CAJ | 학술논문

目的探讨糖耐量异常对心室重塑的影响及可能的机制,从而预防心室重塑的发生和发展.方法入选患者均接受葡萄糖耐量试验(OGTT)和心脏彩色超声检查,测定E波与A波流速比值(E/A)、计算左室心肌重量(LVM)、左室心肌指数(LVMI),行24 h动态血压检测,分析糖耐量异常与心室重塑相关指标的关系.结果合并糖耐量异常高血压组左室舒张功能减低发生率(74%)高于单纯高血压组(39%)(x2=6.5,P＜0.05),糖耐量异常组左室舒张功能减低(34%)发生率高于对照组(10%)(x2=5.2,P＜0.05).合并糖耐量异常高血压组左室肥厚发生率(24%)明显高于高血压组、糖耐量异常组及正常组(分别为7%、0、0)(x2=4.561,P＜0.05).多因素逐步回归分析显示,年龄和餐后2 h血糖值是E/A比值的独立危险因素.结论糖耐量异常是导致左室肥厚和舒张功能减低的一个危险因素和病理基础之一,且导致左室舒张功能减低发生率高于左室肥厚.
목적 탐토당내량이상대심실중소적영향급가능적궤제,종이예방심실중소적발생화발전.방법 입선환자균접수포도당내량시험(OGTT)화심장채색초성검사,측정E파여A파류속비치(E/A)、계산좌실심기중량(LVM)、좌실심기지수(LVMI),행24 h동태혈압검측,분석당내량이상여심실중소상관지표적관계.결과 합병당내량이상고혈압조좌실서장공능감저발생솔(74%)고우단순고혈압조(39%)(x2=6.5,P＜0.05),당내량이상조좌실서장공능감저(34%)발생솔고우대조조(10%)(x2=5.2,P＜0.05).합병당내량이상고혈압조좌실비후발생솔(24%)명현고우고혈압조、당내량이상조급정상조(분별위7%、0、0)(x2=4.561,P＜0.05).다인소축보회귀분석현시,년령화찬후2 h혈당치시E/A비치적독립위험인소.결론 당내량이상시도치좌실비후화서장공능감저적일개위험인소화병리기출지일,차도치좌실서장공능감저발생솔고우좌실비후.
Objective To evaluate the effects of impaired glucose tolerance (IGT) on ventricular remodeling. Methods Parameters of every subject including left ventricular mass ( LVM), left ventricular mass index (LVMI), E/A ratio, 75 g oral glucose tolerance test (OGTT), ambulatory blood pressure monitoring(ABPM) data including 24-hour mean systolic blood pressure(mSBP) and 24-hour mean diastolic blood pressure(mDBP) were collected. Then the relationship of IGT and myocardial remodeling related parameters were analyzed. Results The rate of diastolic dysfunction was higher in the IGT combined with hypertensive group(74% ) compared with the hypertensive group( 39% )( x2 = 6. 5, P ＜ 0. 05 ). The rate of diastolic dysfunction was higher in the IGT group( 34% ) compared with the normal group( 10% ) (x2 = 5.2,P ＜0. 05). The rate of Left Ventricular Hypertrophy (LVH)in the IGT combined with hypertensive group (24%) was higher than the other three groups (Hypertension group 7%, IGT group 0, Normal group 0) (x2 =4.561,P ＜0.05), and there was no significance between the rest three groups (P ＞0.05).Stepwise multiple regression showed age and 2 Hours' Postprandial Blood Glucose were independent risk factors of E/A ratio. Conclusions These results suggested that IGT is a possible contributor to left ventricular hypertrophy and diastolic dysfunction, and is one of the histopathology of left ventricular remodeling.