Spatial relationship between coronary microvascular dysfunction and delayed contrast enhancement in patients with hypertrophic cardiomyopathy.
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).


CONCLUSIONS
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.
Department of Clinical Physiopathology-Nuclear Medicine Unit, Azienda Ospedaliera Universitaria Careggi, Florence, Italy.
Barbara
B
Sotgia
Roberto
R
Sciagrà
Iacopo
I
Olivotto
Giancarlo
G
Casolo
Luigi
L
Rega
Irene
I
Betti
Alberto
A
Pupi
Paolo G
PG
Camici
Franco
F
Cecchi
D000293:Adolescent; D000328:Adult; D000368:Aged; D000641:Ammonia; D002312:Cardiomyopathy, Hypertrophic / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology; D003287:Contrast Media; D003326:Coronary Circulation; D004176:Dipyridamole; D005260:Female; D005355:Fibrosis; D006801:Humans; D006940:Hyperemia / Q000139:chemically induced / Q000503:physiopathology; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D009590:Nitrogen Radioisotopes; D049268:Positron-Emission Tomography
D003287:Contrast Media; D009590:Nitrogen Radioisotopes; D004176:Dipyridamole; D000641:Ammonia