Spatial Relationship Between Coronary Microvascular Dysfunction and Delayed Contrast Enhancement in Patients with Hypertrophic Cardiomyopathy

¹ Department of Clinical Physiopathology—Nuclear Medicine Unit, Azienda Ospedaliera Universitaria Careggi, Florence, Italy
² Regional Referral Center for Myocardial Diseases, Azienda Ospedaliera Universitaria Careggi, Florence, Italy
³ Division of Cardiology, Ospedale Versilia, Lido di Camaiore, Italy
⁴ Centre for Magnetic Resonance, Azienda Ospedaliera Universitaria Careggi, Florence, Italy
⁵ Medical Research Council Clinical Sciences Centre, Hammersmith Hospital, Imperial College, London, United Kingdom

^* To whom correspondence should be addressed. E-mail: r.sciagra{at}dfc.unifi.it.

	Abstract

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 = -0.37, P < 0.0001) and directly correlated with hMBF (Spearman = 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.

Key Words: coronary microvascular dysfunction, fibrosis, hyperthrophic cardiomyopathy, myocardial blood flow, positron emission tomography

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