钙化性主动脉瓣狭窄患者左室长轴功能和心电图ST-T变化的临床研究
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摘要
研究目的：
1.探讨正常左室射血分数的钙化性主动脉瓣狭窄患者亚临床左室收缩功能不全和血Ⅲ型前胶原氨基末端肽之间的关系。
2.调查原发性高血压对无症状钙化性主动脉瓣狭窄患者左室长轴收缩功能和左室舒张功能的影响。
3.观察钙化性主动脉瓣狭窄患者主动脉瓣置换术前后心电图侧壁导联ST段偏移程度和T波幅度的变化,并明确主动脉瓣压力阶差和左室质量指数与ST段偏移程度和T波幅度之间的关系。
研究方法：
1.入选57例正常左室射血分数的钙化性主动脉瓣狭窄患者,30例左室射血分数和主动脉瓣均正常的受试者构成了对照组。应用超声心动图组织多普勒成像和斑点追踪成像技术评估左室舒张功能和左室长轴收缩功能。应用酶联免疫吸附法测定血Ⅲ型前胶原氨基末端肽水平。
2.入选219例无症状钙化性主动脉瓣狭窄患者。根据原发性高血压病史,将所有研究对象分为正常血压组和高血压组。应用超声心动图组织多普勒成像和斑点追踪成像技术测定左室舒张功能和左室长轴收缩功能。
3.对72例接受无支架生物瓣主动脉瓣膜置换术的钙化性主动脉瓣狭窄患者进行研究,分别于主动脉瓣膜置换术前、术后1周、6月、12月和24月记录数字化12导联同步心电图和超声心动图。应用超声心动图测量并计算平均主动脉瓣压力阶差和左室质量指数。应用心电图机的内置软件,在等电位线水平测量每份心电图I、aVL、V5和V6导联的ST段偏移程度和T波幅度,取这4个导联的平均值。
研究结果：
1.钙化性主动脉瓣狭窄组与正常对照组比较,左室收缩期长轴峰值应变降低(-17.1±2.1vs.-18.8±1.4%,P<0.001),血Ⅲ型前胶原氨基末端肽水平增高(2.5±0.6vs.2.1±0.4ug/l, P<0.001)。单因素相关分析发现左室收缩期长轴峰值应变和血Ⅲ型前胶原氨基末端肽水平负性相关(r=-0.67,P<0.001)。异常左室舒张功能患者比正常左室舒张功能患者左室收缩期长轴峰值应变降低(-16.3±1.5vs.-18.8±2.1%,P<0.001)和血Ⅲ型前胶原氨基末端肽水平增高(2.8±0.5vs.2.0±0.3ug/1, P<0.001).多元回归分析表明,左室收缩期长轴峰值应变和舒张压是血Ⅲ型前胶原氨基末端肽水平的独立危险因素(R=0.71,P<0.001)。
2.与正常血压组比较,高血压组的年龄较大,且具有较高的身体质量指数(P<0.001)。此外,高血压组的二尖瓣口舒张早期血流峰值速度(E)和二尖瓣环舒张早期运动峰值速度(e')的比值(E/e')较大,左室收缩期长轴峰值应变降低和左室质量指数增加(所有P<0.001)。多元回归分析表明,左室质量指数和高血压是E/e'值和左室收缩期长轴峰值应变的独立预测因素。
3.在主动脉瓣膜置换术前、后,平均主动脉瓣压力阶差由43.3±16.9mm Hg降至10.3±5.0mm Hg (P<0.001);而ST段压低程度由术前-39.4±40.8uV改善为术后1周-3.7±40.7uV(P<0.001),并且在术后24月维持不变。左室质量指数在术后6月时下降(129.6±31.3g/m2vs.174.7■39.0g/m2, P<0.01),T波幅度的改善发生在术后12月(64.2±108.7uV vs.-11.5±189.4uV, p<0.001)。多元回归分析发现,平均主动脉瓣压力阶差和左室质量指数分别是ST段偏移程度和T波幅度变化最为重要的预测因素(分别r=-0.42和r=-0.35,P<0.001)。
研究结论：
1.正常左室射血分数的钙化性主动脉瓣狭窄患者血Ⅲ型前胶原氨基末端肽水平升高可反映亚临床左室收缩功能不全(左室长轴收缩功能受损)。此外,受损的左室长轴收缩功能和升高的血Ⅲ型前胶原氨基末端肽水平在异常左室舒张功能的患者最为明显。
2.原发性高血压在很大程度上促进了无症状钙化性主动脉瓣狭窄患者左室舒张功能不全和亚临床收缩功能不全(左室长轴收缩功能受损)的发展。
3.在钙化性主动脉瓣狭窄患者,ST段压低主要是由主动脉瓣压力阶差引起,因此术后变化会立即出现,并回升趋向正常基线水平；T波幅度低平或倒置主要是由左室肥厚引起,并在左室肥厚消退时才逐渐恢复至正常水平。因此,在钙化性主动脉瓣狭窄患者,心电图ST段偏移程度和T波幅度的改变应被视为两种具有不同临床病理生理意义的现象。
Objectives:1). To observe the association of plasma amino-terminal propeptide of procollagen type Ⅲ (PIIINP) with subclinical left ventricular (LV) systolic dysfunction in patients with calcific aortic stenosis (AS) and normal LV ejection fraction (LVEF).2). To investigate the impact of systemic hypertension on LV diastolic function and longitudinal systolic function in patients with asymptomatic calcific AS.3). To observe the time course of the electrocardiographic (ECG) ST-T changes in lateral leads after aortic valve replacement (AVR) for calcific AS, and to determine the association of aortic valve pressure gradient (AVPG) and left ventricular mass index (LVMI) with ST Segment level and T wave amplitude.
Methods:1). The study was performed in57calcific AS patients with normal LVEF and in30control subjects with normal aortic valve and normal LVEF. Tissue Doppler Imaging and Speckle Tracking Imaging were performed to assess LV diastolic function and longitudinal systolic function. Plasma PIIINP level was measured by Enzyme-linked Immunosorbent Assay (ELISA).2). A total of219consecutive patients with asymptomatic calcific AS were prospectively studied. According to history of hypertension, patients were divided into the normotensive and hypertensive groups. The severity of AS and left ventricular structure were assessed by conventional echocardiography. Tissue Doppler Imaging and Speckle Tracking Imaging were performed to evaluate left ventricular diastolic function and longitudinal systolic function.3). Seventy-two patients with calcific AS who underwent stentless AVR were prospectively studied by digital12-lead ECG and echocardiography before AVR and at1week,6,12and24months after the operation. Mean AVPG and LVMI were measured by echocardiography. ST segment level and T wave amplitude with respect to ECG isoelectric line were measured by built-in software in lead I, aVL, V5and V6. The mean ST segment level and T wave amplitude of4leads were calculated.
Results:1). In calcific AS patients, LV peak systolic longitudinal strain was significantly reduced and plasma PⅢNP was increased compared with controls (both P<0.001). A significant correlation was found between LV peak systolic longitudinal strain and PⅢNP (r=-0.67, P<0.001). In patients with abnormal LV diastolic function, LV peak systolic longitudinal strain was reduced compared with patients with normal LV diastolic function and plasma PIIINP was increased (both P<0.001). Stepwise multivariate regression analysis revealed that LV peak systolic longitudinal strain and diastolic blood pressure were independent predictors of plasma PIIINP (multiple r=0.71, P<0.001).2). Patients in the hypertensive group were older with higher body mass index (both P<0.001). Furthermore, higher E/e’, lower LV peak systolic longitudinal strain and higher LVMI were present in the hypertensive group (all P<0.001). Stepwise multivariate regression analysis revealed that LVMI and history of hypertension were independent predictors of the E/e’ ratio and LV peak systolic longitudinal strain.3). After correcting AS, mean AVPG fell and the pre-operative ST depression was improved immediately (both P<0.001) at one week after AVR and remained unchanged up to24months afterwards. Despite LVMI had regressed significantly at6months after AVR (P<0.01), the improvement of T wave amplitude from pre-AVR occurred at12month after AVR (P<0.001). Stepwise regression analysis of whole dataset identified that mean AVPG or LVMI was the most significant echo predicator of ST segment level or T wave amplitude, respectively (r=-0.42and-0.35, P<0.001).
Conclusions:1). Plasma PIIINP is associated with subclinical LV systolic dysfunction in patients with calcific AS and normal LVEF. In addition, the impaired LV systolic long axis function and increased plasma PIIINP concentration are most marked in patients with abnormal LV diastolic function.2). Systemic hypertension contributes to the development of left ventricular diastolic dysfunction and subclinical systolic dysfunction in patients with asymptomatic calcific AS.3). In patients with calcific AS, ST segment depression is mainly caused by AVPG, it therefore improves immediately after AVR. T wave amplitude reduction is, however, resulted from LV hypertrophy, and it improves only after LV hypertrophy has regressed towards normal level.
1.探讨正常左室射血分数的钙化性主动脉瓣狭窄患者亚临床左室收缩功能不全和血Ⅲ型前胶原氨基末端肽之间的关系。
2.调查原发性高血压对无症状钙化性主动脉瓣狭窄患者左室长轴收缩功能和左室舒张功能的影响。
3.观察钙化性主动脉瓣狭窄患者主动脉瓣置换术前后心电图侧壁导联ST段偏移程度和T波幅度的变化,并明确主动脉瓣压力阶差和左室质量指数与ST段偏移程度和T波幅度之间的关系。
研究方法：
1.入选57例正常左室射血分数的钙化性主动脉瓣狭窄患者,30例左室射血分数和主动脉瓣均正常的受试者构成了对照组。应用超声心动图组织多普勒成像和斑点追踪成像技术评估左室舒张功能和左室长轴收缩功能。应用酶联免疫吸附法测定血Ⅲ型前胶原氨基末端肽水平。
2.入选219例无症状钙化性主动脉瓣狭窄患者。根据原发性高血压病史,将所有研究对象分为正常血压组和高血压组。应用超声心动图组织多普勒成像和斑点追踪成像技术测定左室舒张功能和左室长轴收缩功能。
3.对72例接受无支架生物瓣主动脉瓣膜置换术的钙化性主动脉瓣狭窄患者进行研究,分别于主动脉瓣膜置换术前、术后1周、6月、12月和24月记录数字化12导联同步心电图和超声心动图。应用超声心动图测量并计算平均主动脉瓣压力阶差和左室质量指数。应用心电图机的内置软件,在等电位线水平测量每份心电图I、aVL、V5和V6导联的ST段偏移程度和T波幅度,取这4个导联的平均值。
研究结果：
1.钙化性主动脉瓣狭窄组与正常对照组比较,左室收缩期长轴峰值应变降低(-17.1±2.1vs.-18.8±1.4%,P<0.001),血Ⅲ型前胶原氨基末端肽水平增高(2.5±0.6vs.2.1±0.4ug/l, P<0.001)。单因素相关分析发现左室收缩期长轴峰值应变和血Ⅲ型前胶原氨基末端肽水平负性相关(r=-0.67,P<0.001)。异常左室舒张功能患者比正常左室舒张功能患者左室收缩期长轴峰值应变降低(-16.3±1.5vs.-18.8±2.1%,P<0.001)和血Ⅲ型前胶原氨基末端肽水平增高(2.8±0.5vs.2.0±0.3ug/1, P<0.001).多元回归分析表明,左室收缩期长轴峰值应变和舒张压是血Ⅲ型前胶原氨基末端肽水平的独立危险因素(R=0.71,P<0.001)。
2.与正常血压组比较,高血压组的年龄较大,且具有较高的身体质量指数(P<0.001)。此外,高血压组的二尖瓣口舒张早期血流峰值速度(E)和二尖瓣环舒张早期运动峰值速度(e')的比值(E/e')较大,左室收缩期长轴峰值应变降低和左室质量指数增加(所有P<0.001)。多元回归分析表明,左室质量指数和高血压是E/e'值和左室收缩期长轴峰值应变的独立预测因素。
3.在主动脉瓣膜置换术前、后,平均主动脉瓣压力阶差由43.3±16.9mm Hg降至10.3±5.0mm Hg (P<0.001);而ST段压低程度由术前-39.4±40.8uV改善为术后1周-3.7±40.7uV(P<0.001),并且在术后24月维持不变。左室质量指数在术后6月时下降(129.6±31.3g/m2vs.174.7■39.0g/m2, P<0.01),T波幅度的改善发生在术后12月(64.2±108.7uV vs.-11.5±189.4uV, p<0.001)。多元回归分析发现,平均主动脉瓣压力阶差和左室质量指数分别是ST段偏移程度和T波幅度变化最为重要的预测因素(分别r=-0.42和r=-0.35,P<0.001)。
研究结论：
1.正常左室射血分数的钙化性主动脉瓣狭窄患者血Ⅲ型前胶原氨基末端肽水平升高可反映亚临床左室收缩功能不全(左室长轴收缩功能受损)。此外,受损的左室长轴收缩功能和升高的血Ⅲ型前胶原氨基末端肽水平在异常左室舒张功能的患者最为明显。
2.原发性高血压在很大程度上促进了无症状钙化性主动脉瓣狭窄患者左室舒张功能不全和亚临床收缩功能不全(左室长轴收缩功能受损)的发展。
3.在钙化性主动脉瓣狭窄患者,ST段压低主要是由主动脉瓣压力阶差引起,因此术后变化会立即出现,并回升趋向正常基线水平；T波幅度低平或倒置主要是由左室肥厚引起,并在左室肥厚消退时才逐渐恢复至正常水平。因此,在钙化性主动脉瓣狭窄患者,心电图ST段偏移程度和T波幅度的改变应被视为两种具有不同临床病理生理意义的现象。
Objectives:1). To observe the association of plasma amino-terminal propeptide of procollagen type Ⅲ (PIIINP) with subclinical left ventricular (LV) systolic dysfunction in patients with calcific aortic stenosis (AS) and normal LV ejection fraction (LVEF).2). To investigate the impact of systemic hypertension on LV diastolic function and longitudinal systolic function in patients with asymptomatic calcific AS.3). To observe the time course of the electrocardiographic (ECG) ST-T changes in lateral leads after aortic valve replacement (AVR) for calcific AS, and to determine the association of aortic valve pressure gradient (AVPG) and left ventricular mass index (LVMI) with ST Segment level and T wave amplitude.
Methods:1). The study was performed in57calcific AS patients with normal LVEF and in30control subjects with normal aortic valve and normal LVEF. Tissue Doppler Imaging and Speckle Tracking Imaging were performed to assess LV diastolic function and longitudinal systolic function. Plasma PIIINP level was measured by Enzyme-linked Immunosorbent Assay (ELISA).2). A total of219consecutive patients with asymptomatic calcific AS were prospectively studied. According to history of hypertension, patients were divided into the normotensive and hypertensive groups. The severity of AS and left ventricular structure were assessed by conventional echocardiography. Tissue Doppler Imaging and Speckle Tracking Imaging were performed to evaluate left ventricular diastolic function and longitudinal systolic function.3). Seventy-two patients with calcific AS who underwent stentless AVR were prospectively studied by digital12-lead ECG and echocardiography before AVR and at1week,6,12and24months after the operation. Mean AVPG and LVMI were measured by echocardiography. ST segment level and T wave amplitude with respect to ECG isoelectric line were measured by built-in software in lead I, aVL, V5and V6. The mean ST segment level and T wave amplitude of4leads were calculated.
Results:1). In calcific AS patients, LV peak systolic longitudinal strain was significantly reduced and plasma PⅢNP was increased compared with controls (both P<0.001). A significant correlation was found between LV peak systolic longitudinal strain and PⅢNP (r=-0.67, P<0.001). In patients with abnormal LV diastolic function, LV peak systolic longitudinal strain was reduced compared with patients with normal LV diastolic function and plasma PIIINP was increased (both P<0.001). Stepwise multivariate regression analysis revealed that LV peak systolic longitudinal strain and diastolic blood pressure were independent predictors of plasma PIIINP (multiple r=0.71, P<0.001).2). Patients in the hypertensive group were older with higher body mass index (both P<0.001). Furthermore, higher E/e’, lower LV peak systolic longitudinal strain and higher LVMI were present in the hypertensive group (all P<0.001). Stepwise multivariate regression analysis revealed that LVMI and history of hypertension were independent predictors of the E/e’ ratio and LV peak systolic longitudinal strain.3). After correcting AS, mean AVPG fell and the pre-operative ST depression was improved immediately (both P<0.001) at one week after AVR and remained unchanged up to24months afterwards. Despite LVMI had regressed significantly at6months after AVR (P<0.01), the improvement of T wave amplitude from pre-AVR occurred at12month after AVR (P<0.001). Stepwise regression analysis of whole dataset identified that mean AVPG or LVMI was the most significant echo predicator of ST segment level or T wave amplitude, respectively (r=-0.42and-0.35, P<0.001).
Conclusions:1). Plasma PIIINP is associated with subclinical LV systolic dysfunction in patients with calcific AS and normal LVEF. In addition, the impaired LV systolic long axis function and increased plasma PIIINP concentration are most marked in patients with abnormal LV diastolic function.2). Systemic hypertension contributes to the development of left ventricular diastolic dysfunction and subclinical systolic dysfunction in patients with asymptomatic calcific AS.3). In patients with calcific AS, ST segment depression is mainly caused by AVPG, it therefore improves immediately after AVR. T wave amplitude reduction is, however, resulted from LV hypertrophy, and it improves only after LV hypertrophy has regressed towards normal level.
引文
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