TY - JOUR
T1 - Spatial relationship between coronary microvascular dysfunction and delayed contrast enhancement in patients with hypertrophic cardiomyopathy
AU - Sotgia, Barbara
AU - Sciagrà, Roberto
AU - Olivotto, Iacopo
AU - Casolo, Giancarlo
AU - Rega, Luigi
AU - Betti, Irene
AU - Pupi, Alberto
AU - Camici, Paolo G.
AU - Cecchi, Franco
PY - 2008/7/1
Y1 - 2008/7/1
N2 - 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 13N-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 ρ = -0.37, P <0.0001) and directly correlated with hMBF (Spearman ρ = 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.
AB - 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 13N-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 ρ = -0.37, P <0.0001) and directly correlated with hMBF (Spearman ρ = 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.
KW - Coronary microvascular dysfunction
KW - Fibrosis
KW - Hyperthrophic cardiomyopathy
KW - Myocardial blood flow
KW - Positron emission tomography
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U2 - 10.2967/jnumed.107.050138
DO - 10.2967/jnumed.107.050138
M3 - Article
C2 - 18552138
AN - SCOPUS:46749099836
SN - 0161-5505
VL - 49
SP - 1090
EP - 1096
JO - Journal of Nuclear Medicine
JF - Journal of Nuclear Medicine
IS - 7
ER -