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.
METHODS: 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).
RESULTS: 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).
CONCLUSION: 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.