Key result
MyoTT differentiates HCM from controls with 0.93 AUC, outperforming native T1 and ECV mapping.
Why the study?
Coronary microvascular dysfunction occurs in non-ischemic cardiomyopathies with left-ventricular hypertrophy, prompting evaluation of the novel CMR parameter myocardial transit-time (MyoTT) to distinguish cardiac amyloidosis from other hypertrophic cardiomyopathies.
Does the novel CMR parameter MyoTT improve diagnostic accuracy in distinguishing cardiac amyloidosis from hypertrophic cardiomyopathy compared to native T1 and ECV?
Observational (n=60)
Blinded readers
No
Does the novel CMR parameter MyoTT improve diagnostic accuracy in distinguishing cardiac amyloidosis from hypertrophic cardiomyopathy compared to native T1 and ECV?
Effect estimate: AUC 0.93 (95% CI 0.81-1.00)
p-value: p=0.003
The novel CMR parameter MyoTT reflects coronary microvascular dysfunction and is superior to native T1 and ECV for differentiating HCM from controls, though inferior for diagnosing cardiac amyloidosis.
MyoTT may aid HCM detection on CMR; hypothesis-generating for amyloidosis differentiation pending validation.
BACKGROUND: Coronary microvascular dysfunction (CMD) is present in various non-ischemic cardiomyopathies and in particular in those with left-ventricular hypertrophy. This study evaluated the diagnostic value of the novel cardiovascular magnetic resonance (CMR) parameter "myocardial transit-time" (MyoTT) in distinguishing cardiac amyloidosis from other hypertrophic cardiomyopathies. METHODS: N = 20 patients with biopsy-proven cardiac amyloidosis (CA), N = 20 patients with known hypertrophic cardiomyopathy (HCM), and N = 20 control patients without relevant cardiac disease underwent dedicated CMR studies on a 1.5-T MR scanner. The CMR protocol comprised cine and late-gadolinium-enhancement (LGE) imaging as well as first-pass perfusion acquisitions at rest for MyoTT measurement. MyoTT was defined as the blood circulation time from the orifice of the coronary arteries to the pooling in the coronary sinus (CS) reflecting the transit-time of gadolinium in the myocardial microvasculature. RESULTS: MyoTT was significantly prolonged in patients with CA compared to both groups: 14.8 ± 4.1 s in CA vs. 12.2 ± 2.5 s in HCM (p = 0.043) vs. 7.2 ± 2.6 s in controls (p < 0.001). Native T1 and extracellular volume (ECV) were significantly higher in CA compared to HCM and controls (p < 0.001). Both parameters were associated with a higher diagnostic accuracy in predicting the presence of CA compared to MyoTT: area under the curve (AUC) for native T1 = 0.93 (95% confidence interval (CI) = 0.83-1.00; p < 0.001) and AUC for ECV = 0.95 (95% CI = 0.88-1.00; p < 0.001)-compared to the AUC for MyoTT = 0.76 (95% CI = 0.60-0.92; p = 0.008). In contrast, MyoTT performed better than all other CMR parameters in differentiating HCM from controls (AUC for MyoTT = 0.93; 95% CI = 0.81-1.00; p = 0.003 vs. AUC for native T1 = 0.69; 95% CI = 0.44-0.93; p = 0.20 vs. AUC for ECV = 0.85; 95% CI = 0.66-1.00; p = 0.017). CONCLUSION: The relative severity of CMD (measured by MyoTT) in relationship to extracellular changes (measured by native T1 and/or ECV) is more pronounced in HCM compared to CA-in spite of a higher absolute MyoTT value in CA patients. Hence, MyoTT may improve our understanding of the interplay between extracellular/intracellular and intravasal changes that occur in the myocardium during the disease course of different cardiomyopathies.
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Chatzantonis et al. (2020) conducted an observational in Cardiac amyloidosis and hypertrophic cardiomyopathy (n=60). Myocardial transit-time (MyoTT) measurement via CMR vs. Healthy controls and established CMR parameters (native T1, ECV) was evaluated on Diagnostic accuracy (AUC) of MyoTT for differentiating hypertrophic cardiomyopathy from controls (AUC 0.93, 95% CI 0.81-1.00, p=0.003). Myocardial transit-time (MyoTT) demonstrated high diagnostic accuracy (AUC 0.93) for differentiating hypertrophic cardiomyopathy from healthy controls, outperforming native T1 and ECV mapping.
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