Impact of noncontrast PCI for ACS

Purpose : Contrast-induced acute kidney injury (CI-AKI) is one of the common serious complications of percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS). This study aimed to assess the significance of noncontrast strategy in the setting of ACS. Methods : CI-AKI was defined as an increase in serum creatinine of ≥ 0.5 mg / dL or ≥ 1.25 times from the baseline. One-year worsening renal function (WRF) was defined as an increase of ≥ 0.3 mg / dL in serum creatinine from the baseline after PCI. Results : Of 250 ACS patients, 81 were treated with noncontrast PCI. The average doses of contrast medium in the noncontrast and conventional groups were 17 (9–22) ml and 150 (120–200) ml, respectively. CI-AKI was observed in 4 patients (5%) in the noncontrast group and 29 patients (17%) in the conventional group. Noncontrast PCI was associated with a lower incidence of CI-AKI (adjusted odds ratio, 0.26 ; 95% confidence interval [CI], 0.08–0.82). The bootstrap method and inverse probability weighting led to similar results. CI-AKI was associated with a higher incidence of 1-year WRF (adjusted hazard ratio, 2.30 ; 95% CI, 1.12–4.69), while noncontrast PCI was not. Conclusions : Noncontrast PCI was associated with the lower incidence of CI-AKI in ACS patients

Oral infection-inflammatory pathway, periodontitis, is a risk factor for endothelial dysfunction in patients with coronary artery disease

Objective: Several studies have shown that periodontitis is a risk factor for cardiovascular diseases. There is an association between inflammation and endothelial dysfunction. The purpose of this study was to evaluate endothelial function in patients with coronary artery disease (CAD) who had periodontitis. Methods and results: We evaluated forearm blood flow (FBF) responses to acetylcholine (ACh), an endothelium-dependent vasodilator, and to sodium nitroprusside (SNP), an endothelium-independent vasodilator, in 101 CAD patients with periodontitis (37 men and 11 women, 63 +/- 12 yr) and without periodontitis (36 men and 17 women, 62 +/- 13 yr). FBF was measured by using strain-gauge plethysmography. Circulating levels of C-reactive protein and interleukin-6 were significantly higher in the periodontitis group than in the non-periodontitis group. FBF response to ACh was significantly smaller in the periodontitis group than in the non-periodontitis group. SNP-stimulated vasodilation was similar in the two groups. Periodontal therapy reduced serum concentrations of C-reactive protein from 2.7 +/- 1.9 to 1.8 +/- 0.9 mg/L (P < 0.05) and interleukin-6 from 2.6 +/- 3.4 to 1.6 +/- 2.6 ng/L (P < 0.05) and augmented ACh-induced vasodilation from 14.7 +/- 5.2 to 20.1 +/- 6.1 mL/(min 100 mL) tissue (P < 0.05) in patients with periodontitis. The SNP-stimulated vasodilation was similar before and after treatment. After administration of NG-monomethyl-l-arginine, a nitric oxide synthase inhibitor, FBF response to ACh was similar before and after treatment. Conclusion: These findings suggest that periodontitis is associated with endothelial dysfunction in patients with CAD through a decrease in nitric oxide bioavailability. Systemic inflammation may be, at least in part, a cause and predictor of progression of endothelial dysfunction