Zile M R, Tomita M, Ishihara K, Nakano K, Lindroth J, Spinale F, Swindle M, Carabello B A
Gazes Cardiac Research Institute, Department of Medicine, Medical University of South Carolina, Charleston 29425.
Circulation. 1993 Apr;87(4):1378-88. doi: 10.1161/01.cir.87.4.1378.
Mitral regurgitation (MR) causes an augmentation in left ventricular (LV) diastolic function, increasing early diastolic filling rate and decreasing LV stiffness. Whether these changes in diastolic function persist, return to normal, or become abnormal after mitral valve replacement (MVR) is unknown.
Simultaneous LV echocardiography and catheterization studies were performed in six dogs in the baseline state (baseline), 3 months after creation of MR (chronic MR), and 3 months after MVR. Chronic MR caused LV dilation (end-diastolic dimension increased from 4.5 +/- 0.1 cm in baseline to 5.8 +/- 0.1 cm in chronic MR, p < 0.05) and eccentric LV hypertrophy (LV-to-body weight ratio increased from 3.6 +/- 0.2 g/kg in baseline to 4.9 +/- 0.4 g/kg in chronic MR, p < 0.05). Chronic MR caused an increase in LV early diastolic filling rate (peak rate of increase in minor-axis dimension increased from 11 +/- 1 cm/sec in baseline to 18 +/- 1 cm/sec in chronic MR, p < 0.05), did not change the time constant of myocardial relaxation (tau was 31 +/- 4 msec in baseline and 30 +/- 2 msec in chronic MR), and caused a decrease in the modulus of regional chamber stiffness from 7.7 +/- 1.2 in baseline to 2.4 +/- 0.03 in chronic MR, p < 0.05. MVR caused the resolution of LV dilation (end-diastolic dimension returned to normal [4.8 +/- 0.2 cm]), but three months after MVR, regression of LV hypertrophy was incomplete (LV-to-body weight ratio remained elevated [4.4 +/- 0.5 g/kg]). After MVR, LV early diastolic filling rate (8 +/- 1 cm/sec), the relaxation time constant (31 +/- 2 msec), chamber stiffness (7.1 +/- 1.8), myocardial stiffness (11.2 +/- 3.1), and LV end-diastolic pressure (8 +/- 1 mm Hg) returned to normal.
The enhanced diastolic function seen in chronic MR returned to normal after correction of the chronic volume overload by MVR.
二尖瓣反流（MR）导致左心室（LV）舒张功能增强，增加舒张早期充盈率并降低左心室僵硬度。二尖瓣置换术（MVR）后，这些舒张功能的变化是持续存在、恢复正常还是变得异常尚不清楚。
对6只犬在基线状态（基线）、MR形成后3个月（慢性MR）和MVR后3个月进行同步左心室超声心动图和导管检查。慢性MR导致左心室扩张（舒张末期内径从基线时的4.5±0.1 cm增加到慢性MR时的5.8±0.1 cm，p<0.05）和离心性左心室肥厚（左心室与体重比从基线时的3.6±0.2 g/kg增加到慢性MR时的4.9±0.4 g/kg，p<0.05）。慢性MR导致左心室舒张早期充盈率增加（短轴维度峰值增加率从基线时的11±1 cm/秒增加到慢性MR时的18±1 cm/秒，p<0.05），未改变心肌松弛时间常数（基线时τ为31±4毫秒，慢性MR时为30±2毫秒），并导致局部心室僵硬度模量从基线时的7.7±1.2降至慢性MR时的2.4±0.03，p<0.05。MVR使左心室扩张得到缓解（舒张末期内径恢复正常[4.8±0.2 cm]），但MVR后3个月，左心室肥厚的消退不完全（左心室与体重比仍升高[4.4±0.5 g/kg]）。MVR后，左心室舒张早期充盈率（8±1 cm/秒）、松弛时间常数（31±2毫秒）、心室僵硬度（7.1±1.8）、心肌僵硬度（11.2±3.1）和左心室舒张末期压力（8±1 mmHg）恢复正常。
通过MVR纠正慢性容量超负荷后，慢性MR中所见的增强舒张功能恢复正常。
