Department of Cardiovascular Medicine, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Department of Cardiovascular Medicine, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
J Am Soc Echocardiogr. 2017 Nov;30(11):1070-1080. doi: 10.1016/j.echo.2017.06.023. Epub 2017 Aug 16.
Left ventricular (LV) filling following atrial contraction generates LV myocardial stretch that propagates from base to apex with a speed proportional to myocardial elasticity. The aim of this study was to test the hypothesis that intrinsic velocity propagation of myocardial stretch (iVP) would be altered in patients with valvular disease and chronic LV pressure overload or volume overload, which may adversely affect mechanical properties of the LV tissue. A second aim was to compare iVP with flow propagation velocity in the chamber.
Sixty subjects were prospectively recruited: 20 with severe aortic stenosis (AS), 20 with severe degenerative mitral regurgitation (MR), and 20 normal control subjects. LV iVP was measured using ultrahigh-frame rate tissue Doppler (350-460 frames/sec) and flow propagation velocity by color flow M-mode imaging. Follow-up data (up to 2 years) were retrieved from medical records.
iVP was highest in patients with AS (2.2 ± 0.7 m/sec), intermediate in those with MR (1.6 ± 0.5 m/sec), and lowest in control subjects (1.4 ± 0.2 m/sec; P < .0001). Fourteen patients with AS and eight with MR had iVP > 1.8 m/sec. Overall, iVP correlated with age, LV morphology, severity of aortic valve obstruction, and measures of LV preload and afterload. At follow-up, patients with high iVP had lower survival free of major adverse cardiac events (P = .002). Flow propagation velocity was similar between groups and correlated poorly with iVP (r = 0.26, P = .10).
A significant number of patients with severe AS and severe MR had rapid transmission of myocardial stretch, indicating increased myocardial stiffness. This information was not conveyed by measurement of flow propagation. Larger studies are needed to investigate the clinical utility of this novel measurement.
心房收缩后左心室(LV)充盈会产生 LV 心肌拉伸,这种拉伸从基底向心尖传播,其传播速度与心肌弹性呈比例关系。本研究旨在验证以下假设:在瓣膜性疾病和慢性 LV 压力或容量超负荷患者中,心肌拉伸固有速度传播(iVP)会发生改变,这可能会对 LV 组织的机械性能产生不利影响。第二个目的是比较 iVP 与腔室内的血流传播速度。
前瞻性招募 60 名受试者:20 名严重主动脉瓣狭窄(AS)患者,20 名严重退行性二尖瓣反流(MR)患者和 20 名正常对照者。使用超高帧率组织多普勒(350-460 帧/秒)测量 LV iVP,使用彩色血流 M 型成像测量血流传播速度。从病历中检索随访数据(最长 2 年)。
AS 患者的 iVP 最高(2.2±0.7 m/sec),MR 患者次之(1.6±0.5 m/sec),对照组最低(1.4±0.2 m/sec;P<.0001)。14 名 AS 患者和 8 名 MR 患者的 iVP>1.8 m/sec。总体而言,iVP 与年龄、LV 形态、主动脉瓣梗阻严重程度以及 LV 前负荷和后负荷的测量值相关。在随访中,iVP 较高的患者主要不良心脏事件无复发的生存率较低(P=.002)。各组之间的血流传播速度相似,与 iVP 的相关性较差(r=0.26,P=.10)。
相当数量的严重 AS 和严重 MR 患者的心肌拉伸传播速度较快,表明心肌僵硬度增加。这种信息无法通过测量血流传播来传达。需要进行更大规模的研究来探讨这种新测量方法的临床应用价值。