| objective:Evaluation of left ventricular (LV) systolic function was common during stress echocardiography and assessment of LV diastolic function was relatively scarce especially domestic. The purpose of this study was to use adenosine stress echocardiography and N-terminal pro-B-type natriuretic peptide (NT-proBNP) to assess coronary stenosis in patients with chest pain syndrome or anginal equivalent noninvasively. Methods:NT-proBNP was measured after overnight fast in fifty-five patients (M 45, F 10,57±11 years) who then underwent echocardiography before, during and 3 minutes after adenosine administration. LV diastolic function analyzed included mitral annular early (E’) and late velocity (A’) both at mitral septal and lateral level and the mitral inflow to annulus ratio (E/E’). Coronary angiography was performed the following day by which patients were assigned into three groups:normal results(<50%,18patients), stenosis 50%-70%(18 patients) and stenosis≥70%(19 patients). Difference of inter-groups and intra-group were analyzed. Receiver operating characteristic (ROC) curves of the LV diastolic parameters were analyzed to identify predictors of coronary stenosis.ΔE’septal/A’septal represented E’septal/A’septal during adenosine stress subtracted that of the baseline. Results:NT-proBNP levels in groups of stenosis 50%~70% and> 70% were significantly higher than that in group of normal results(P=0.014, P=0.040). There were no significant differences of these diastolic parameters, heart rate and blood pressure among the three groups before adenosine administration. The heart rates in the patients in the three groups became significantly faster during adenosine stress than before, although went down significantly 3 minutes after asenosine administration but was still higher than before (P<0.05). The systolic blood pressure went significantly lower during stress continuing to 3 minutes after adenosine administration than before; the diastolic blood pressure also went significantly lower during stress than before, but got significantly higher 3 minutes after the admininstration when was no difference from before. The ejection fraction (EF)in the normal and coronary stenosis 50%-70% groups increased significantly during adenosine stress when compared with baseline values, while in the stenosis 70% group it also increased but not significantly; 3 minutes after the stress EF of the 3 groups had no difference from baseline. During adenosine stress, the E/E’scptal in group of stenosis≥70% were higher than that in the group of normal results (P=0.024); while 3 minutes after adenosine administration, E/E’septal in group of coronary stenosis 50%-70% and >70% were higher than that in group of normal coronary artery (P=0.036,0.048). The variation of E’septal/A’septal of during and before adenosine stress (ΔE’septal/A’septal) between group of normal results and stenosis≥70% were significantly different (P =0.001). E lateral’/A lateral’ in group of stenosis 50%~70% and E’septal/A’septal and E’lateral/A’lateral in group of stenosis≥70% were also decreased during stress compared with baseline (P=0.003,0.001,0.022). By ROC curve, the specificity ofΔE’septal/A’septal≥0.037 predicting coronary stenosis<70% was 94%. The sensitivity and specificity of NT-proBNP≥544.6fmol/ml in predicting coronary stenosis≥70% were 93% and 75%, respectively. NT-proBNP inversely correlated with E’lateral/A’lateral (r=-0.390, P=0.014) and positively correlated with E/E’lateral(r=0.550, P=0.001).Conclusions: Adenosine might induce diastolic dysfunction in patients with coronary stenosis more than 70% and NT-proBNP could reflect LV diastolic function to a certain extent. We support the prediction that most patients having chest pain syndromes or anginal equivalent with NT-proBNP<544.6fmol/ml and in ASEΔE’septal/A’septal≥0.037 might be spared coronary angiography. objective:The currently available data is quite limited on evaluation of left atrial mechanical function by stress echocardiography especially with adenosine stress echocardiography (ASE). We hypothesized that patients with coronary artery disease might have changes in left ventricular and left atrial mechanical functions, which should be correlated with each other due to atherosclerosis and abnormal coronary blood supply. So we were intented to assess left cardiac mechanical function by ASE in patients of stable angina pectoris with preserved ejection fraction (EF) to explore the mechanism of left cardiac remodeling. Method:Fifty-five patients (M 45, F 10,57±11 years) underwent echocardiography before, during and 3 minutes after adenosine administration. The volumes were measured and were indexed to body surface area. The parameters analyzed included left ventricular (LV) end-diastolic volume index (LVEDVi), LV end-systolic volume index (LVESVi), LV stroke volume (LV-SVi), left atrial (LA) volume index (LAVi), LA volume index before atrial contraction [LAV(pre-a)i], LA passive emptying volume index (LAPVi), LA active emptying volume index(LAAVi), LA conduit volume index (LACVi), and LA total emptying volume index (LATVi). Ejection fraction of LA (LAEF), LA passive emptying percent of total emptying and LA active emptying percent of total emptying were calculated as LAEF% [(LAVmax-LAVmin)/LAVmax] X 100, ([LAVmax-LAVpre-a]/[LAVmax-LAVmin])×100 and ([LAVa-LAVmin]/[LAVmax-LAVmin])×100. Coronary angiography was performed the following day by which patients were assigned into three groups:normal results(<50%,18patients), stenosis 50%~70%(18 patients) and stenosis≥70%(19 patients).ΔLAAVi represented LAAVi during adenosine stress subtracted that of the baseline. Results:There were no significant differences of these volume parameters, heart rate and blood pressure among the three groups before adenosine administration. The heart rates in the patients in the three groups became significantly faster during adenosine stress than before, although went down significantly 3 minutes after asenosine administration but was still higher than before (P<0.05). The systolic blood pressure went significantly lower during stress continuing to 3 minutes after adenosine administration than before; the diastolic blood pressure also went significantly lower during stress than before, but got significantly higher 3 minutes after the admininstration when was no difference from before. The ejection fraction (EF)in the normal and coronary stenosis 50%-70% groups increased significantly during adenosine stress when compared with baseline values, while in the stenosis 70%group it also increased but not significantly; 3 minutes after the stress EF of the 3 groups had no difference from baseline. In all the 3 groups, LATVi were elevated during adenosine stress when compared to measurements taken before (P=0.046,0.041,0.034). LAV(pre-a)i and LAAVi in group of coronary stenosis≥70% increased significantly during adenosine stress when compared with that of baseline (P=0.021,0.007). LAV(pre-a)i and LAAVi in group of normal coronary went lower even than that before adenosine stress (P=0.002, 0.029). LAAVi in group of coronary stenosis 50~70% was smaller 3 minutes after the stress than baseline almost reaching statistical significance (P=0.057), while that in group of coronary stenosis≥70% wasn’t different from baseline. LAEF in all the 3 groups increased significantly during the stress when compared with baseline (P=0.001,0.045, 0.005) and had recovered 3 minutes after the stress.The iner-group comparisons showed LAAVi in group of coronary stenosis≥70% 3 minutes after the stress was higher than that in group of normal coronary artery(P=0.016). The inter-group and intra-group analysis didn’t show any statistical significance of LV volume index parameters before, during and after the adenosine stress. The largest area under the ROC curve for predicting coronary stenosis≥70% followed byΔLAAVi was 0.689 (P=0.042),95% CI 0.520~0.857. The specificity ofΔLAAVi≥1.67 ml/m2 for diagnosing more than≥70% coronary stenosis was 61%, and the sensitivity was 63%. The correlation coefficient of LAAVi and heart rate in group of coronary stenosis≥70% by Pearson analysis was r=0.554, P=0.000; while that in amalgamation of noraml coronary artery group and stenosis 50~70% group was r=0.264, P=0.019 and there were no correlation when in either of the above two group. What’s more LAAVi inversely correlated with E’septal/A’septal in all the 3 groups (r=-0.300, P=0.017 in group of normal coronary artery; r=-0.304, P=0.011 in group of coronary stenosis 50-70%; r=-0.469, P=0.001 in group of coronary stenosis≥70%). And LAAVi correlated with E’lateral/A’lateral only in group of coronary stenosis≥70%(r=-0.400, P=0.004). LAPVi in group of coronary stenosis >70% inversely correlated with heart rate (r=-0.3, P=0.038). Conclusions:Under adenosine stress, the LA compensates for changes in LV diastolic properties by augmenting active atrial contraction in patients of stable angina pectoris with preserved EF of coronary stenosis≥70%. LAAVi inversely correlated with E’septal/A’septal.LACVi and LAPVi didn’t vary in the acute adenosine stress situation. The LA compliance of patients of coronary stenosis<70% was better than that of coronary stenosis≥70%. The variation of LAAVi during adenosine stress and baseline could be used to predict the degree of coronary stenosis:the specificity and sensitivity ofΔLAAVi≥1.67 ml/m2 for diagnosing more than≥70% coronary stenosis was 61% and 63% respectively. objective:The purpose of this part was to observe the effects of adenosine on left atrial function in patients of stable angina pectoris with preserved EF assessed by two-dimensional speckle tracking echocardiography (2DSTE). Method:Fifty-five patients (M 45, F 10,57±11 years) underwent echocardiography before, during and 3 minutes after adenosine administration.2DSTE of the LA was acquired from the apical 4-chamber view (frame rate:47±11 frame/sec, Philip CX-50) using prototype speckle tracking software (QLAB 7.0, Philips Medical Systems, Andover, MA). LA wall was tracked on a frame-by-frame basis, and LA volume waveforms were generated. Maximum LA volume (LAVmax) and minimal LA volume (LAVmin), and the LA volume before atrial contraction LAV(pre-a) were measured. These values were corrected by body surface area. Ejection fraction of LA (LAEF), LA passive emptying percent of total emptying and LA active emptying percent of total emptying were calculated as LAEF%=[(LAVmax-LAVmin)/LAVmax] X 100, ([LAVmax-LAVpre-a]/[LAVmax-LAVmin]) X 100 and ([LAVa-LAVmin]/[LAVmax-LAVmin]) X 100. Coronary angiography was performed the following day by which patients were assigned into three groups:normal results(<50%,18 patients), stenosis 50%~70% (18patients) and stenosis≥70%(19patients).The results were analyzed with those from Part 1 and Part 2 by Pearson analysis. Results:Adequate LA volume waveforms were obtained in 71% subjects. A good correlation was obtained between speckle tracking-derived LA volume measurements and manually traced LA volume measurements of the identical 2D image from Part 2(r=0.92, P=0.000). LAAVi in group of coronary stenosis≥70% increased significantly during adenosine stress when compared with that of baseline (P=0.005). LAEF in all the 3 groups increased significantly during the stress when compared with baseline (P=0.04,0.035,0.04) Conclusions:2DSTE can effectively and easily measure LA volume and has a potential for the noninvasive assessment of LA function in daily clinical practice.Under adenosine stress, the LA compensates for changes in LV diastolic properties by augmenting active atrial contraction in patients of stable angina pectoris with preserved EF of coronary stenosis≥70%. |