PDF(Pubmed)
Abstract：
UNASSIGNED: Quantification of left atrial (LA) conduit function and its contribution to left ventricular (LV) filling is challenging because it requires simultaneous measurements of both LA and LV volumes. The functional relationship between LA conduit function and the severity of diastolic dysfunction remains controversial. We studied the role of LA conduit function in maintaining LV filling in advanced diastolic dysfunction.
UNASSIGNED: We performed volumetric and flow analyses of LA function across the spectrum of LV diastolic dysfunction, derived from a set of consecutive patients undergoing multiphasic cardiac computed tomography scanning (n=489). From LA and LV time-volume curves, we calculated 3 volumetric components: (1) early passive emptying volume; (2) late active (booster) volume; and (3) conduit volume. Results were prospectively validated on a group of patients with severe aortic stenosis (n=110).
UNASSIGNED: The early passive filling progressively decreased with worsening diastolic function (P<0.001). The atrial booster contribution to stroke volume modestly increases with impaired relaxation (P=0.021) and declines with more advanced diastolic function (P<0.001), thus failing to compensate for the reduction in early filling. The conduit volume increased progressively (P<0.001), accounting for 75% of stroke volume (interquartile range, 63-81%) with a restrictive filling pattern, compensating for the reduction in both early and booster functions. Similar results were obtained in patients with severe aortic stenosis. The pulmonary artery systolic pressure increased in a near-linear fashion when the conduit contribution to stroke volume increased above 60%. Maximal conduit flow rate strongly correlated with mitral E-wave velocity (r=0.71; P<0.0001), indicating that the increase in mitral E wave in diastolic dysfunction represents the increased conduit flow.
UNASSIGNED: An increase in conduit volume contribution to stroke volume represents a compensatory mechanism to maintain LV filling in advanced diastolic dysfunction. The increase in conduit volume despite increasing LV diastolic pressures is accomplished by an increase in pulmonary venous pressure.
UNASSIGNED: We performed volumetric and flow analyses of LA function across the spectrum of LV diastolic dysfunction, derived from a set of consecutive patients undergoing multiphasic cardiac computed tomography scanning (n=489). From LA and LV time-volume curves, we calculated 3 volumetric components: (1) early passive emptying volume; (2) late active (booster) volume; and (3) conduit volume. Results were prospectively validated on a group of patients with severe aortic stenosis (n=110).
UNASSIGNED: The early passive filling progressively decreased with worsening diastolic function (P<0.001). The atrial booster contribution to stroke volume modestly increases with impaired relaxation (P=0.021) and declines with more advanced diastolic function (P<0.001), thus failing to compensate for the reduction in early filling. The conduit volume increased progressively (P<0.001), accounting for 75% of stroke volume (interquartile range, 63-81%) with a restrictive filling pattern, compensating for the reduction in both early and booster functions. Similar results were obtained in patients with severe aortic stenosis. The pulmonary artery systolic pressure increased in a near-linear fashion when the conduit contribution to stroke volume increased above 60%. Maximal conduit flow rate strongly correlated with mitral E-wave velocity (r=0.71; P<0.0001), indicating that the increase in mitral E wave in diastolic dysfunction represents the increased conduit flow.
UNASSIGNED: An increase in conduit volume contribution to stroke volume represents a compensatory mechanism to maintain LV filling in advanced diastolic dysfunction. The increase in conduit volume despite increasing LV diastolic pressures is accomplished by an increase in pulmonary venous pressure.
摘要：
■定量左心房（LA）导管功能及其对左心室（LV）充盈的贡献具有挑战性，因为它需要同时测量LA和LV体积。LA导管功能与舒张功能障碍严重程度之间的功能关系仍存在争议。我们研究了LA导管功能在维持晚期舒张功能障碍中的LV充盈中的作用。
■我们在左心室舒张功能障碍的范围内对LA功能进行了容积和流量分析，来自一组接受多相心脏计算机断层扫描的连续患者（n=489）。从LA和LV时间-体积曲线来看，我们计算了3种体积成分：（1）早期被动排空体积；（2）晚期主动（增压）体积；（3）导管体积。结果在一组严重主动脉瓣狭窄患者（n=110）中得到了前瞻性验证。
■随着舒张功能的恶化，早期被动充盈逐渐减少（P<0.001）。心房增压剂对每搏量的贡献随着舒张功能受损而适度增加(P=0.021)，随着舒张功能进展而下降(P<0.001)，因此无法弥补早期填充的减少。导管容积逐渐增加(P<0.001),占每搏输出量的75%(四分位数间距，63-81%)具有限制性填充模式，补偿早期和助推器功能的减少。在严重的主动脉瓣狭窄患者中也获得了类似的结果。当导管对每搏输出量的贡献增加到60％以上时，肺动脉收缩压以接近线性的方式增加。最大导管流速与二尖瓣E波速度密切相关(r=0.71;P<0.0001),表明舒张功能障碍中二尖瓣E波的增加代表导管流量的增加。
■导管容积对每搏输出量的增加代表了在晚期舒张功能障碍中维持左心室充盈的代偿机制。尽管LV舒张压增加，但导管体积增加是通过肺静脉压增加来实现的。
■我们在左心室舒张功能障碍的范围内对LA功能进行了容积和流量分析，来自一组接受多相心脏计算机断层扫描的连续患者（n=489）。从LA和LV时间-体积曲线来看，我们计算了3种体积成分：（1）早期被动排空体积；（2）晚期主动（增压）体积；（3）导管体积。结果在一组严重主动脉瓣狭窄患者（n=110）中得到了前瞻性验证。
■随着舒张功能的恶化，早期被动充盈逐渐减少（P<0.001）。心房增压剂对每搏量的贡献随着舒张功能受损而适度增加(P=0.021)，随着舒张功能进展而下降(P<0.001)，因此无法弥补早期填充的减少。导管容积逐渐增加(P<0.001),占每搏输出量的75%(四分位数间距，63-81%)具有限制性填充模式，补偿早期和助推器功能的减少。在严重的主动脉瓣狭窄患者中也获得了类似的结果。当导管对每搏输出量的贡献增加到60％以上时，肺动脉收缩压以接近线性的方式增加。最大导管流速与二尖瓣E波速度密切相关(r=0.71;P<0.0001),表明舒张功能障碍中二尖瓣E波的增加代表导管流量的增加。
■导管容积对每搏输出量的增加代表了在晚期舒张功能障碍中维持左心室充盈的代偿机制。尽管LV舒张压增加，但导管体积增加是通过肺静脉压增加来实现的。
