Paced QRS axis as a predictor of pacing-induced left ventricular dysfunction.

PURPOSE: The selection of the optimal right ventricular (RV) pacing site remains unclear. We hypothesized that a normal paced QRS axis would provide a physiological ventricular activation and lead to a better long-term outcome. METHODS: We evaluated 187 patients who underwent a permanent pacemaker implantation and were dependent on RV pacing. The pacing sites were classified as the apex and non-apex according to the chest radiography. A paced QRS axis was defined as that between -30° and 90°. Preservation of the left ventricular (LV) systolic function was defined as that with a <10 % decrease in the ejection fraction after the pacemaker implantation. RESULTS: The median follow-up period was 5.8 years (interquartile 3.9-9.0). Radiographically, the RV leads were located in the apex (n = 148, 79 %) or non-apex (n = 39, 21 %). In the electrocardiogram, normal paced and abnormal paced QRS axes were observed in 28 patients (15 %) and 159 patients (85 %), respectively. The LV ejection fraction was decreased in the patients with an abnormal paced QRS axis (-10 ± 10 %, P < 0.001), but not in those with a normal axis (0 ± 6 %, P = 0.80). The electrocardiographic determinant differentiated a preserved LV function (95 % vs. 35 %, log-rank P = 0.04). Among the patients with radiographically non-apical pacing, a normal paced QRS axis was an additional meaningful predictor of a preserved LV function after the pacemaker implantation (95 % vs. 24 %, log-rank P = 0.002). CONCLUSION: Compared with the radiographic method, a normal paced QRS axis was associated with a preserved LV function.

Decaffeinated green tea extract improves hypertension and insulin resistance in a rat model of metabolic syndrome.

BACKGROUND: Oxidative stress and endothelial dysfunction are closely associated with hypertension and insulin resistance (IR) in metabolic syndrome (MetS). It is still controversial whether green tea extract (GTE) may have blood pressure (BP) lowering effect. Decaffeinated GTE might be presumed to have strong antioxidative effect and BP-lowering effect as compared with catechins. Thus we investigated whether decaffeinated-GTE could attenuate hypertension and IR by improving endothelial dysfunction and reducing oxidative stress in a rat model of MetS. METHODS AND RESULTS: 20 Otsuka Long-Evans Tokushima Fatty (OLETF) rats at 13 weeks old, MetS rats, were randomized into a saline treated group (OLETF; n = 10) and a group treated with decaffeinated-GTE (25 mg/kg/day) (GTE-OLETF; n = 10). Intraperitoneal glucose tolerance tests and BP measurements were performed at 13 and 25 weeks. Decaffeinated-GTE significantly reduced BP (OLETF vs. GTE-OLETF; 130 ± 7 vs. 121 ± 3 mmHg, p = 0.01), fasting/postprandial 2 h glucose (141 ± 18/159 ± 13 vs. 115 ± 7/132 ± 16 mg/dL, p = 0.009/0.002) and insulin levels (4.8 ± 2.3 vs. 2.4 ± 1.3 ng/mL, p < 0.001). Decaffeinated-GTE significantly reduced vascular reactive oxygen species (ROS) formation and NADPH oxidase activity, and improved endothelium dependent relaxation in the thoracic aorta of OLETF rats. Decaffeinated-GTE also suppressed the expression of p47 and p22phox (NADPH oxidase subunits) in the immunohistochemical staining, and stimulated phosphorylation of endothelial nitric oxide synthase (eNOS) and Akt in the immunoblotting of aortas. CONCLUSIONS: Decaffeinated-GTE reduced the formation of ROS and NADPH oxidase activity and stimulated phosphorylation of eNOS and Akt in the aorta of a rat model of MetS, which resulted in improved endothelial dysfunction and IR, and eventually lowered BP.