Coronary microvascular dysfunction is related to abnormalities in myocardial structure and function in cardiac amyloidosis.

Coronary microvascular dysfunction is related to abnormalities in myocardial structure and function in cardiac amyloidosis.
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DOI:
10.1016/j.jchf.2014.03.009
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发表时间:
2014-08
期刊:
JACC. Heart failure
影响因子:
--
通讯作者:
Falk R
Falk R
中科院分区:
其他
文献类型:
--
作者:
Dorbala S;Vangala D;Bruyere J Jr;Quarta C;Kruger J;Padera R;Foster C;Hanley M;Di Carli MF;Falk R

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我们试图验证冠状动脉微血管功能在心脏淀粉样变性患者中受损的假设。心力型心绞痛常见于心脏淀粉样变性患者,即使没有心外膜冠状动脉疾病(CAD)。本研究前瞻性纳入31名受试者,包括21名确诊无心外膜CAD的心脏淀粉样变性患者和10名高血压左心室肥厚(LVH)患者。所有受试者均接受休息和血管舒张剂应激N-13氨正电子发射断层扫描和二维超声心动图检查。测量静息和充血高峰时左室心肌血流(MBF),计算冠状动脉血流储备(CFR)(峰值应激MBF /静息MBF)。与LVH组相比,淀粉样蛋白组表现出较低的静止MBF(0.59±0.15 vs. 0.88±0.23 ml/g/min, P = 0.004)、应激MBF(0.85±0.29 vs. 1.85±0.45 vs. ml/min/g, P < 0.0001)、CFR(1.19±0.38 vs. 2.23±0.88,P < 0.0001)和较高的最小冠状动脉阻力(111±40 vs. 70±19 mmhg / ml/g/min, P = 0.004)。值得注意的是,几乎所有的淀粉样蛋白受试者(> 95%)表现出显著降低的峰值应激MBF (< 1.3 mL/g/min)。在多变量线性回归分析中,淀粉样变诊断、左室体积增加和年龄是冠状动脉血管扩张功能受损的唯一独立预测因素。即使没有心外膜CAD,冠状动脉微血管功能障碍在心脏淀粉样变性患者中也非常普遍,这可能解释了他们的心绞痛症状。针对淀粉样变的特异性治疗是否能改善淀粉样变患者的冠状动脉血管舒缩,还需要进一步的研究。
We sought to test the hypothesis that coronary microvascular function is impaired in subjects with cardiac amyloidosis. Effort angina is common in subjects with cardiac amyloidosis even in the absence of epicardial coronary artery disease (CAD). Thirty one subjects were prospectively enrolled in this study including 21 subjects with definite cardiac amyloidosis without epicardial CAD and 10 subjects with hypertensive left ventricular hypertrophy (LVH). All subjects underwent rest and vasodilator stress N-13 ammonia positron emission tomography and 2D echocardiography. Global LV myocardial blood flow (MBF) was quantified at rest and during peak hyperemia, and coronary flow reserve (CFR) was computed (peak stress MBF / rest MBF) adjusting for rest rate pressure product. Compared to the LVH group, the amyloid group showed lower rest MBF (0.59 ± 0.15 vs. 0.88 ± 0.23 ml/g/min, P = 0.004), stress MBF (0.85 ± 0.29 vs. 1.85 ± 0.45 vs. ml/min/g, P < 0.0001), CFR (1.19 ± 0.38 vs. 2.23 ± 0.88, P < 0.0001), and higher minimal coronary vascular resistance (111 ± 40 vs. 70 ± 19 mm Hg/mL/g/min, P = 0.004). Of note, almost all amyloid subjects (> 95%) demonstrated significantly reduced peak stress MBF (< 1.3 mL/g/min). In multivariable linear regression analyses, a diagnosis of amyloidosis, increased LV mass and age were the only independent predictors of impaired coronary vasodilator function. Coronary microvascular dysfunction is highly prevalent in subjects with cardiac amyloidosis even in the absence of epicardial CAD, and may explain their anginal symptoms. Further study is required to understand whether specific therapy directed at amyloidosis may improve coronary vasomotion in amyloidosis.
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