腺苷负荷超声心动图对心绞痛患者舒张功能及左心机械功能变化的研究
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摘要
背景和目的：应用负荷超声心动图观察左心室舒张功能改变的研究较少见,国内尚无相关报道。目前研究发现N末端脑钠肽(NT-proBNP)可以反映左心室舒张功能及冠状动脉狭窄程度。本研究通过腺苷负荷超声心动图观察稳定性心绞痛(SAP)患者左心室舒张功能的变化,旨在明确：(1)SAP患者在腺苷负荷过程中左心室舒张功能是否发生变化；(2)以冠状动脉造影为金标准,探索舒张功能变化与冠状动脉狭窄程度的关系；(3)结合血浆NT-proBNP浓度,无创预测SAP患者冠状动脉狭窄程度。方法：55名SAP患者(男45人,女10人,平均年龄57±11岁)腺苷负荷前空腹测定NT-proBNP浓度。在腺苷负荷前、负荷试验过程中及负荷后3分钟行超声心动图检查,应用组织多普勒模式(TDI)分别在二尖瓣环间隔侧及侧壁侧得到二尖瓣环舒张早期和舒张晚期运动速度之比(E’间隔/A间隔、E’侧壁/A’侧壁)；并得到E/E’间隔、E/E’侧壁。由此得出二尖瓣环运动速度变化值(E’间隔/A’间隔)腺苷负荷中—(E’间隔/A’间隔)基础=△E’间隔/A’间隔。次日行冠状动脉造影。按其结果分组：冠状动脉狭窄<50%组(正常组)；冠状动脉狭窄50%～70%;冠状动脉狭窄≥70%。比较组间及组内差异。并行受试者工作曲线(ROC曲线)进行分析。结果：冠状动脉狭窄50%-70%组和冠状动脉狭窄≥70%组NT-proBNP大于正常组(P=-0.014、P=0.040)。用药前各组间左心室舒张功能、心率、血压无统计学差异。3组在腺苷负荷过程中心率均较腺苷负荷前明显增快,用药后3分钟明显降低,但仍明显快于基础状态,均有统计学意义；收缩压在腺苷负荷中均较基础状态减低,腺苷负荷后3分钟仍较基础状态减低,均有统计学意义；舒张压在腺苷负荷中均较基础状态减低,有统计学意义,用药后3分钟与基础状态无明显差异。腺苷负荷中正常组与冠状动脉狭窄≥70%组E/E间隔’差别具有显著性(P=0.024)；腺苷负荷后3分钟,冠状动脉狭窄50～70%组和≥70%组E/E间隔’均大于冠状动脉正常组(P=0.036,0.048)；除了△E’间隔/A’间隔在正常组和冠状动脉狭窄≥70%组有显著性差异(P=0.001)外,其他变量各组间无显著性差异。腺苷负荷中冠状动脉狭窄50%～70%组E’侧壁/A’侧壁和冠状动脉狭窄≥70%组E’间隔/A’间隔、E’侧壁/A’侧壁均较用药前降低(P值分别为0.003、0.001、0.022),用药后3分钟上述指标恢复到基础状态。冠状动脉正常组和狭窄50～70%组左室EF值在腺苷负荷中较基础状态增加,有统计学意义,腺苷负荷后3分钟恢复到基础状态；而狭窄≥70%组在腺苷负荷中增加不明显。ROC曲线显示△E’间隔/A’间隔≥0.037判定无显著冠状动脉狭窄(即狭窄<70%)的敏感性69%,特异性94%；NT-proBNP≥544.6 fmol/ml诊断冠状动脉狭窄≥70%的敏感性是93%,特异性是75%。NT-proBNP与E’侧壁/A’侧壁呈负相关(r=-0.361,P=0.014),与E/E’侧壁呈正相关(r=0.550,P=0.001)。结论：腺苷负荷可诱发冠状动脉狭窄≥70%者左室舒张功能降低,NT-proBNP在一定程度反映左心室舒张功能改变。NT-proBNP<544.6 fmol/ml和腺苷负荷超声心动图中△E’侧壁/A’间隔≥0.037的大部分SAP患者可能负于冠状动脉造影检查。
背景和目的：目前,以负荷超声心动图研究冠心病患者左房容积和机械功能的报导较少见,尤其是腺苷负荷超声心动图。我们推测冠心病患者在腺苷负荷下,不同冠状动脉狭窄程度的患者左房和左室的容积和机械功能将随着舒张功能的改变发生不同的变化,从而探讨在稳定性心绞痛心功能正常患者左心机械功能的变化。
方法：55名稳定性心绞痛患者在腺苷负荷前、负荷试验过程中及负荷后3分钟分别行超声心动图检查,由左房、左室容积除以体表面积得到相应的容积指数：左室舒张末期容积指数(LVEDVi);左室收缩末期容积指数(LVESVi);左室每搏搏出量容积指数(SVi)；左房容积指数(LAVi);左房收缩前容积指数[LA V(pre-a)i]；左房被动排空容积指数(LAPVi);左房主动排空容积指数(LAAVi);左房管道容积(LACVi);左房蓄储容积(LATVi)。计算得到左室射血分数(LVEF%)左房射血分数(LAEF%)；左房被动排空分数(LAPV%);左房主动排空分数(LAAV%);LAAVi腺苷负荷中与基础状态之差△LAAVi=LAAVi负荷LAAVi基础。次日行冠状动脉造影。按其结果分组：冠状动脉狭窄<50%组(正常组)；冠状动脉狭窄50%～70%;冠状动脉狭窄≥70%。比较组间及组内差异。并行受试者工作曲线(ROC曲线)进行分析。结果：LATVi在3组内,腺苷负荷中均较基础状态增加,有统计学意义,在腺苷用药后3分钟恢复。LAV(pre-a)i在冠状动脉狭窄≥70%组腺苷负荷中较基础状态增加,有统计学意义；冠状动脉狭窄<50%组用药后3分钟LAV(pre-a)i较基础状态明显减少。LAAVi在冠状动脉狭窄≥70%组在腺苷负荷中较基础状态明显增加,其他两组虽有增加,但是未达到统计学意义；冠状动脉狭窄<50%组用药后3分钟LAAVi较基础状态明显减少,狭窄50～70%组用药后3分钟亦较基础状态减少,几乎达到统计学意义(P=0.057),而狭窄≥70%组用药后3分钟与基础状态无明显差别。LAEF在3组内腺苷负荷中较基础状态增加,均有统计学差异。冠状动脉狭窄<50%组和狭窄50～70%组左心室EF值在腺苷负荷中较基础状态明显增加,而狭窄≥70%组增加不明显。左房容积与机械功能的组间比较显示LAAVi在腺苷负荷后3分钟冠状动脉狭窄≥70%组较狭窄<50%组增加,有统计学意义。左心室容积在腺苷负荷前、过程中及用药后3分钟组内及组间比较未发现统计学意义的差别。受试者工作曲线(ROC曲线)显示△LAAVi诊断冠状动脉狭窄≥70%的曲线下面积是0.689,P=0.042,95%可信区间是(0.520～0.857),△LAAVi≥1.67判断冠状动脉狭窄≥70%的敏感性是63%,特异性是61%。Pearson相关分析显示LAAVi在冠状动脉狭窄≥0%组与心率的相关系数r=0.554,P=0.000；而在冠状动脉狭窄<50%组和50～70%狭窄组则无明显相关性；如果将冠状动脉狭窄<50%组和50～70%狭窄组合并,则r=0.264,P=0.019。LAPVi在冠状动脉狭窄≥70%组与心率的相关系数是r=-0.3,P=0.038,在其他两组则没有此相关性,将这两组合并亦未发现二者存在相关性。血压与各观察指标之间无明确相关性。LAAVi与第一部分的测量指标进行Pearson相关分析的结果显示,LAAVi与E’间隔/A’间隔在3组均呈负相关,冠状动脉狭窄<50%组r=-0.300,P=0.017；冠状动脉50～70%狭窄组r=-0.304,P=0.011；冠状动脉狭窄≥70%组r=-0.469,P=0.001。在冠状动脉狭窄<50%组和50～70%狭窄组LAAVi与E’侧壁/A’侧壁无明显相关性,而在狭窄≥70%组则其相关性为r=-0.400,P=0.004。LAAVi与E/E’间隔及E/E’侧壁无明显相关性。结论：本研究发现,在腺苷负荷状态下,冠状动脉狭窄≥70%者左心室舒张功能减低主要通过左房主动收缩来进行代偿；LAAVi与E’间隔/A’间隔呈负相关。在腺苷负荷状态下,LACVi和LAPVi无明显变化。冠状动脉狭窄<70%者左房的顺应性较狭窄≥70%者好。△LAAVi可以用来预测冠状动脉狭窄的程度。腺苷负荷过程中LAAVi较基础状态增加量≥1.67ml/m2判断冠状动脉狭窄≥70%的敏感性是63%,特异性是61%。
目的：应用二维斑点追踪技术(2DSTE)通过腺苷负荷超声心动图(ASE)研究左房容积和功能的变化。方法：55名稳定性心绞痛心功能正常患者在腺苷负荷前、过程中及腺苷负荷后3分钟分别行超声心动图检查。在心尖四腔心切面(帧频：47±11帧/秒/；Philip CX-50)应用QLAB 7.0 TMQ(Philips Medical Systems)得到左房容积曲线,从曲线上测量得到左房最大容积(LAVmax).左房最小容积(LAVmin)以及左房收缩前容积LAV(pre-a).所测容积除以体表面积得到相应的容积指数。通过计算得到左室每搏搏出量容积指数(SVi)；左房被动排空容积指数(LAPVi);左房主动排空容积指数(LAAVi);左房管道容积(LACVi);左房蓄储容积(LATVi)以及左房射血分数(LAEF%)=[(LAVmax-LAVmin)/LAVmax]×10016,17；左房被动排空分数(LAPV%)=(LAPV/LATV)×100;左心室主动排空分数(LAAV%) =(LAAV/LATV)×100。所得结果与本研究第一、二部分进行相关分析。结果：71%患者可以得到完整的左房容积曲线。2DSTE测量的结果与第二部分的左房容积测量结果有很好的相关性(r=0.92,P=0.000)。LAAVi在冠状动脉狭窄≥70%组在腺苷负荷中较基础状态明显增加,其他两组虽有增加,但是未达到统计学意义。LAEF在3组中均为腺苷负荷中较基础状态明显增加,有统计学意义。结论：本研究发现2DSTE可以简便、准确地得到左房容积曲线,为左房容积测量和功能评估提供可靠的数据,可以在临床中推广。结合ASE,发现在腺苷负荷状态下,冠状动脉狭窄≥70%组左心室舒张功能减低主要通过左房主动收缩来进行代偿。
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%.
背景和目的：目前,以负荷超声心动图研究冠心病患者左房容积和机械功能的报导较少见,尤其是腺苷负荷超声心动图。我们推测冠心病患者在腺苷负荷下,不同冠状动脉狭窄程度的患者左房和左室的容积和机械功能将随着舒张功能的改变发生不同的变化,从而探讨在稳定性心绞痛心功能正常患者左心机械功能的变化。
方法：55名稳定性心绞痛患者在腺苷负荷前、负荷试验过程中及负荷后3分钟分别行超声心动图检查,由左房、左室容积除以体表面积得到相应的容积指数：左室舒张末期容积指数(LVEDVi);左室收缩末期容积指数(LVESVi);左室每搏搏出量容积指数(SVi)；左房容积指数(LAVi);左房收缩前容积指数[LA V(pre-a)i]；左房被动排空容积指数(LAPVi);左房主动排空容积指数(LAAVi);左房管道容积(LACVi);左房蓄储容积(LATVi)。计算得到左室射血分数(LVEF%)左房射血分数(LAEF%)；左房被动排空分数(LAPV%);左房主动排空分数(LAAV%);LAAVi腺苷负荷中与基础状态之差△LAAVi=LAAVi负荷LAAVi基础。次日行冠状动脉造影。按其结果分组：冠状动脉狭窄<50%组(正常组)；冠状动脉狭窄50%～70%;冠状动脉狭窄≥70%。比较组间及组内差异。并行受试者工作曲线(ROC曲线)进行分析。结果：LATVi在3组内,腺苷负荷中均较基础状态增加,有统计学意义,在腺苷用药后3分钟恢复。LAV(pre-a)i在冠状动脉狭窄≥70%组腺苷负荷中较基础状态增加,有统计学意义；冠状动脉狭窄<50%组用药后3分钟LAV(pre-a)i较基础状态明显减少。LAAVi在冠状动脉狭窄≥70%组在腺苷负荷中较基础状态明显增加,其他两组虽有增加,但是未达到统计学意义；冠状动脉狭窄<50%组用药后3分钟LAAVi较基础状态明显减少,狭窄50～70%组用药后3分钟亦较基础状态减少,几乎达到统计学意义(P=0.057),而狭窄≥70%组用药后3分钟与基础状态无明显差别。LAEF在3组内腺苷负荷中较基础状态增加,均有统计学差异。冠状动脉狭窄<50%组和狭窄50～70%组左心室EF值在腺苷负荷中较基础状态明显增加,而狭窄≥70%组增加不明显。左房容积与机械功能的组间比较显示LAAVi在腺苷负荷后3分钟冠状动脉狭窄≥70%组较狭窄<50%组增加,有统计学意义。左心室容积在腺苷负荷前、过程中及用药后3分钟组内及组间比较未发现统计学意义的差别。受试者工作曲线(ROC曲线)显示△LAAVi诊断冠状动脉狭窄≥70%的曲线下面积是0.689,P=0.042,95%可信区间是(0.520～0.857),△LAAVi≥1.67判断冠状动脉狭窄≥70%的敏感性是63%,特异性是61%。Pearson相关分析显示LAAVi在冠状动脉狭窄≥0%组与心率的相关系数r=0.554,P=0.000；而在冠状动脉狭窄<50%组和50～70%狭窄组则无明显相关性；如果将冠状动脉狭窄<50%组和50～70%狭窄组合并,则r=0.264,P=0.019。LAPVi在冠状动脉狭窄≥70%组与心率的相关系数是r=-0.3,P=0.038,在其他两组则没有此相关性,将这两组合并亦未发现二者存在相关性。血压与各观察指标之间无明确相关性。LAAVi与第一部分的测量指标进行Pearson相关分析的结果显示,LAAVi与E’间隔/A’间隔在3组均呈负相关,冠状动脉狭窄<50%组r=-0.300,P=0.017；冠状动脉50～70%狭窄组r=-0.304,P=0.011；冠状动脉狭窄≥70%组r=-0.469,P=0.001。在冠状动脉狭窄<50%组和50～70%狭窄组LAAVi与E’侧壁/A’侧壁无明显相关性,而在狭窄≥70%组则其相关性为r=-0.400,P=0.004。LAAVi与E/E’间隔及E/E’侧壁无明显相关性。结论：本研究发现,在腺苷负荷状态下,冠状动脉狭窄≥70%者左心室舒张功能减低主要通过左房主动收缩来进行代偿；LAAVi与E’间隔/A’间隔呈负相关。在腺苷负荷状态下,LACVi和LAPVi无明显变化。冠状动脉狭窄<70%者左房的顺应性较狭窄≥70%者好。△LAAVi可以用来预测冠状动脉狭窄的程度。腺苷负荷过程中LAAVi较基础状态增加量≥1.67ml/m2判断冠状动脉狭窄≥70%的敏感性是63%,特异性是61%。
目的：应用二维斑点追踪技术(2DSTE)通过腺苷负荷超声心动图(ASE)研究左房容积和功能的变化。方法：55名稳定性心绞痛心功能正常患者在腺苷负荷前、过程中及腺苷负荷后3分钟分别行超声心动图检查。在心尖四腔心切面(帧频：47±11帧/秒/；Philip CX-50)应用QLAB 7.0 TMQ(Philips Medical Systems)得到左房容积曲线,从曲线上测量得到左房最大容积(LAVmax).左房最小容积(LAVmin)以及左房收缩前容积LAV(pre-a).所测容积除以体表面积得到相应的容积指数。通过计算得到左室每搏搏出量容积指数(SVi)；左房被动排空容积指数(LAPVi);左房主动排空容积指数(LAAVi);左房管道容积(LACVi);左房蓄储容积(LATVi)以及左房射血分数(LAEF%)=[(LAVmax-LAVmin)/LAVmax]×10016,17；左房被动排空分数(LAPV%)=(LAPV/LATV)×100;左心室主动排空分数(LAAV%) =(LAAV/LATV)×100。所得结果与本研究第一、二部分进行相关分析。结果：71%患者可以得到完整的左房容积曲线。2DSTE测量的结果与第二部分的左房容积测量结果有很好的相关性(r=0.92,P=0.000)。LAAVi在冠状动脉狭窄≥70%组在腺苷负荷中较基础状态明显增加,其他两组虽有增加,但是未达到统计学意义。LAEF在3组中均为腺苷负荷中较基础状态明显增加,有统计学意义。结论：本研究发现2DSTE可以简便、准确地得到左房容积曲线,为左房容积测量和功能评估提供可靠的数据,可以在临床中推广。结合ASE,发现在腺苷负荷状态下,冠状动脉狭窄≥70%组左心室舒张功能减低主要通过左房主动收缩来进行代偿。
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%.
引文
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