心脏X综合征：微循环障碍导致心肌灌注缺损

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心血管磁共振显示负荷诱导的心肌灌注缺损与心脏X综合征患者冠脉微血管功能障碍的关系

背景：尽管大多数心脏X综合征患者存在心脏微血管功能障碍，心脏X综合征患者缺血原因尚存在争议。目前尚没有研究探讨心肌灌注不良与冠脉微血管功能障碍是否存在区域相关性。

方法：18名心脏X综合征患者（平均年龄58 ± 7岁，男性7名）和10名健康对照者（平均年龄54 ± 8岁，男性4名）分别在静息状态下和多巴胺负荷试验峰值状态（最大剂量40 礸/kg/min）下的接受钆增强心血管磁共振心肌灌注扫描。通过经胸高分辨率超声多普勒测量腺苷峰值状态和静息状态下的冠脉血流速度比值以评价冠状动脉左前降支血流对腺苷（140 礸/kg/min，90秒）的反应。

结果：在多巴胺负荷试验峰值状态下，10名心脏X综合征（56％）患者被检测出心脏磁共振下可逆性灌注缺损，但对照组患者中没有检测出（P＝0.004）。心脏X综合征患者冠脉左前降支血流对腺苷的反应低于对照组(2.03 ± 0.63 vs. 3.29 ± 1.0, p = 0.0004)。心脏X综合征患者中，左前降支区域存在多巴胺负荷诱导的灌注缺损的患者冠脉血流对腺苷的反应比这一区域没有灌注缺损的患者低（1.69 ± 0.5 vs. 2.31 ± 0.6, p = 0.01）。冠脉血流对腺苷的反应与心血管磁共振下多巴胺负荷试验诱导的左前降支区域灌注缺损评分有显著的相关性(r = –0.45, p = 0.019)。

结论：我们的数据显示心脏X综合征患者左前降支区域同时存在心血管磁共振下多巴胺负荷试验诱导的心肌灌注缺损和冠脉血流对腺苷的反应降低，因此以强有力的证据证明冠脉微循环障碍导致心肌灌注不良存在于心脏X综合征患者。

Relation Between Stress-Induced Myocardial Perfusion Defects on Cardiovascular Magnetic Resonance and Coronary Microvascular Dysfunction in Patients With Cardiac Syndrome X

Gaetano A. Lanza, MD*,*, Antonino Buffon, MD*, Alfonso Sestito, MD*, Luigi Natale, MD, Gregory A. Sgueglia, MD*, Leda Galiuto, MD, FACC*, Fabio Infusino, MD*, Luca Mariani, MD*, Antonio Centola, MD* and Filippo Crea, MD, FACC*
* Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Rome, Italy
Istituto di Radiologia, Università Cattolica del Sacro Cuore, Rome, Italy.

Objectives: The purpose of this study was to investigate whether a direct relation can be demonstrated between myocardial perfusion defects detected during dobutamine stress test (DST) by cardiovascular magnetic resonance (CMR) and impairment of coronary microvascular dilatory function in patients with cardiac syndrome X (CSX).

Background: Despite the fact that coronary microvascular dysfunction has been shown in most patients with CSX, the ischemic origin of CSX remains debated. No previous study assessed whether a strict relation exists between abnormalities in myocardial perfusion and coronary microvascular dysfunction in CSX patients.

Methods: Eighteen CSX patients (mean age 58 ± 7 years, 7 men) and 10 healthy control subjects (mean age 54 ± 8 years, 4 men) underwent myocardial perfusion study by gadolinium-enhanced CMR at rest and at peak DST (maximal dose 40 礸/kg/min). Coronary flow response (CFR) to adenosine (140 礸/kg/min in 90 s) in the left anterior descending (LAD) coronary artery was assessed by high-resolution transthoracic echo-Doppler and expressed as the ratio between coronary flow velocity at peak adenosine and at rest.

Results: At peak DST, reversible perfusion defects on CMR were found in 10 CSX patients (56%) but in none of the control subjects (p = 0.004). The CFR to adenosine in the LAD coronary artery was lower in CSX patients than in control subjects (2.03 ± 0.63 vs. 3.29 ± 1.0, p = 0.0004). The CSX patients with DST-induced myocardial perfusion defects in the LAD territory on CMR had a lower CFR to adenosine compared with those without perfusion defects in the LAD territory (1.69 ± 0.5 vs. 2.31 ± 0.6, p = 0.01). A significant correlation was found in CSX patients between CFR to adenosine and a DST perfusion defect score on CMR in the LAD territory (r = –0.45, p = 0.019).

Conclusions: Our data concurrently show DST-induced myocardial perfusion defects on CMR and reduced CFR in the LAD coronary artery territory in CSX patients, thus giving strong evidence that a dysfunction of coronary microcirculation resulting in myocardial perfusion abnormalities is present in these patients.