The CMR examinations were performed with a 1.5 Tesla Siemens Avanto scanner (Siemens AG, Erlangen, Germany). For dynamic stress, all patients received an adenosine infusion of 140 μg/kg body weight/minute. After 3 minutes of infusion, a contrast injection with 0.05 mmol/kg dimeglumine gadopentetate (Dotarem – Guerbet, Paris, France) at a flow rate of 5 mL/s was started. Simultaneously, the stress pCMR image acquisition was initiated. The patient was asked to stop breathing when contrast arrived in right ventricle. The image acquisition lasted for 120 heartbeats with three short-axis slices sampled on each heartbeat. Adenosine infusion was stopped after approx. 50 heartbeats. We applied the following imaging parameters: Saturation recovery segmented gradient echo pulse sequence with TR/TE/TI of 167/1.11/120 ms, 108 × 144 matrix, 340–430 mm field of view, 1 NEX, 8 mm slice thickness.
After 10 minutes, rest of the pCMR imaging was performed without adenosine infusion, but with otherwise identical contrast parameters and pulse sequence parameters.
After another 10 minutes, LGE imaging was performed with 3 long-axis slices and short-axis slices that covered the entire left ventricle. Imaging parameters are phase sensitive gradient echo pulse sequence triggered on every second heart beat in diastolic phase with typical TR/TE/TI of 800/3.33/300 ms, 156 × 256 matrix, 330 mm field of view, 1 NEX, 8 mm slice thickness.
For CMR, a 16 segment score sheet, where the apical part had been excluded from a 17 segment sheet,6 (link) was filled in for all patients. Each segment was assessed for perfusion and late gadolinium enhancement (LGE) pathology. The diagnosis of perfusion defect was based on a visual analysis with comparison between regions to identify relative hypo-perfusion according to current guidelines from the Society of Cardiovascular Magnetic Resonance.7 (link) A comparison between stress and rest images was performed to identify inducible perfusion defects and artifacts. Perfusion defects in regions with LGE were only interpreted as reversible if the extent of the perfusion defect was clearly beyond the extent of LGE.
For evaluation of ischemia and infarct, a score was assigned to each segment indicating a normal (0), borderline (1), or pathologic (2) finding. The final overall score for LGE was deemed pathologic if at least one of the segments was classified as pathologic with a high degree of confidence. Similarly, the final score for pCMR was deemed pathologic if there was at least one segment with a high confidence of transmural pathology or two adjacent segments with high confidence of subendocardial pathology.8 (link)
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