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Figure 1

Schematic depiction of our standard stress perfusion CMR protocol.
Schematic depiction of our standard stress perfusion CMR protocol.

Figure 2

Short-axis mid-ventricular slices acquired during stress and rest, showing the splenic switch-off phenomenon, defined as a visible decrease in splenic signal intensity during adenosine stress as compared to rest (yellow arrow). During adenosine-induced hypotension, the splenic blood flow is reduced presumably due reactive sympathetic vasoconstriction. During stress, a perfusion defect is seen on the lateral wall (red arrow). This defect is no longer seen on rest perfusion acquisition. The yellow arrowhead indicates a dark-rim artifact which is the most common artifact seen in stress perfusion CMR.
Short-axis mid-ventricular slices acquired during stress and rest, showing the splenic switch-off phenomenon, defined as a visible decrease in splenic signal intensity during adenosine stress as compared to rest (yellow arrow). During adenosine-induced hypotension, the splenic blood flow is reduced presumably due reactive sympathetic vasoconstriction. During stress, a perfusion defect is seen on the lateral wall (red arrow). This defect is no longer seen on rest perfusion acquisition. The yellow arrowhead indicates a dark-rim artifact which is the most common artifact seen in stress perfusion CMR.

Figure 3

The final diagnosis after stress perfusion cardiovascular magnetic resonance.
The final diagnosis after stress perfusion cardiovascular magnetic resonance.

Figure 4

Stress Perfusion CMR in a 61-year-old patient with intermediate lesions on invasive coronary angiography, without a clinical history of myocardial infarction. Perfusion imaging acquired during adequate vasodilator stress (upper row) show a large perfusion defect in the right coronary (RCA) territory (basal infero-septum, inferior and infero-lateral walls, mid inferior and infero-lateral walls and apical inferior segment) (yellow arrowhead). The rest acquisition (middle row) shows no evidence of perfusion defect. Late Gadolinium imaging (lower row) shows a small subendocardial scar (hyperenhancement) in the RCA territory (red arrowheads). Of note, the stress perfusion defect extends well beyond the myocardial scar.
Stress Perfusion CMR in a 61-year-old patient with intermediate lesions on invasive coronary angiography, without a clinical history of myocardial infarction. Perfusion imaging acquired during adequate vasodilator stress (upper row) show a large perfusion defect in the right coronary (RCA) territory (basal infero-septum, inferior and infero-lateral walls, mid inferior and infero-lateral walls and apical inferior segment) (yellow arrowhead). The rest acquisition (middle row) shows no evidence of perfusion defect. Late Gadolinium imaging (lower row) shows a small subendocardial scar (hyperenhancement) in the RCA territory (red arrowheads). Of note, the stress perfusion defect extends well beyond the myocardial scar.

Figure 5

Stress perfusion CMR in a 70-year-old patient with a history of complex PCIs. His initial culprit lesion was a severe left main stenosis for which he was revascularized with a 2-stent technique. After one year, the stent on circumflex artery (Cx) had a severe ostial restenosis with chronic occlusion of the large ramus intermedius (RI). The Cx lesion was dilated with a DES but the RI could not be opened. Basal, mid and apical short axis slices acquired during maximal vasodilatory stress showing a perfusion defect in 3 myocardial segments: basal anterior, mid lateral and apical lateral wall respectively (yellow arrows). The topography of hypoperfused myocardium is compatible with the territory of the occluded intermediate ramus.
Stress perfusion CMR in a 70-year-old patient with a history of complex PCIs. His initial culprit lesion was a severe left main stenosis for which he was revascularized with a 2-stent technique. After one year, the stent on circumflex artery (Cx) had a severe ostial restenosis with chronic occlusion of the large ramus intermedius (RI). The Cx lesion was dilated with a DES but the RI could not be opened. Basal, mid and apical short axis slices acquired during maximal vasodilatory stress showing a perfusion defect in 3 myocardial segments: basal anterior, mid lateral and apical lateral wall respectively (yellow arrows). The topography of hypoperfused myocardium is compatible with the territory of the occluded intermediate ramus.

Figure 6

Stress perfusion CMR in a 60-year-old patient with intermediate lesions on invasive coronary angiography, with a dual chamber pacemaker implanted for intermittent AV block. During CMR examination, the pacemaker was set in DOO mode, 80 bpm. Basal, mid and apical short axis slices show the pacemaker right ventricular lead (yellow arrow) which does not induce any metallic artifacts. However, the pulse generator (red arrow), induces a significant artifact which precludes the optimal visualisation of the apical anterior segment only. Overall, the image quality permits reliable interpretation of the stress test.
Stress perfusion CMR in a 60-year-old patient with intermediate lesions on invasive coronary angiography, with a dual chamber pacemaker implanted for intermittent AV block. During CMR examination, the pacemaker was set in DOO mode, 80 bpm. Basal, mid and apical short axis slices show the pacemaker right ventricular lead (yellow arrow) which does not induce any metallic artifacts. However, the pulse generator (red arrow), induces a significant artifact which precludes the optimal visualisation of the apical anterior segment only. Overall, the image quality permits reliable interpretation of the stress test.

Clinical indications for which patients underwent stress perfusion CMR

Clinical indication Total (n=120) Positive test Negative test
Detection of ischaemia in patients with risk factors or atypical chest pain 36 (30%) 3 (8.33%) 32 (88.88%)
Etiology of DCM 4 (3.33%) 1 (25%) 3 (75%)
Detection of ischaemia in patients with history of MI or previous revascularisation 51 (42.5%) 11 (21.56%) 40 (78,43%)
Detection of functional significance of intermediate lesions 37 (30.83%) 9 (24,32%) 27 (72,97%)
Ventricular arrhytmia substrate detection 5 (4.16%) 0 5 (100%)

Clinical end electrocardiography data of the analyzed patients

Demographics (n=120)
Age, years 57 ± 11
Men 95 (79.1%)
BMI (kg/m2) 28.9 ± 3.6
Outpatient referral 48 (40%)
Cardiovascular risk factors (data available for 75 patients)
Hypertension 53 (70.67%)
Hypercholesterolemia 57 (76%)
Diabetes 19 (25.33%)
Tobacco use 33 (44%)
Median number of aggregated risk factors 2
Cardiovascular history
Previous non-invasive ischaemia testing 28 (23.33%)
Previous myocardial infarction 51 (42.5%)
ICA before CMR 77 (64.16%)
Number of affected vessels on ICA

0

1 vessel

2 vessels

3 vessels

6 (7.79%)

23 (29.87%)

22 (28.57%)

26 (33.76%)

History of PCI 40 (33.3%)
History of CABG 7 (5.83%)
ECG at the time of CMR
Sinus rhythm 113 (94%)
Atrial fibrillation 7 (6%)
Extrasystoles 8 (6.66%)
Narrow QRS 106 (88.33%)
LBBB 5 (4.16%)
RBBB 9 (7.5%)

Selected CMR findings

General CMR findings
Artifacts 4 (3.33%)
Extracardiac findings 34 (28,33%)
Efficient vasodilatory stress 113 (94.16%)
Positive stress test 21 (17.5%)
LV dimensions and function
LV motion abnormalities 44 (36,66%)
LV EDV (ml) 188.35 ± 59.09
LV EDVi (ml/m2) 92,68 ± 29.13
LV ESV (ml) 87.12 ± 55.34
LV SV 100.78 ± 24.78
LV EF 56.87 ± 13.52
LV myocardial mass (g/m2) 56.74 ± 15.21
Tissue characterization
Oedema 2 (1.66%)
Native T1 (ms) 982.60 ± 151.20
ECV (%) 25.71 ± 2.51
T2 (ms) 46.06 ± 2.56
Characterization of focal scars
Scar present 63 (52.5%)
Ischaemic scar 49 (40.83%)
Non-ischaemic scar 14(11.66%)
Number of scars

1 scar

2 scars

3 scars

49 (77.77%)

11 (17.46%)

3 (4.76%)

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