FOCAL COMPENSATORY ENLARGEMENT OF HUMAN ARTERIES IN RESPONSE TO PROGRESSIVE ATHEROSCLEROSIS - IN-VIVO DOCUMENTATION USING INTRAVASCULAR ULTRASOUND
FOCAL COMPENSATORY ENLARGEMENT OF HUMAN ARTERIES IN RESPONSE TO PROGRESSIVE ATHEROSCLEROSIS - IN-VIVO DOCUMENTATION USING INTRAVASCULAR ULTRASOUND
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DOI：
10.1161/01.cir.89.6.2570
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发表时间：
1994-06-01
期刊：
影响因子：
37.8
通讯作者：
ISNER, JM
中科院分区：
文献类型：
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作者：
LOSORDO, DW;ROSENFIELD, K;ISNER, JM
背景先前的尸检研究表明，动物模型和患者的动脉粥样硬化动脉呈代偿性增大。关于这些变化的结论是基于对一组受试者的病变动脉和另一组受试者的正常动脉的尺寸进行比较而得出的。该方法考虑了潜在的混杂变量，如人口统计学和其他疾病状态，这些变量也可能对动脉大小产生影响。方法和结果应用血管内超声，我们研究了20例接受外周血管介入治疗的患者股浅动脉62个成对的、相邻的正常和病变部位。使用基于计算机的图像分析系统进行形态评估。测量动脉管腔横截面积、动脉粥样硬化斑块和动脉外缘。然后比较这些维度，以确定进行性动脉粥样硬化对动脉形态的影响。管腔横截面积从正常节段的21.1+/-2.2 mm(2)减少到邻近动脉粥样硬化节段的16.7+/-0.8 mm(2)(P=0.0001)。同样，最小管腔直径从5.7±0.2 mm减小到5.0±0.1 mm(2)，最大管腔直径从6.2+/-0.2 mm减小到5.7+/-0.2 mm(2)。在这些部位，正常和病变节段的总动脉面积分别为32.9±1.6 mm(2)和37.9±1.9 mm(2)(P=0.0001)。动脉最小直径和最大直径增加相似(分别为7.3+/-0.2至7.7+/-0.2 mm(2)[P=0.0015]和7.6+/-0.2至8.3+/-0.2 mm(2)[P=0.0001])。回归分析显示斑块横截面积与总动脉面积相关(R=.70，P=.0001)。这种代偿机制导致动脉大小增加，与血管中积累的斑块横截面积成比例。血管内超声显示，这一过程是动脉粥样硬化狭窄的离散部位的局灶性代偿性扩大，紧邻动脉较小的正常区域。
Background Previous postmortem studies have demonstrated compensatory enlargement of atherosclerotic arteries in animal models and patients. Conclusions regarding these changes were drawn based on a comparison of the dimensions of diseased arteries in one group of subjects with the dimensions of normal arteries in another group. This method admits potential confounding variables, such as demographics and other disease states, which might also have an impact on arterial size.Methods and Results Using intravascular ultrasound, we studied a total of 62 paired, adjacent normal and diseased sites in the superficial femoral arteries of 20 patients undergoing peripheral vascular interventions. Morphological assessment was performed using a computer-based image analysis system. Measurements were made of the cross-sectional area of the arterial lumen, the atherosclerotic plaque, and the outer border of the artery. These dimensions were then compared to determine the effects of progressive atherosclerosis on arterial morphology. Luminal cross-sectional area decreased from 21.1+/-2.2 mm(2) in normal segments to 16.7+/-0.8 mm(2) (P=.0001) in adjacent atherosclerotic segments. Similarly, minimal luminal diameter decreased from 5.7+/-0.2 to 5.0+/-0.1 mm(2), and maximal luminal diameter decreased from 6.2+/-0.2 to 5.7+/-0.2 mm(2). At these same sites, total arterial area was 32.9+/-1.6 and 37.9+/-1.9 mm(2) (P=.0001) in normal and diseased segments, respectively. Minimal and maximal arterial diameters demonstrated similar increases (7.3+/-0.2 to 7.7+/-0.2 mm(2) [P=.0015] and 7.6+/-0.2 to 8.3+/-0.2 mm(2) [P=.0001], respectively). Regression analysis disclosed correlation of the cross-sectional area of plaque to the total arterial area (R=.70, P=.0001).Conclusions Human arteries enlarge in response to progressive atherosclerosis. This compensatory mechanism results in an increase in arterial size that is proportionate to the cross-sectional area of plaque that has accumulated in the vessel. Intravascular ultrasound demonstrates that this process is focal compensatory enlargement at discrete sites of atherosclerotic narrowing immediately adjacent to more normal areas in which arterial size is smaller.