Sotgia Barbara, Sciagrà Roberto, Olivotto Iacopo, Casolo Giancarlo, Rega Luigi, Betti Irene, Pupi Alberto, Camici Paolo G, Cecchi Franco
Department of Clinical Physiopathology-Nuclear Medicine Unit, Azienda Ospedaliera Universitaria Careggi, Florence, Italy.
J Nucl Med. 2008 Jul;49(7):1090-6. doi: 10.2967/jnumed.107.050138. Epub 2008 Jun 13.
To clarify the spatial relationship between coronary microvascular dysfunction and myocardial fibrosis in hypertrophic cardiomyopathy (HCM), we compared the measurement of hyperemic myocardial blood flow (hMBF) by PET with the extent of delayed contrast enhancement (DCE) detected by MRI.
In 34 patients with HCM, PET was performed using (13)N-labeled ammonia during hyperemia induced by intravenous dipyridamole. DCE and systolic thickening were assessed by MRI. Left ventricular myocardial segments were classified as with DCE, either transmural (DCE-T) or nontransmural (DCE-NT), and without DCE, either contiguous to DCE segments (NoDCE-C) or remote from them (NoDCE-R).
In the group with DCE, hMBF was significantly lower than in the group without DCE (1.81 +/- 0.94 vs. 2.13 +/- 1.11 mL/min/g; P < 0.001). DCE-T segments had lower hMBF than did DCE-NT segments (1.43 +/- 0.52 vs. 1.91 +/- 1 mL/min/g, P < 0.001). Similarly, NoDCE-C segments had lower hMBF than did NoDCE-R (1.98 +/- 1.10 vs. 2.29 +/- 1.10 mL/min/g, P < 0.01) and had no significant difference from DCE-NT segments. Severe coronary microvascular dysfunction (hMBF in the lowest tertile of all segments) was more prevalent among NoDCE-C than NoDCE-R segments (33% vs. 24%, P < 0.05). Systolic thickening was inversely correlated with percentage transmurality of DCE (Spearman rho = -0.37, P < 0.0001) and directly correlated with hMBF (Spearman rho = 0.20, P < 0.0001).
In myocardial segments exhibiting DCE, hMBF is reduced. DCE extent is inversely correlated and hMBF directly correlated with systolic thickening. In segments without DCE but contiguous to DCE areas, hMBF is significantly lower than in those remote from DCE and is similar to the value obtained in nontransmural DCE segments. These results suggest that increasing degrees of coronary microvascular dysfunction might play a causative role for myocardial fibrosis in HCM.
为阐明肥厚型心肌病（HCM）中冠状动脉微血管功能障碍与心肌纤维化之间的空间关系，我们比较了PET测量的充血性心肌血流量（hMBF）与MRI检测到的延迟强化（DCE）范围。
对34例HCM患者，在静脉注射双嘧达莫诱导充血期间，使用（13）N标记的氨进行PET检查。通过MRI评估DCE和收缩期增厚情况。左心室心肌节段分为有DCE的节段，即透壁性（DCE-T）或非透壁性（DCE-NT），以及无DCE的节段，即与DCE节段相邻（NoDCE-C）或远离DCE节段（NoDCE-R）。
在有DCE的组中，hMBF显著低于无DCE的组（1.81±0.94 vs. 2.13±1.11 mL/min/g；P<0.001）。DCE-T节段的hMBF低于DCE-NT节段（1.
