Department of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN, USA.
Department of Cardiology, Miyazaki Medical Association Hospital, Funado, Shinbeppu-chou, Miyazaki city, Miyazaki, Japan.
Eur Heart J Cardiovasc Imaging. 2019 Apr 1;20(4):396-406. doi: 10.1093/ehjci/jey177.
Mechanisms of chronic ischaemic mitral regurgitation (IMR) are well-characterized by apically tethered leaflet caused by papillary muscles (PMs) displacement and adynamic mitral apparatus. We investigated the unique geometry and dynamics of the mitral apparatus in first acute myocardial infarction (MI) by using quantified 3D echocardiography.
We prospectively performed 3D echocardiography 2.3 ± 1.8 days after first MI, in 174 matched patients with (n = 87) and without IMR (n = 87). 3D echocardiography of left ventricular (LV) volumes and of mitral apparatus dynamics throughout cardiac cycle was quantified. Similar mitral quantification was obtained at chronic post-MI stage (n = 44). Mechanistically, acute IMR was associated with larger and flatter annulus (area 9.29 ± 1.74 cm2 vs. 8.57 ± 1.94 cm2, P = 0.002, saddle shape 12.7 ± 4.5% vs. 15.0 ± 4.6%, P = 0.001), and larger tenting (length 6.36 ± 1.78 mm vs. 5.60 ± 1.55 mm, P = 0.003) but vs. chronic MI, mitral apparatus displayed smaller alterations (all P < 0.01) and annular size, PM movement remained dynamic (all P < 0.01). Specific to acute IMR, without PM apical displacement (P > 0.70), greater separation (21.7 ± 4.9 mm vs. 20.0 ± 3.4 mm, P = 0.01), and widest angulation of PM (38.4 ± 6.2° for moderate vs. 33.5 ± 7.3° for mild vs. 31.4 ± 6.3° for no-IMR, P = 0.0009) wider vs. chronic MI (P < 0.01).
3D echocardiography of patients with first MI provides insights into unique 4D dynamics of the mitral apparatus in acute IMR. Mitral apparatus remained dynamic in acute MI and distinct IMR mechanism in acute MI is not PM displacement seen in chronic IMR but separation and excess angulation of PM deforming the mitral valve, probably because of sudden-onset regional wall motion abnormality without apparent global LV remodelling. This specific mechanism should be considered in novel therapeutic strategies for IMR complicating acute MI.
通过观察乳头肌位移导致的瓣叶顶端牵曳以及二尖瓣装置动力不足,对慢性缺血性二尖瓣反流(IMR)的机制进行了深入研究。我们使用定量 3D 超声心动图来研究首次急性心肌梗死(MI)时二尖瓣装置的独特几何形状和动力学特性。
我们前瞻性地对 174 例首次 MI 后 2.3±1.8 天的患者进行了 3D 超声心动图检查,其中 87 例有 IMR(n=87),87 例无 IMR(n=87)。对左心室(LV)容积和整个心动周期内二尖瓣装置动力学的 3D 超声心动图进行了定量分析。在慢性 MI 后阶段(n=44)获得了类似的二尖瓣定量数据。在机制上,急性 IMR 与更大和更平坦的瓣环(面积 9.29±1.74 cm2 与 8.57±1.94 cm2,P=0.002,鞍形 12.7±4.5%与 15.0±4.6%,P=0.001)和更大的瓣叶膨出(长度 6.36±1.78 mm 与 5.60±1.55 mm,P=0.003)有关,但与慢性 MI 相比,二尖瓣装置的变化较小(均 P<0.01),瓣环大小、PM 运动仍然活跃(均 P<0.01)。对于急性 IMR,无 PM 顶端移位(P>0.70),PM 分离更大(21.7±4.9 mm 与 20.0±3.4 mm,P=0.01),PM 最大成角更大(中重度 38.4±6.2°与轻度 33.5±7.3°与无 IMR 31.4±6.3°,P=0.0009),且更宽(与慢性 MI 相比,P<0.01)。
首次 MI 患者的 3D 超声心动图为急性 IMR 时二尖瓣装置的独特 4D 动力学提供了新的见解。急性 MI 时二尖瓣装置仍然具有动力性,急性 IMR 的独特机制不是慢性 IMR 中所见的 PM 位移,而是 PM 的分离和过度成角导致二尖瓣变形,可能是由于突然出现的区域性壁运动异常,而没有明显的整体 LV 重构。在急性 MI 并发 IMR 的新型治疗策略中,应考虑这种特定的机制。