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How We Do CMR Perfusion

How We Do CMR Perfusion. Robert Manka, Rolf Gebker, Eike Nagel German Heart Institute Berlin and www.cmr-academy.com Created October 2007 for SCMR

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How We Do CMR Perfusion

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  1. How We Do CMR Perfusion Robert Manka, Rolf Gebker, Eike Nagel German Heart Institute Berlin and www.cmr-academy.com Created October 2007 for SCMR This presentation posted for members of scmr as an educational guide – it represents the views and practices of the author, and not necessarily those of SCMR.

  2. Perfusion • The occurrence of myocardial perfusion deficits is a very sensitive indicator of ischemia in the presence of significant coronary artery stenoses. • Most perfusion defects occur during stress, such as pharmacological vasodilation. • Adenosine is a safe and well tolerated pharmacological stress agent. • In-plane resolution of 2-3 mm allows separate visualization of the endo- and epicardial layers of the left ventricle.

  3. Pharmacological Agent • Stressor agent: • Adenosine: i.v. 140 mcg/kg/min (preferable concentration 5mg/ml) - A potent vasodilator of most vascular beds, except for hepatic and renal arterioles. It exerts its pharmacological effect through the activation of purine A1 and A2 cell-surface adenosine receptors - Half-life 4-10 seconds • Antidote: • Adenosine infusion should be discontinued • Aminophylline i.v (250mg slowly injected under ECG monitoring) • Patient instruction: • No caffeine (tea, coffee, chocolate) • No aminophyline or nitrates for 24 hours

  4. Adenosine- Side-Effects • Mild-to-moderate reduction in systolic, diastolic and mean arterial blood pressure (< 10 mmHg) with a reflex increase in heart rate. • Some patients complain about chest pain, which is rather nonspecific and does not reliably indicate the presence of CAD. • Direct depressant effect on the SA and AV nodes transient first-, second- and third-degree AV block and sinus bradycardia have been reported in 2.8%, 4.1% and 0.8% of patients. • Increases in minute ventilation, reduction in arterial PCO2 and respiratory alkalosis. • Approximately 14% of patients complain of dyspnea.

  5. Contraindication for Adenosine Myocardial infarction <3 Days Unstable angina pectoris Asthma or severe obstruktive pulmonary disease AV-block >IIa Claustrophobia Non compatible biometallic implants (pacemaker/AICD) Caution Stenotic valvular disease Autonomic dysfunction Cerebrovascular insufficiency Termination criteria Persistent or symptomatik AV-block Significant drop in systolic pressure (>20 mmHg) Persistent or symptomatic hypotension Severe respiratory difficulty Contraindications/Termination

  6. Scanner environment • The pts lies in the supine position • 1.5 or 3 Tesla (T) whole body scanner • Gradient strength 30 mT/m, slew rate 150 mT/m/ms • 5 element cardiac synergy coil • Multichannel ECG (Vector-ECG)

  7. Contrast Agents and Injection Scheme • Bolus with a dosage of 0.05 mmol/kg bw of an extracellular Gd-based CA (dose may be lower with Gd-DTPA-BMA) • Injection speed of 4 ml/s is used at the German Heart Institute Berlin • The bolus is followed by a 20 ml saline flush using the same injection rate to facilitate a compact bolus passage • We recommend the use of an automatic infusion system • Two 18 gauge venflons for separate administration of the stress agent and CA

  8. Imaging Procedure • Cine wall motion imaging of the heart at rest, perfusion imaging under vasodilator stress, and finally delayed enhancement imaging • Examination time may vary between 40-75 minutes • Breathhold should be performed during expiration to ensure reproducible slice geometry • First is a about 6 to 10 seconds during baseline acquisition of myocardial signal intensity. • Then the patient is asked to inhale and exhale once more and to hold his breath as long as possible. Right before starting this breathhold command the contrast bolus is administered. • The patient should stop breathing at least for 15 to 20 seconds resulting in a fixed slice geometry during the first-pass of the contrast agent

  9. Survey • Transversal • Single-angulated view • Double-angulated view Perfusion Flowchart • Resting wall motion • Short axis (apical, mid, basal slice) • 4 chamber/3 chamber • 2 chamber Carefully exclude any wraparound If necessary enlarge field of view • Perfusion test scan • Slice geometry identical to (4) • acquisition of 5 dynamic images RR, rhythm & respiratory monitoring Adenosine infusion (140 µg/kg/min) over 4 minutes Inject gadolinium 0.05 mmol/kg • Stress Perfusion • Start imaging (60 dynamics) after • 4 minutes of adenosine infusion Stop adenosine infusion wait 10 min Inject gadolinium 0.05 mmol/kg • Rest Perfusion • Repeat (8) without adenosine • infusion Inject gadolinium 0.1 mmol/kg wait 10 min • Delayed Enhancement • Determine optimal inversion time

  10. RV contrast uptake: 2nd breath hold command LV contrast uptake First pass myocardial contrast uptake Second pass myocardial contrast uptake Scanning procedure start scan contrast injection 2nd breathhold free breathing 1stbreathhold 1 breathing cycle scanning interval Baseline 5 dyn, start contrast injection

  11. Pulse Sequences • T1-weighted • In-plane resolution of 2-3 mm to separately visualize the endo- and epicardial layers. • We use a balanced SSFP-technique which shows a higher peak enhancement and superior image quality compared with other sequences (T1-GrE, GrE-EPI).

  12. Monitoring requirements • Heart rate & rhythm: continuously • Blood pressure: every minute • Pulse oximetry: not required when the vector-ECG used • Symptoms: continuously • Defibrillator • All medications for emergency treatment

  13. Analysis of MR Perfusion Studiescover 16 out of 17 myocardial segments • Visual Analysis • For routine clinical use, we do a qualitative analysis by visual comparison of the contrast enhancement in different myocardial regions (see next slide) • Quantitative • Absolute Tissue Perfusion (Unit: ml/g/min) (requires mathematical modeling) • Semiquantification (stress induced change of upslope)

  14. Abnormalities: Signal intensity Pattern and Location Dark regions arising from the subendocardium with usually irregular intramyocardial border or with completely transmural extent. Dynamic myocardial filling pattern Initially, slow or missing enhancement persistent over a few dynamics with consecutive signal intensity increase starting from the defects epicardial border. Comparison Stress vs. Rest If a regional defect is found in the stress scan, but not in the rest scan, inducible ischemia is confirmed. Regional persistence of the perfusion deficit shows myocardial scar. Visual assessment of regional myocardial perfusion Evaluate the equatorial slice first, then check whether the suspected perfusion defect can be followed in corresponding segments of the apical or basal slice

  15. Report • Data is reported for 16/17 segments (segment 1 – 16). The apical segment (17) is not visualized with 3 short axis views. • Perfusion defects are reported with their transmurality (transmural defect vs. subendocardial defect). • Perfusion images are compared to cine and late enhancement images

  16. Stress-Perfusion RV contrast uptake Early mycardial contrast uptake Late myocardial contrast uptake Baseline

  17. RV contrast uptake LV contrast uptake Myocardial contrast uptake Baseline Stress- Perfusion Rest- Perfusion Viability and coronary angiography

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