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Updated: Apr 25, 2026
In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
Published on: February 16, 2016
Coronary microvascular ischemia in hypertrophic cardiomyopathy - a pixel-wise quantitative cardiovascular magnetic
Insights
Quantitative cardiovascular magnetic resonance (CMR) perfusion imaging reveals localized microvascular dysfunction in hypertrophic cardiomyopathy (HCM). This technique identifies patients with potential myocardial ischemia due to impaired blood flow.
Area of Science:
- Cardiology
- Medical Imaging
- Physiology
Background:
- Microvascular dysfunction in hypertrophic cardiomyopathy (HCM) is linked to poor clinical outcomes.
- Quantitative cardiovascular magnetic resonance (CMR) perfusion imaging enables pixel-level myocardial blood flow (MBF) assessment.
Purpose of the Study:
- Investigate the spectrum of microvascular dysfunction in HCM using quantitative CMR perfusion imaging.
- Explore the relationship between microvascular dysfunction, myocardial fibrosis, and wall thickness in HCM patients.
Main Methods:
- Utilized CMR perfusion imaging during adenosine-induced hyperemia and at rest in 35 HCM patients.
- Quantified MBF pixel-by-pixel using Fermi-constrained deconvolution.
- Correlated MBF with late gadolinium enhancement (LGE) for fibrosis and regional wall thickness.
Main Results:
- Observed distinct endocardial and epicardial MBF patterns at rest and during stress.
- Identified 31% of patients with reduced stress MBF compared to resting values.
- Found significant inverse associations between hyperemic MBF, wall thickness, and fibrosis probability.
Conclusions:
- Pixel-wise quantitative CMR perfusion imaging effectively detects localized severe microvascular dysfunction in HCM.
- This imaging approach may identify patients at risk of myocardial ischemia.
Background:
Microvascular dysfunction in HCM has been associated with adverse clinical outcomes. Advances in quantitative cardiovascular magnetic resonance (CMR) perfusion imaging now allow myocardial blood flow to be quantified at the pixel level. We applied these techniques to investigate the spectrum of microvascular dysfunction in hypertrophic cardiomyopathy (HCM) and to explore its relationship with fibrosis and wall thickness.
Methods:
CMR perfusion imaging was undertaken during adenosine-induced hyperemia and again at rest in 35 patients together with late gadolinium enhancement (LGE) imaging. Myocardial blood flow (MBF) was quantified on a pixel-by-pixel basis from CMR perfusion images using a Fermi-constrained deconvolution algorithm. Regions-of-interest (ROI) in hypoperfused and hyperemic myocardium were identified from the MBF pixel maps. The myocardium was also divided into 16 AHA segments.
Results:
Resting MBF was significantly higher in the endocardium than in the epicardium (mean ± SD: 1.25 ± 0.35 ml/g/min versus 1.20 ± 0.35 ml/g/min, P<0.001), a pattern that reversed with stress (2.00 ± 0.76 ml/g/min versus 2.36 ± 0.83 ml/g/min, P<0.001). ROI analysis revealed 11 (31%) patients with stress MBF lower than resting values (1.05 ± 0.39 ml/g/min versus 1.22 ± 0.36 ml/g/min, P=0.021). There was a significant negative association between hyperemic MBF and wall thickness (β=-0.047 ml/g/min per mm, 95% CI: -0.057 to -0.038, P<0.001) and a significantly lower probability of fibrosis in a segment with increasing hyperemic MBF (odds ratio per ml/g/min: 0.086, 95% CI: 0.078 to 0.095, P=0.003).
Conclusions:
Pixel-wise quantitative CMR perfusion imaging identifies a subgroup of patients with HCM that have localised severe microvascular dysfunction which may give rise to myocardial ischemia.
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