protein kinase C catalysed the phosphorylation reaction of P47 protein, platelet myosin light chain, histone III-S with Km of 0.8±0.2, 4.2±0.5, 4.7±0.7μM, and Vmax of 0.312, 0.189, 0.874 nmole/min/mg, respectively. Some data previously obtained in this laboratory and others utilizing histone III-S as substrate are consistent with the synergistic effect by diacylglycerol (DG) in the presence of Ca++ , phosphatidylserine (PS). Using P47 as substrate, the enzyme required both Ca++ and PS, but not DG for activity. 125I labelled unphosphorylated P47 had an ability to bind with platelet membrane fraction in the presense of phosphatidylserine. Effect of diacylglycerol was inhibitory in this PS dependent P47 binding with membrane. Unphosphorylated P47 had a inhibitory activity in platelet actin polymerization. Molar ratio to inhibit actin polymerization was 1:8(P47:actin). These activities were Ca++ independent. Purified 32P-labelled P47 lost the binding ability with membrane, also the inhibitory activity in actin polymerization.Therefore, we propose the hypothesis that unphosphorylated P47 may loosely bind with the inside of plasma membrane of platelet and inhibit actin polymerization as a modulator, when stimulated, protein Kinase C rapidly phosphorylate P47 and induce the activation of cytoskeletal network and subsequently release reaction. On the other hand, whether DG in fact can act as a second messenger remain uncertain, (supported by MESC of Japan)