Jones Noah J, Bates Eric R, Chetcuti Stanley J, Lederman Robert J, Grossman P Michael
Cardiovascular Center, University of Michigan, Ann Arbor, Michigan 48109, USA.
Catheter Cardiovasc Interv. 2006 Sep;68(3):429-34. doi: 10.1002/ccd.20697.
We sought to determine the hemodynamic significance of intermediate RAS by measuring translesional systolic pressure gradients (TSPG), using a pressure-sensing guidewire at baseline and after acetylcholine (ACh) induced hyperemia, following selective renal artery angiography.
Renal artery stenosis (RAS) is a cause of reversible hypertension and nephropathy. Stenting effectively relieves RAS, however improvement in blood pressure control or renal function is variable and unpredictable. Hemodynamic significance is usually present with RAS when diameter stenosis is >75%, but is less predictable in intermediate (30%-75%) RAS.
Twenty-two patients (26 renal arteries) with uncontrolled hypertension underwent invasive hemodynamic assessment because of intermediate RAS, defined as radiocontrast angiographic diameter stenosis (DS) between 30% and 75% (quantitative DS was measured prospectively). Translesional pressure gradients were measured using a 0.014" pressure-sensing wire. Hyperemia was induced by administration of intrarenal ACh.
Visual and measured angiographic lesion severity did not correlate with TSPG either at baseline (visual DS, R(2) = 0.091, P = 0.13; measured DS, R(2) = 0.124, P = 0.07) or with hyperemia (visual DS, R(2) = 0.057, P = 0.24; measured DS, R(2) = 0.101, P = 0.12). Baseline and maximal hyperemic gradient did correlate (R(2) = 0.567; P < 0.05). Pharmacological provocation produced a significant increase in TSPG (mean; baseline, 18 +/- 21 vs. hyperemia, 34 +/- 41 mm Hg; P < 0.05). A hemodynamically significant lesion (TSPG > 20 mm Hg) was found in 14/26 (54%) arteries (13 patients); 13 (60%) patients subsequently underwent renal artery stenting for hemodynamically significant RAS. At follow-up (at least 30 days), there was a significant decrease in systolic blood pressure (mean; 167 +/- 24 vs. 134 +/- 19 mm Hg; P < 0.001).
Intrarenal administration of ACh induces hyperemia and can be used to unmask resistive renal artery lesions. Gradient measurement and induced hyperemia may be warranted in the invasive assessment of intermediate renal artery stenoses, rather than relying on stenosis severity alone. Further study is needed to determine whether translesional pressure gradients and pharmacological provocation predict clinical benefit after renal artery stenting.
我们试图通过在选择性肾动脉血管造影术的基线期和乙酰胆碱(ACh)诱发充血后,使用压力感应导丝测量跨病变收缩压梯度(TSPG),来确定中度肾动脉狭窄(RAS)的血流动力学意义。
肾动脉狭窄(RAS)是可逆性高血压和肾病的一个病因。支架置入术可有效缓解RAS,然而血压控制或肾功能的改善却不尽相同且难以预测。当直径狭窄>75%时,RAS通常具有血流动力学意义,但在中度(30%-75%)RAS中则较难预测。
22例(26条肾动脉)高血压控制不佳的患者因中度RAS接受了有创血流动力学评估,中度RAS定义为放射造影血管直径狭窄(DS)在30%至75%之间(前瞻性测量定量DS)。使用0.014英寸的压力感应导丝测量跨病变压力梯度。通过肾内注射ACh诱发充血。
无论是在基线期(视觉DS,R² = 0.091,P = 0.13;测量DS,R² = 0.124,P = 0.07)还是充血期(视觉DS,R² = 0.057,P = 0.24;测量DS,R² = 0.101,P = 0.12),视觉和测量的血管造影病变严重程度均与TSPG无关。基线期和最大充血梯度存在相关性(R² = 0.567;P < 0.05)。药物激发使TSPG显著升高(平均值;基线期,18±21 vs.充血期,34±41 mmHg;P < 0.05)。在14/26(54%)条动脉(13例患者)中发现了具有血流动力学意义的病变(TSPG>20 mmHg);13例(60%)患者随后因具有血流动力学意义的RAS接受了肾动脉支架置入术。在随访期(至少30天),收缩压显著降低(平均值;167±24 vs. 134±19 mmHg;P < 0.001)。
肾内注射ACh可诱发充血,并可用于揭示有阻力的肾动脉病变。在中度肾动脉狭窄的有创评估中,可能有必要进行梯度测量和诱发充血,而不是仅依赖狭窄严重程度。需要进一步研究以确定跨病变压力梯度和药物激发是否能预测肾动脉支架置入术后的临床获益。