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In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
Published on: February 16, 2016
Spatial relationship between coronary microvascular dysfunction and delayed contrast enhancement in patients with
Barbara Sotgia1, Roberto Sciagrà, Iacopo Olivotto
1Department of Clinical Physiopathology-Nuclear Medicine Unit, Azienda Ospedaliera Universitaria Careggi, Florence, Italy.
Insights
Coronary microvascular dysfunction is linked to myocardial fibrosis in hypertrophic cardiomyopathy (HCM). Reduced hyperemic myocardial blood flow (hMBF) in segments with delayed contrast enhancement (DCE) suggests a causative role.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Medical Physics
Background:
- Hypertrophic cardiomyopathy (HCM) is associated with myocardial fibrosis.
- The relationship between coronary microvascular dysfunction and fibrosis in HCM requires further clarification.
- Assessing hyperemic myocardial blood flow (hMBF) and delayed contrast enhancement (DCE) can provide insights into myocardial health.
Purpose of the Study:
- To investigate the spatial relationship between coronary microvascular dysfunction and myocardial fibrosis in HCM.
- To compare hMBF measured by PET with DCE extent detected by MRI in HCM patients.
Main Methods:
- 34 patients with HCM underwent PET for hMBF measurement using (13)N-labeled ammonia and dipyridamole-induced hyperemia.
- MRI was used to assess DCE and systolic thickening.
- Myocardial segments were categorized based on DCE presence (transmural/nontransmural) and proximity to DCE areas (contiguous/remote).
Main Results:
- Segments with DCE showed significantly lower hMBF compared to segments without DCE.
- Transmural DCE segments had lower hMBF than nontransmural DCE segments.
- Segments without DCE but contiguous to DCE areas exhibited reduced hMBF, similar to nontransmural DCE segments.
- Systolic thickening was inversely correlated with DCE transmurality and directly correlated with hMBF.
Conclusions:
- Reduced hMBF is observed in myocardial segments with DCE in HCM patients.
- The extent of DCE and hMBF are correlated with systolic thickening.
- Coronary microvascular dysfunction in segments adjacent to fibrotic areas suggests a potential causative role in the development of myocardial fibrosis in HCM.
Unlabelled:
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.
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