Refine
Document Type
- Article (2)
Language
- English (2)
Has Fulltext
- yes (2)
Is part of the Bibliography
- no (2)
Keywords
- adenosine (1)
- dyssynchrony analysis (1)
- gadolinium (1)
- perfusion (1)
Institute
- Medizin (2)
BACKGROUND: Microvascular ischemia is one of the hallmarks of hypertrophic cardiomyopathy (HCM) and has been associated with poor outcome. However, myocardial fibrosis, seen on cardiovascular magnetic resonance (CMR) as late gadolinium enhancement (LGE), can be responsible for rest perfusion defects in up to 30% of patients with HCM, potentially leading to an overestimation of the ischemic burden. We investigated the effect of left ventricle (LV) scar on the total LV ischemic burden using novel high-resolution perfusion analysis techniques in conjunction with LGE quantification.
METHODS: 30 patients with HCM and unobstructed epicardial coronary arteries underwent CMR with Fermi constrained quantitative perfusion analysis on segmental and high-resolution data. The latter were corrected for the presence of fibrosis on a pixel-by-pixel basis.
RESULTS: High-resolution quantification proved more sensitive for the detection of microvascular ischemia in comparison to segmental analysis. Areas of LGE were associated with significant reduction of myocardial perfusion reserve (MPR) leading to an overestimation of the total ischemic burden on non-corrected perfusion maps. Using a threshold MPR of 1.5, the presence of LGE caused an overestimation of the ischemic burden of 28%. The ischemic burden was more severe in patients with fibrosis, also after correction of the perfusion maps, in keeping with more severe disease in this subgroup.
CONCLUSIONS: LGE is an important confounder in the assessment of the ischemic burden in patients with HCM. High-resolution quantitative analysis with LGE correction enables the independent evaluation of microvascular ischemia and fibrosis and should be used when evaluating patients with HCM.
Aims: We sought to describe perfusion dyssynchrony analysis specifically to exploit the high temporal resolution of stress perfusion CMR. This novel approach detects differences in the temporal distribution of the wash-in of contrast agent across the left ventricular wall.
Methods and results: Ninety-eight patients with suspected coronary artery disease (CAD) were retrospectively identified. All patients had undergone perfusion CMR at 3T and invasive angiography with fractional flow reserve (FFR) of lesions visually judged >50% stenosis. Stress images were analysed using four different perfusion dyssynchrony indices: the variance and coefficient of variation of the time to maximum signal upslope (V-TTMU and C-TTMU) and the variance and coefficient of variation of the time to peak myocardial signal enhancement (V-TTP and C-TTP). Patients were classified according to the number of vessels with haemodynamically significant CAD indicated by FFR <0.8. All indices of perfusion dyssynchrony were capable of identifying the presence of significant CAD. C-TTP >10% identified CAD with sensitivity 0.889, specificity 0.857 (P < 0.0001). All indices correlated with the number of diseased vessels. C-TTP >12% identified multi-vessel disease with sensitivity 0.806, specificity 0.657 (P < 0.0001). C-TTP was also the dyssynchrony index with the best inter- and intra-observer reproducibility. Perfusion dyssynchrony indices showed weak correlation with other invasive and non-invasive measurements of the severity of ischaemia, including FFR, visual ischaemic burden, and MPR.
Conclusion: These findings suggest that perfusion dyssynchrony analysis is a robust novel approach to the analysis of first-pass perfusion and has the potential to add complementary information to aid assessment of CAD.