Relationship of delayed enhancement by magnetic resonance to myocardial perfusion by positron emission tomography in hypertrophic cardiomyopathy.
Relationship of delayed enhancement by magnetic resonance to myocardial perfusion by positron emission tomography in hypertrophic cardiomyopathy.
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DOI：
10.1161/circimaging.112.000110
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发表时间：
2013-03-01
期刊：
影响因子：
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通讯作者：
Abraham TP
中科院分区：
文献类型：
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作者：
Bravo PE;Zimmerman SL;Luo HC;Pozios I;Rajaram M;Pinheiro A;Steenbergen C;Kamel IR;Wahl RL;Bluemke DA;Bengel FM;Abraham MR;Abraham TP
磁共振（CMR）上出现延迟增强（DE）与肥厚型心肌病（HCM）的临床结局较差相关。我们研究了DE对CMR和HCM心肌缺血的关系。HCM患者（n=47）接受CMR以评估DE和血管扩张剂应力氨正电子发射断层扫描（PET），以定量心肌血流量（MBF）和冠状动脉血流储备（CFR）。还评估了局部心肌灌注（rMP）的总差异评分（SDS）。DE组患者（n=35）的LV壁厚度更大（2.09 ± 0.44 vs 1.78 ± 0.34 cm; P 0.03）。DE阳性患者的负荷MBF（2.25 ± 0.46 vs.1.78 ± 0.43ml/min/g，P = 0.01）和CFR（2.78 ± 0.32 vs.2.01 ± 0.52，P < 0.001）显著降低。DE组SDS评分（7.3 ± 6.6）显著高于对照组（0.9 ± 1.4）（P < 0.0001）。18例DE患者（51%）CFR < 2.00，而DE阴性患者无CFR < 2.00（P <0.0001）。CMR和PET显示31例患者视觉上一致的DE和rMP异常，9例患者无DE和灌注缺陷。4例DE阳性患者显示正常rMP，3例DE阴性患者（心尖）rMP异常。我们发现，在大多数研究的患者中，CMR的DE与微血管功能之间存在密切关系。然而，一小部分患者在没有灌注异常的情况下发生DE，表明微血管功能障碍和缺血不是HCM患者DE的唯一原因。
Presence of delayed enhancement (DE) on magnetic resonance (CMR) is associated with worse clinical outcomes in hypertrophic cardiomyopathy (HCM). We investigated the relationship between DE on CMR, and myocardial ischemia in HCM. HCM patients (n=47) underwent CMR for assessment of DE and vasodilator stress ammonia positron emission tomography (PET) to quantify myocardial blood flow (MBF) and coronary flow reserve (CFR). The summed difference score (SDS) for regional myocardial perfusion (rMP) was also assessed. Patients in the DE-group (n=35) had greater LV wall thickness (2.09 ± 0.44 vs. 1.78 ± 0.34 cm; P 0.03). Stress MBF (2.25 ± 0.46 vs. 1.78 ± 0.43 ml/min/g, P = 0.01), and CFR (2.78 ± 0.32 vs. 2.01 ± 0.52, P < 0.001) were significantly lower in DE-positive patients. SDS (7.3 ± 6.6 vs. 0.9 ± 1.4, P < 0.0001) was significantly higher in patients with DE. A CFR < 2.00 was seen in 18 patients (51%) with DE, but in none of the DE-negative patients (P <0.0001). CMR and PET showed visually concordant DE and rMP abnormalities in 31 patients and absence of DE and perfusion defects in 9 patients. Four DE-positive patients demonstrated normal rMP, and 3 DE-negative patients had (apical) rMP abnormalities. We found a close relationship between DE by CMR and microvascular function in the majority of the patients studied. However, a small proportion of patients had DE in the absence of perfusion abnormalities, suggesting that microvascular dysfunction and ischemia are not the sole causes of DE in HCM patients.