Background Central aortic systolic blood pressure(CASP) has been shown to be a stronger predictor of target-organ damage and cardiovascular events than brachial systolic blood pressure(BSBP), but there was no data...Background Central aortic systolic blood pressure(CASP) has been shown to be a stronger predictor of target-organ damage and cardiovascular events than brachial systolic blood pressure(BSBP), but there was no data about whether CASP can predict prolonged QRS duration more than BSBP. We examined the association of CASP and BSBP with QRS duration in rural community residents. Methods We retrospectively analyzed 490 rural community residents. Standard resting 12-lead ECG and central aortic blood pressure(CABP) were measured noninvasively in all subjects at baseline. The QRS duration was equal to or more than 120 ms being defined as prolonged QRS duration. Results The prolonged QRS duration group showed higher CASP(139.38 ± 11.67 vs. 135.36 ± 16.22, P = 0.031) and BSBP(136.03 ± 6.74 vs. 124.44 ± 13.01, P 〈 0.001) as compared with controls. Multivariate linear regression analysis showed that CASP, BSBP and heart rate were independently affecting QRS duration. Logistic regression analyses showed that CASP(OR 1.057, 95%CI: 1.027, 1.088, P 〈 0.001)and BSBP(OR 1.056, 95%CI: 1.027, 1.086, P = 0.032) were independent predictors of prolonged QRS duration after adjustment for age, sex, body mass index, heart rate. CASP had a better predictive value for prolonged QRS duration than(AUC: 0.793 vs. 0.601, P 〈 0.001) BSBP. Conclusions Our findings demonstrate that both CASP and BSBP are risks for prolonged QRS duration, but CASP can predict prolonged QRS duration better than BSBP.展开更多
Background: Previous studies have shown that reduced renal plasma flow (RPF) may play a role in progression of renal disease in autosomal dominant polycystic kidney disease (ADPKD). Tolvaptan, a vasopressin 2 antagoni...Background: Previous studies have shown that reduced renal plasma flow (RPF) may play a role in progression of renal disease in autosomal dominant polycystic kidney disease (ADPKD). Tolvaptan, a vasopressin 2 antagonist, reduces growth of total kidney volume and slows the decrease in estimated glomerular filtration rate (eGFR) in ADPKD. The purpose of this randomized, cross-over, double-blind, placebo-controlled study was to investigate if acute tolvaptan treatment increases RPF in ADPKD patients. Methods: Eighteen ADPKD patients (chronic kidney disease stages I-III) were investigated twice (min. 10 days apart) after acute treatment with either tolvaptan 60 mg or placebo. Two hours after treatment RPF and GFR were estimated by Technetium-99m diethylenetriamine penta-acetic acid (99-mTc-DTPA) renography. During the examination day, central and brachial blood pressures (BP) were measured using Mobil-O-Graph? PWA. We also measured plasma concentrations of vasopressin (p-AVP), renin (PRC), angiotensin II (p-AngII) and aldosterone (p-Aldo), urine excretion of aquaporin 2 (u-AQP2), urine output (OU), urine osmolality (u-Osm) and fractional excretion of sodium (FENa). Results: 99-mTc-DTPA renography showed a similar RPF (673 ± 262 ml/min after tolvaptan vs. 650 ± 209 ml/min after placebo, p = 0.571) and GFR (78 ± 26 ml/min after tolvaptan vs. 79 ± 21 ml/min after placebo p = 0.774) after tolvaptan and placebo treatment. P-AVP and UO increased and u-Osm decreased after tolvaptan and remained unchanged during placebo. Systolic BP tended to decrease during renography during tolvaptan. Very small or insignificant changes were seen in PRC, p-AngII and p-Aldo. Conclusions: Acute tolvaptan treatment did not change renal hemodynamics in ADPKD.展开更多
基金supported by the grants from Guangdong Natural Science Foundation(No.2015A030313660)the Technology Project Foundation of Guangzhou(No.2014y2-00140/No.1563000381/201604020186/201604020018)+1 种基金the Technology Project Foundation of Guangdong Province(No.2014B020212008)National Natural Science Foundation of China(No.81300230)
文摘Background Central aortic systolic blood pressure(CASP) has been shown to be a stronger predictor of target-organ damage and cardiovascular events than brachial systolic blood pressure(BSBP), but there was no data about whether CASP can predict prolonged QRS duration more than BSBP. We examined the association of CASP and BSBP with QRS duration in rural community residents. Methods We retrospectively analyzed 490 rural community residents. Standard resting 12-lead ECG and central aortic blood pressure(CABP) were measured noninvasively in all subjects at baseline. The QRS duration was equal to or more than 120 ms being defined as prolonged QRS duration. Results The prolonged QRS duration group showed higher CASP(139.38 ± 11.67 vs. 135.36 ± 16.22, P = 0.031) and BSBP(136.03 ± 6.74 vs. 124.44 ± 13.01, P 〈 0.001) as compared with controls. Multivariate linear regression analysis showed that CASP, BSBP and heart rate were independently affecting QRS duration. Logistic regression analyses showed that CASP(OR 1.057, 95%CI: 1.027, 1.088, P 〈 0.001)and BSBP(OR 1.056, 95%CI: 1.027, 1.086, P = 0.032) were independent predictors of prolonged QRS duration after adjustment for age, sex, body mass index, heart rate. CASP had a better predictive value for prolonged QRS duration than(AUC: 0.793 vs. 0.601, P 〈 0.001) BSBP. Conclusions Our findings demonstrate that both CASP and BSBP are risks for prolonged QRS duration, but CASP can predict prolonged QRS duration better than BSBP.
文摘Background: Previous studies have shown that reduced renal plasma flow (RPF) may play a role in progression of renal disease in autosomal dominant polycystic kidney disease (ADPKD). Tolvaptan, a vasopressin 2 antagonist, reduces growth of total kidney volume and slows the decrease in estimated glomerular filtration rate (eGFR) in ADPKD. The purpose of this randomized, cross-over, double-blind, placebo-controlled study was to investigate if acute tolvaptan treatment increases RPF in ADPKD patients. Methods: Eighteen ADPKD patients (chronic kidney disease stages I-III) were investigated twice (min. 10 days apart) after acute treatment with either tolvaptan 60 mg or placebo. Two hours after treatment RPF and GFR were estimated by Technetium-99m diethylenetriamine penta-acetic acid (99-mTc-DTPA) renography. During the examination day, central and brachial blood pressures (BP) were measured using Mobil-O-Graph? PWA. We also measured plasma concentrations of vasopressin (p-AVP), renin (PRC), angiotensin II (p-AngII) and aldosterone (p-Aldo), urine excretion of aquaporin 2 (u-AQP2), urine output (OU), urine osmolality (u-Osm) and fractional excretion of sodium (FENa). Results: 99-mTc-DTPA renography showed a similar RPF (673 ± 262 ml/min after tolvaptan vs. 650 ± 209 ml/min after placebo, p = 0.571) and GFR (78 ± 26 ml/min after tolvaptan vs. 79 ± 21 ml/min after placebo p = 0.774) after tolvaptan and placebo treatment. P-AVP and UO increased and u-Osm decreased after tolvaptan and remained unchanged during placebo. Systolic BP tended to decrease during renography during tolvaptan. Very small or insignificant changes were seen in PRC, p-AngII and p-Aldo. Conclusions: Acute tolvaptan treatment did not change renal hemodynamics in ADPKD.