Aim The aim of this study was to assess the ability of stress T1 mapping to detect perfusion abnormalities and inducible ischaemia in hypertrophic cardiomyopathy (HCM).

Background Impaired perfusion reserve in HCM has been shown to be an independent predictor of adverse cardiovascular outcomes. CMR perfusion imaging currently requires the administration of gadolinium based contrast agents, which are contraindicated in allergy and renal failure, making non-contrast methods such as T1 mapping a safer and more affordable alternative. As adenosine stress T1 mapping has been shown to detect inducible ischaemia in patients with coronary disease, we hypothesised that stress T1 may be used to detect perfusion abnormalities in HCM with reasonable accuracy and T1 reactivity correlates with impaired myocardial blood flow (MBF) reserve and global longitudinal strain (GLS).

Method 62 subjects with no known history of coronary disease (31 controls and 31 HCM patients) underwent CMR at 3T including cine imaging, tagging, rest and stress (adenosine 140 mcg/kg/min) blood oxygen level dependent imaging (BOLD), T1 mapping (ShMOLLI), first-pass perfusion imaging and late gadolinium imaging (LGE). Rest and stress T1 values from mid ventricular slice were derived and T1 reactivity determined. ^1,2 MBF was estimated using Fermi function de-convolution method as previous described.^3,4

Results Baseline characteristics are listed in Table 1. T1 reactivity was significantly reduced in regions of interest (ROI) with LGE and perfusion defects compared to the remaining ‘unaffected’ myocardium (Figure 1). Using a diagnostic threshold of 3.5% on ROC analysis for detecting impaired MBF in HCM, T1 reactivity had a sensitivity and specificity of 82% and 88% respectively (AUC 0.894, p<0.01) (Figure 1). Adenosine induced rise in MBF, T1 reactivity, oxygenation and global longitudinal strain (GLS) were significantly reduced in HCM compared with controls (p<0.01 for all comparisons) Stress T1 reactivity moderately correlated with MBF reactivity (r=0.55, p<0.01) and GLS (r=−0.44, p<0.01).

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Abstract 011 Figure 1

A. Comparison of T1 reactivity profiles for ‘Unaffected’ myocardium versus regions with abnormal perfusion versus LGE; B. ROC curve depicting sensitivity and specificity of stress T1 reactivity to predict perfusion deficits in HCM.

Conclusions

1. Stress T1 mapping is capable of distinguishing regions with perfusion defects versus normal perfusion in HCM without the need of contrast.

2. Stress T1 reactivity, MBF reactivity, oxygenation and GLS were significantly reduced in HCM compared to controls.

References

1. . Liu A, Wijesurendra RS, Francis JM, et al. Adenosine Stress and Rest T1 Mapping Can Differentiate Between Ischaemic, Infarcted, Remote, and Normal Myocardium Without the Need for Gadolinium Contrast Agents. JACC Cardiovasc Imaging2016;9(1):27–36.

2. Mahmod M, Piechnik SK, Levelt E, et al. Adenosine stress native T1 mapping in severe aortic stenosis: evidence for a role of the intravascular compartment on myocardial T1 values. J Cardiovasc Magn Reson 2014;16:92.

3. Jerosch-Herold M. Quantification of myocardial perfusion by cardiovascular magnetic resonance. J Cardiov Magn Reson 2010;12(1):57.

4. McCommis KS, Zhang H, Goldstein TA, et al. Myocardial Blood Volume Is Associated with Myocardial Oxygen Consumption: An Experimental Study with CMR in a Canine Model. JACC Cardiovascular imaging 2009;2(11):1313–1320.