McGinley Joseph C, Berretta Remus M, Bratinov George D, Dhar Sunil, Gaughan John P, Margulies Kenneth B
The Cardiovasc Res Center, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.
J Card Fail. 2005 Jun;11(5):343-50. doi: 10.1016/j.cardfail.2004.12.003.
Alterations in transmitral pressure, valve structure, subvalvular geometry, and abnormal myocardial function have all been implicated in the pathophysiology of functional/progressive mitral valve regurgitation (MR). In this study, we hypothesized that a relatively small structural lesion to the mitral valve apparatus predisposes to severe MR in the setting of progressive left ventricular dilation. While examining this hypothesis, an additional purpose of this study was to determine the extent of papillary muscle (PM) distortion and mitral annular dilation with increasing MR resulting from progressive dilated cardiomyopathy.
Mild MR was produced via a limited, fixed structural lesion to the mitral valve apparatus of 8 dogs (20 to 22 kg). Incremental tachypacing induced left ventricular dilation over an 8-month period. The pacer was deactivated and the dogs followed for an additional 6 weeks. Echocardiographic measurements demonstrated significant cardiac remodeling (left ventricular end diastolic diameter) and MR progression with a 54% increase in left ventricular end diastolic diameter and a 44% increase in MR jet area (P < .05). Tachypacing induced decreases in left ventricular ejection fraction recovered nearly to baseline levels by 6 weeks after pacing cessation. Nevertheless, left ventricular dilation persisted and MR remained severe after pacing cessation. There was a significant increase in the short axis PM segment length and PM angular separation from baseline (6.28 +/- 0.83 versus 4.02 +/- 0.56 cm and 99.7 +/- 2.6 versus 90.1 +/- 3.2 deg, respectively, P < .05) with no change in mitral annulus circumference (8.71 +/- 0.70 versus 8.15 +/- 0.35 cm, P = NS).
Progressive MR severity in nonischemic dilated cardiomyopathy resulted from changes in left ventricular shape and altered papillary muscle geometries and does not require mitral annulus dilation or a reduced left ventricular ejection fraction.
跨二尖瓣压力改变、瓣膜结构、瓣下结构几何形态以及心肌功能异常均与功能性/进行性二尖瓣反流（MR）的病理生理学相关。在本研究中，我们假设二尖瓣装置相对较小的结构性病变在左心室逐渐扩张的情况下易导致严重MR。在检验这一假设时，本研究的另一个目的是确定因进行性扩张型心肌病导致MR加重时乳头肌（PM）变形和二尖瓣环扩张的程度。
通过对8只犬（体重20至22千克）的二尖瓣装置造成有限的、固定的结构性病变来产生轻度MR。在8个月的时间里，通过递增性快速起搏诱导左心室扩张。停用起搏器后，对犬再随访6周。超声心动图测量显示心脏发生显著重塑（左心室舒张末期内径）以及MR进展，左心室舒张末期内径增加54%，MR反流束面积增加44%（P<0.05）。快速起搏导致左心室射血分数降低，在起搏停止后6周几乎恢复到基线水平。然而，起搏停止后左心室扩张持续存在，MR仍很严重。与基线相比，短轴PM段长度和PM角分离显著增加（分别为6.28±0.83对4.02±0.56厘米和99.7±2.6对90.1±3.2度，P<0.05），而二尖瓣环周长无变化（8.71±0.70对8.15±0.35厘米，P=无显著性差异）。
非缺血性扩张型心肌病中MR严重程度的进展是由左心室形状改变以及乳头肌几何形态改变所致，并不需要二尖瓣环扩张或左心室射血分数降低。
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