Relation of QT-interval variability to ventricular arrhythmias during percutaneous transluminal coronary angioplasty.

The present study investigated the role of the dispersion of QT interval in percutaneous transluminal coronary angioplasty (PTCA)-induced ventricular tachyarrhythmias. Patients with effort angina without a previous myocardial infarction (n = 22), who had single-vessel disease of the anterior descending coronary artery (LAD), underwent PTCA if the coronary lesion was 75% or more stenosed in segment 6 or 7 of the LAD. The standard 12-lead ECG was continuously recorded during the procedure. Averaged QTc and QTac intervals, where QTac was the interval from the beginning of QRS complex to the nadir of T wave corrected by Bazett's formula, did not change significantly during PTCA. Of the 22 patients, 7 showed ventricular arrhythmias during PTCA. The maximum difference (deltaQTc) and the standard deviation (QTcSD) of the corrected QT interval in the standard 12-lead ECG increased significantly during PTCA in the 7 patients with ventricular arrhythmias, whereas they decrreased in the 15 patients without ventricular arrhythmias. deltaQTac and QTacSD were not affected by PTCA regardless of ventricular arrhythmias, which shows that the increases in the variation of the ventricular repolarization process play a role in PTCA-induced ventricular arrhythmias.

Morphologic correlation between atherosclerotic lesions of the carotid and coronary arteries in patients with angina pectoris.

The morphology of atherosclerosis between the carotid and coronary artery systems was studied in 63 patients with ischemic heart disease to determine if there was a correlation with coronary heart disease. The sclerotic lesions of the carotid and coronary artery systems were imaged with ultrasonography and coronary arteriography, respectively, and divided into 4 types. Hemodynamic variables, serum lipid levels, and serum uric acid concentration were not different among the groups, but the serum C-reactive protein (CRP) concentration in patients without significant atheroma in the carotid artery system was lower than the mean concentration of the other 3 groups with carotid atheroma. The morphological stability of carotid arterial plaques correlated well to coronary artery stenosis. Morphologically unstable plaques of the carotid artery predicted unstable forms of coronary obstruction with a sensitivity of 68%, specificity of 85%, predictive power of 72% and a likelihood ratio of 4.5. These results suggest that ultrasonic examination of the carotid artery is useful for predicting the presence or absence of unstable lesions in coronary arteries.

Soluble CD14-dependent intercellular adhesion molecular-1 induction by Porphyromonas gingivalis lipopolysaccharide in human gingival fibroblasts.

BACKGROUND: Intercellular adhesion molecule-1 (ICAM-1) is involved in the accumulation and activation of leukocytes in inflammatory sites through binding to beta2 integrins expressed on leukocytes. We investigated whether or not lipopolysaccharide (LPS) derived from the periodontopathic bacterium Porphyromonas gingiualis affects ICAM-1 expression on human gingival fibroblasts (HGF). CD14 is a receptor for LPS on monocytes and macrophages and is also present in serum as a soluble protein. We further examined the effects of serum and soluble CD14 (sCD14) on ICAM-1 expression in HGF stimulated with P. gingivalis LPS. METHODS: HGF were prepared from explants of human gingival tissues and incubated in 96-well culture plates before LPS stimulation. LPS derived from Escherichia coli O55:B5 and P. gingivalis ATCC 33277 LPS were employed. sCD14 was purified from normal human serum (NHS) by affinity chromatography using an anti-CD14 monoclonal antibody. ICAM-1 expression on HGF was measured by a cell enzyme-linked immunosorbent assay. RESULTS: P. gingivalis LPS induced ICAM-1 on HGF in a dose-dependent manner in the presence of either 10% fetal calf serum or 2% NHS. The ability of P. gingivalis LPS to induce ICAM-1 was comparable to that of LPS from E. coli at high LPS concentrations. In the absence of NHS, ICAM-1 induction was negligible in HGF stimulated with P. gingivalis LPS, reaching a maximum at 2% NHS. The ICAM-1 expression induced by P. gingivalis LPS was inhibited by a monoclonal antibody to CD14. Supplementation of serum-free medium with sCD14 alone restored the capacity of HGF to respond to P. gingivalis LPS. CONCLUSIONS: These results indicate that P. gingivalis LPS induces ICAM-1 expression in HGF in an sCD14-dependent manner. The overexpression of ICAM-1 on fibroblasts in gingiva induced by P. gingivalis LPS seems to be involved in the retention of inflammatory cells in periodontitis lesions.

Increased levels of soluble CD14 in sera of periodontitis patients.

Soluble CD14 (sCD14) mediates the response to lipopolysaccharide (LPS) in cells lacking membrane-bound CD14. We determined sCD14 concentrations in the sera of 38 periodontitis patients and 25 healthy controls by enzyme-linked immunosorbent assay. The sCD14 levels in the sera of patients with periodontitis were significantly higher than those of healthy subjects and decreased after treatment. Enhanced levels of sCD14 in serum may contribute to the host response to LPS in periodontitis. Furthermore, we showed in vitro that addition of LPS enhanced the release of sCD14 by monoblastic U937 cells treated with 1alpha,25-dihydroxyvitamin D3. Thus, increased sCD14 levels in periodontitis patients may be due to chronic exposure to LPS.

Soluble CD14 mediates lipopolysaccharide-induced intercellular adhesion molecule 1 expression in cultured human gingival fibroblasts.

Intercellular adhesion molecule 1 (ICAM-1) is involved in the accumulation and activation of leukocytes in inflammatory diseases such as periodontitis. As reported previously, ICAM-1 is up-regulated on cultured human gingival fibroblasts (HGF) by exposure to lipopolysaccharide (LPS), suggesting a specific LPS recognition mechanism. We therefore investigated the role of CD14, an LPS receptor, in stimulation of HGF by LPS. Cell surface CD14 antigen was not observed on HGF by flow cytometric analysis. In addition, expression of CD14 mRNA in HGF was not detected by reverse transcription-PCR analysis. Since HGF did not express endogenous CD14, we investigated the role of human serum-derived soluble CD14 (sCD14) in ICAM-1 induction on HGF by LPS. The serum-dependent ICAM-1 induction by LPS was observed in HGF. In medium containing human serum, anti-CD14 antibody inhibited ICAM-1 induction on HGF by LPS. Depletion of sCD14 from human serum markedly reduced ICAM-1 expression on HGF in response to LPS. Supplementation of the serum-free medium with sCD14 alone restored the capacity of HGF to respond to LPS. These results show that induction of ICAM-1 in HGF by LPS does not involve binding to cell surface CD14 but is mediated by serum-derived sCD14.