| Objectives1. To analyze left ventricular systolic asynchrony for heart failure patients by tissue velocity imaging(TVI);2. To analyze the correlation between the width of QRS wave and left ventricular systolic asynchrony in heart failure pateints;3. To analyze the correlation betweenβ3 receptor gene polymorphism and left ventricular systolic asynchrony in heart failure pateints;4. To observe the interventional effects of carvedilol on NYHA classification,LVEDd,LVEF,NO concentration in blood serum and left ventricular systolic asynchrony in heart failure patients.Methods (1)Selective,exclusive criteria and drug intervention:①Selective and exclusive criteria:Eighty-three heart failure patients with left ventricular ejection fraction (LVEF)≤45% (measured by Simpson method),NYHA classes I,II,III and without reveivingβblocker treatment were enrolled. Patients with valvular heart disease,chronic obstructive pulmonary disease,atrial fibrillation,atrial flutter,sinus bradycardia and pacemaker implantation were excluded. And 30 age-matched healthy control subjects were enrolled as group Control.②Drug intervention:Eleven CHF patients who had left ventricular systolic asynchrony were selected. Besides conventional therapy for heart failure they also accepted carvedilol treatment which started from low dose to maximum tolerated dose or target dose and lasted for 6 months.( 2 ) Detection indices : Echocardiographic parameters and the concentration of NO in blood serum were detected at the beginning of enrolment,1 month,3 months and 6 months after carvedilol treatment. ECG andβ3 receptor gene polymorphism were detected at the beginning of enrolment.①LVEDd and EF ( measured by routine echocardiographic method);②TS-SD,TS-maxD,TSI,TTP-SD,IVC-SD,S-SD and IVC/S-SD (measured by TVI to analyze left ventricular systolic asynchrony);③ECG recording;④β3 receptor gene polymorphism ( Blood samples were drawn through peripheral vein and it was detected by enzyme cutting method);⑤Concentration of NO in blood serum (detected by nitrate reductase method).Results1. The indices of left ventricular systolic asynchrony analyzed by TVI such as TS-SD,TS-max,TSI and the parameters of mitral annular motion in group CHF exceeded group Control significantly(p<0.05). 2. The index of left ventricular systolic asynchrony—Ts-SD in CHF patients with QRS<120ms exceeded that in group Control significantly(p<0.05). But the difference between detectable rates for left ventricular systolic asynchrony in CHF patients applying QRS<120ms and QRS≥120ms is not significant (p>0.05).3. The mutation frequence ofβ3 receptor gene polymorphism for CHF patients with and without left ventricular systolic asynchrony were 59.3% and 68.4% respectively,and the difference was not statistically significant (p>0.05).4. NYHA classification improved for those CHF patients who received carvedilol treatment. LVEDd decreased,LVEF increased,velocity of mitral annular systolic motion speeded up and the index of left ventricular systolic asynchrony Ts-SD shortened obviously after 1 month of carvedilol treatment(p<0.05).5. The concentration of NO in blood serum increased gradually as the treatment continued. The measurements among different follw-up time points had obvious difference(p<0.05).Conclusions1. Left ventricular systolic asynchrony exists in heart failure patients.2. CHF patients with QRS complexes<120ms or QRS complexes≥120ms have left ventricular systolic asynchrony . QRS duration can not assess left ventricular systolic asynchrony accurately and sensitively. 3. Index such as Ts-SD detected by TVI can evaluate left ventricular systolic asynchrony precisely.4. There may be no correlation betweenβ3 receptor gene polymorphism and left ventricular systolic asynchrony in heart failure.5. Carvedilol shows significant improvement to left ventricular systolic asynchrony 1 month after its treatment,the same to left ventricular systolic function and left ventricular remodeling. The improvement may be related to the rise of NO concentration in blood serum. |