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

Barbara Sotgia, Roberto Sciagrà, Iacopo Olivotto, Giancarlo Casolo, Luigi Rega, Irene Betti, Alberto Pupi, Paolo G. Camici, Franco Cecchi

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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 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.

Original languageEnglish
Pages (from-to)1090-1096
Number of pages7
JournalJournal of Nuclear Medicine
Volume49
Issue number7
DOIs
Publication statusPublished - Jul 1 2008

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Hypertrophic Cardiomyopathy
Fibrosis
Dipyridamole
Hyperemia
Ammonia

Keywords

  • Coronary microvascular dysfunction
  • Fibrosis
  • Hyperthrophic cardiomyopathy
  • Myocardial blood flow
  • Positron emission tomography

ASJC Scopus subject areas

  • Radiological and Ultrasound Technology

Cite this

Spatial relationship between coronary microvascular dysfunction and delayed contrast enhancement in patients with hypertrophic cardiomyopathy. / Sotgia, Barbara; Sciagrà, Roberto; Olivotto, Iacopo; Casolo, Giancarlo; Rega, Luigi; Betti, Irene; Pupi, Alberto; Camici, Paolo G.; Cecchi, Franco.

In: Journal of Nuclear Medicine, Vol. 49, No. 7, 01.07.2008, p. 1090-1096.

Research output: Contribution to journalArticle

Sotgia, Barbara ; Sciagrà, Roberto ; Olivotto, Iacopo ; Casolo, Giancarlo ; Rega, Luigi ; Betti, Irene ; Pupi, Alberto ; Camici, Paolo G. ; Cecchi, Franco. / Spatial relationship between coronary microvascular dysfunction and delayed contrast enhancement in patients with hypertrophic cardiomyopathy. In: Journal of Nuclear Medicine. 2008 ; Vol. 49, No. 7. pp. 1090-1096.
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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 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.",
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AU - Sotgia, Barbara

AU - Sciagrà, Roberto

AU - Olivotto, Iacopo

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AU - Rega, Luigi

AU - Betti, Irene

AU - Pupi, Alberto

AU - Camici, Paolo G.

AU - Cecchi, Franco

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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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