在容量超负荷性心肌肥大大鼠模型中，低冠状动脉灌注压与心内膜纤维化有关。

Guido Maria Carolina, Koike Márcia Kiyomi, Frimm Clovis de Carvalho

Laboratory of Medical Investigation 51, Hospital das Clínicas, Faculty of Medicine, University of São Paulo, São Paulo, SP, Brazil.

Rev Hosp Clin Fac Med Sao Paulo. 2004 Oct;59(5):228-35. doi: 10.1590/s0041-87812004000500002. Epub 2004 Oct 29.

UNLABELLED

Left ventricular hypertrophy following volume overload is regarded as an example of cardiac remodeling without increased fibrosis accumulation. However, infarction is associated with increased fibrosis within the noninfarcted, hypertrophied myocardium, particularly in the subendocardial regions. It is conceivable to suppose that, as also occurs postinfarction, low coronary driving pressure may also interfere with accumulation of myocardial fibrosis following aortocaval fistula.

PURPOSE

To investigate the role of acute hemodynamic changes in subsequent deposition of cardiac fibrosis in response to aortocaval fistula.

METHOD

Aortocaval fistula were created in 4 groups of Wistar rats that were followed over 4 and 8 weeks: aortocaval fistula 4 and aortocaval fistula 8 (10 rats each) and their respective controls (sham-operated controls - Sh), Sh4 and Sh8 (8 rats each). Hemodynamic measurements were performed 1 week after surgery. Hypertrophy and fibrosis were quantified by myocyte diameter and collagen volume fraction at the end of follow up.

RESULT

Compared with Sh4 and Sh8, pulse pressure, left ventricular end-diastolic pressure, and +dP/dt were higher in aortocaval fistula 4 and aortocaval fistula 8, but -dP/dt was similar. Coronary driving pressure (mm Hg), used as an estimate of perfusion pressure, was lower in aortocaval fistula 8 (52.6 +/- 4.1) than in Sh8 (100.8 +/- 1.3), but comparable between aortocaval fistula 4 (50.0 +/- 8.9) and Sh4 (84.8 +/- 2.3). Myocyte diameter was greater in aortocaval fistula 8, whereas interstitial and subendocardial fibrosis were greater in aortocaval fistula 4 and aortocaval fistula 8. Coronary driving pressure correlated inversely and independently with subendocardial fibrosis (r(2) = .86, P <.001), whereas left ventricular systolic pressure (r(2) = 0.73, P = .004) and end-diastolic pressure (r(2) = 0.55, P = 012) correlated positively and independently with interstitial fibrosis.

CONCLUSION

Coronary driving pressure falls and ventricular pressures increase early after aortocaval fistula and are associated with subsequent myocardial fibrosis deposition.

未标记

容量超负荷后的左心室肥厚被视为心脏重塑的一个例子，且无纤维化积累增加。然而，梗死与非梗死、肥厚心肌内的纤维化增加有关，尤其是在心内膜下区域。可以设想，正如心肌梗死后的情况一样，低冠状动脉驱动压也可能干扰主动脉腔静脉瘘后心肌纤维化的积累。

目的

研究急性血流动力学变化在主动脉腔静脉瘘后心脏纤维化后续沉积中的作用。

方法

在4组Wistar大鼠中制造主动脉腔静脉瘘，并对其进行4周和8周的跟踪观察：主动脉腔静脉瘘4周组和主动脉腔静脉瘘8周组（每组10只大鼠）及其各自的对照组（假手术对照组 - Sh），Sh4和Sh8（每组8只大鼠）。在手术后1周进行血流动力学测量。在随访结束时，通过心肌细胞直径和胶原容积分数对肥厚和纤维化进行量化。

结果

与Sh4和Sh8相比，主动脉腔静脉瘘4周组和主动脉腔静脉瘘8周组的脉压、左心室舒张末期压力和 +dP/dt 较高，但 -dP/dt 相似。用作灌注压估计值的冠状动脉驱动压（mmHg），在主动脉腔静脉瘘8周组（52.6±4.1）低于Sh8（100.8±1.3），但在主动脉腔静脉瘘4周组（50.0±8.9）和Sh4（84.8±2.3）之间相当。主动脉腔静脉瘘8周组的心肌细胞直径更大，而主动脉腔静脉瘘4周组和主动脉腔静脉瘘8周组的心内膜下纤维化更严重。冠状动脉驱动压与心内膜下纤维化呈负相关且独立相关（r² = 0.86，P <.001），而左心室收缩压（r² = 0.73，P =.004）和舒张末期压力（r² = 0.55，P = 0.012）与间质纤维化呈正相关且独立相关。