Total salivary MMP-8 assessed by immunofluorometric assay method and immunoblot densitometric units was higher in non-AMI than in AMI patients' saliva, but a significantly higher percentage of AMI patients' MMP-8 was activated polymorphonuclear leukocyte (PMN) type (P <0.001) regardless of periodontal diagnosis.Serum MMP-8, MMP-9, and TIMP-1 levels were significantly higher in AMI (for all markers and all comparisons,P <0.05). Characteristic for AMI was dominance of active PMN MMP-8 in saliva [corrected].
Background: The aim of the present study was to investigate whether chronic periodontitis caused the elevated levels of anti‐cardiolipin antibodies (anti‐CL) and oxidized low‐density lipoprotein (oxLDL) in subjects with essential hypertension.
Methods: Seventy‐two subjects were categorized as healthy controls, subjects with essential hypertension and periodontal health (healthy‐hypertension group), subjects with essential hypertension and gingivitis (gingivitis‐hypertension group), or subjects with essential hypertension and chronic periodontitis (periodontitis‐hypertension group). Individuals with essential hypertension who had been taking antihypertensive medication ≥2 years were included in the present study. The presence of supragingival plaque, bleeding on probing (BOP), probing depth (PD), and clinical attachment level were recorded, and blood samples were collected. Serum immunoglobulin M (IgM) and immunoglobulin G (IgG) anti‐CL and oxLDL levels were assessed by enzyme‐linked immunosorbent assay. For IgM and IgG anti‐CL assays, positive tests were defined as ≥15 IgM phospholipid units and ≥10 IgG phospholipid units, respectively.
Results: The mean IgM anti‐CL level and the prevalence of subjects positive for IgM anti‐CL were significantly higher in the periodontitis‐hypertension group compared to the other groups (P = 0.001). No significant differences were observed in the mean IgG anti‐CL and oxLDL levels or in the number of subjects positive for IgG anti‐CL and positive for IgM or IgG anti‐CL among the study groups. The Pearson correlation analysis revealed positive correlations between IgM anti‐CL levels and supragingival plaque, BOP, and PD scores.
Conclusions: Chronic periodontitis might play a causal role in the elevated serum levels of anti‐CL antibodies in individuals with essential hypertension. These elevated anti‐CL levels that are due to chronic periodontitis might contribute to an increased risk for atherosclerosis in individuals with essential hypertension.
Objective: There is conflicting data about the role of renin-angiotensin-aldosterone system (RAAS) blockers in contrast-induced nephropathy (CIN) pathophysiology. In this study, we aimed to investigate the effects of chronic usage of RAAS blocker drugs on development of CIN in low risk patients. Methods: Study was designed as a prospective cohort study. A total of 295 patients were enrolled in the study. Study population was consisted of three subgroups according to prior usage of RAAS blockers: no RAAS blocker group (n=95), angiotensin-converting enzyme inhibitor (ACEI) group (n=106), angiotensin receptor blocker (ARB) group (n=94). CIN was defined as an increase of ≥25% in creatinine over the baseline value or 0.5 mg/dL rise within 48-72 h of angiography. Mehran score was calculated for each patient. Baseline variables and percentage of CIN were compared with ANOVA, Mann-Whitney U, Kruskal-Wallis and Pearson Chi-square tests between groups. In order to determine the independent predictors of CIN, binary logistic regression analyses were performed. Results: CIN occurred in 18 patients (17.0%) in the ACEI group, 17 patients (18.1%) in ARB group and 7 patients (7.4%) in the no RAAS group. CIN occurrence was significantly higher in RAAS than no RAAS group (17.5% vs. 7.4%, p=0.01). Chronic RAAS blocker administration was an independent predictor of CIN (OR=2.69; 95% CI: 1.025-7.067; p=0.04). Mehran score was the only other independent predictor for CIN (OR=1.15; 95% CI: 1.019-1.310; p=0.02).
Men seem to have a higher activity relative to women for the drug efflux transporter P-gp. Our results suggest that carvedilol will cause drug interaction with digoxin following the inhibition of P-gp-mediated transcellular transport of digoxin in males.
SUMMARYThe aim of this study was investigate the effects of carvedilol therapy on ventricular repolarization characteristics as assessed by QT dispersion (QTd) and heart rate variability (HRV) in patients with heart failure.Thirty-one patients with heart failure (mean age, 63.9 years) were included in the study. Carvedilol was administered in addition to standard therapy for CHF at a dose of 6.25 mg/day and uptitrated to the maximum tolerated dose. Control group consisted of 14 patients with heart failure (mean age, 69.4 years) who could not take carvedilol due to several reasons. All patients were followed-up 6 months. QT dispersion (QTd), and corrected QTd (QTcd) values were calculated at baseline and at the end of follow-up. Time domain and frequency domain heart rate variability analysis were performed with ambulatory Holter ECG.Mean carvedilol dose was 23.9 ± 13.9 mg. Significant reductions were observed in the QTd (P = 0.016) and QTcd (P = 0.001) with carvedilol therapy, whereas QTd (P = 0.47) and QTcd (P = 0.43) did not change significantly in the control group. The QT maximum value did not change significantly but the QT minimum value (P = 0.03) was significantly increased after carvedilol therapy. Although the mean SDANN value was improved (P = 0.039), other HRV parameters such as mean SDNN (P = 0.32), rMSSD (P = 0.74), and the LF/HF ratio (P = 0.35) did not change significantly after carvedilol therapy.This prospective controlled study shows that carvedilol therapy decreased QT dispersion and improved ventricular repolarization characteristics but did not change autonomic dysfunction in patients with heart failure. (Int Heart J 2006; 47: 565-573)
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