Impact Of Obesity On Hypertension-induced Subclinical Left Ventricular Hypertrophy And The Exploration To Hydrogen Sulfide Regulation

Objective：To observe peripheral blood level of hydrogen sulfide（H₂S）、Nicotinamide-adeninedinucleotide phosphate oxidase2，the size of Left ventricular diameter（LVD）、Leftventricular posterior wall thickness （LVPWT）、Interventricular septal thickness （IVST） inpatients with the early of Obesity and hypertension,and to investigate the possiblemechanism and impact of obesity on hypertension-induced subclinical cardiac damage.Methods：In this randomized controlled study, A total of106consecutive subject wererecruited in Cardiology outpatient or Health Management Centre of Changsha CentralHospital between August2012and February2013.matching in age、gender and othergeneral information. thirty-three obesity-related hypertension、twenty-four normal bodymass index hypertension （Isolated hypertension group）、twenty-eight obese withouthypertension（Isolated obesity group）、twenty-one normal body mass index withouthypertension （control group）.After overnight fasting （8-12hours）, All patients underwentheight、weight and blood pressure measurements the next morningï¼›blood samples werecollected in vacu tainers， plasma H₂S level by modified methylene blue method、plasmaNADPH oxidase2level by enzyme-linked immunosorbent assay（ELISA） for measurementwere tested. subjects underwent blood routine and routine biochemical evaluationsincluding Fasting blood glucose、renal function and fasting total cholesterol.Measure Leftventricular diameter （LVD）、 Left ventricular posterior wall thickness （LVPWT）、Interventricular septal thickness （IVST） by Echocardiography. According to the formulato calculate Left ventricular mass （LVM） and Left ventricular mass index（LVMI）. Result:（1）LVMI in obesity-related hypertension(43.32±8.79g/m^2.7) was significantlyhigher than in Isolated hypertension group(36.87±7.11g/m^2.7，P＜0.05)、Isolated obesitygroup(35.46±6.03g/m^2.7，P＜0.05)、control group(29.29±4.04g/m^2.7，P＜0.05)ï¼›LVMIin Isolated hypertension group and Isolated obesity group was also significantly higherthan in control group（all P＜0.05）；（2）Plasma H₂S level in obesity-related hypertension （31.86±5.70μmol/L） wassignificantly lower than in Isolated hypertension group（38.72±9.63μmol/L，P＜0.05）、Isolated obesity group（36.65±8.03μmol/L，P＜0.05）、control group（48.23±11.83μmol/L，P＜0.05）； plasma H₂S level in solated hypertension group and Isolated obesity group wasalso significantly lower than in control group（all P＜0.05）；（3） Plasma H₂S level showed a negative correlation with LVMI in obesity-relatedhypertension（r=-0.884，P＜0.05）；（4） Plasma NADPH oxidase2level in obesity-related hypertension（2.63±0.95ng/ml） was significantly higher than in Isolated hypertension group（1.89±0.54ng/ml，P＜0.05）、Isolated obesity group（1.81±0.35ng/ml，P＜0.05）、controlgroup（0.75±0.23ng/ml，P＜0.05）；plasma NADPH oxidase2level in solated hypertensiongroup and Isolated obesity group was also significantly higher than in control group（all P＜0.05）；（5）In obesity-related hypertension、Isolated hypertension group and Isolated obesitygroup，plasma H₂S level showed a significant negative correlation with plasma NADPHoxidase2level（r=-0.615,P＜0.001）. Conclusion:（1） Obesity has a additive role in hypertension-induced subclinical cardiac damage；（2） H₂S is involved in subclinical cardiac damage in obesity-related hypertension viaNADPH oxidase2-generating oxidative stress。...