1350374 - A critical case for CMR guided pre-chemotherapy cardiac risk stratification

A 73-year-old gentleman with diffuse large B cell testicular lymphoma and recent orchidectomy was referred to the cardio-oncology team for optimisation pre anthracycline chemotherapy. He gave a history of crescendo angina with multiple cardiovascular risk factors including hypertension, hypercholesterolaemia and chronic kidney disease. ECG showed normal sinus rhythm with poor R wave progression. An adenosine stress perfusion cardiovascular magnetic resonance (CMR) scan was requested to investigate further for ischaemia.

Diagnostic Techniques and Their Most Important Findings:

CMR performed using a 1.5T Siemens Aera showed normal biventricular sizes and systolic function (left ventricular ejection fraction of 59%) with no regional wall motion abnormalities. Adenosine was infused at 140mcg/kg/minute for 2 minutes with suboptimal heart rate response. The dose of adenosine was increased to 175mcg/kg/minute for a further 3 minutes with a heart rate increment from 58 to 67bpm and the patient developed symptoms of breathlessness and flushing. On stress perfusion imaging, there were near circumferential adenosine induced perfusion defects in the basal, mid and apical slices that were most pronounced subendocardially. Quantitative automated inline myocardial perfusion mapping demonstrated poor global stress myocardial blood flow (MBF) - mean flow 0.64ml/min/g, with only the basal and mid anterolateral wall spared. Good splenic switch off indicated adequate stress. Mean rest MBF (acquired 7 minutes post stress) was paradoxically increased at 0.78ml/kg/min, resulting in very low global myocardial perfusion reserve (0.81). There was no late gadolinium enhancement, and the impression was of critical 3 vessel coronary artery disease without infarction.

The decision was made to hold anthracycline based chemotherapy and proceed to urgent invasive coronary angiography which showed critical distal left mainstem stenosis extending into the ostium of the left anterior descending (LAD) and left circumflex (LCx) arteries with further moderate-severe lesions in the mid LAD and proximal LCx.

The patient was treated with emergency coronary artery bypass grafting without complication.  LV function immediately post CABG remained mildly impaired, and following multidisciplinary team discussion, the patient was treated with a non-anthracycline-based chemotherapy regimen. 

Learning Points from this Case: Quantitative perfusion CMR has added value over conventional qualitative stress perfusion analysis, enabling differentiation between severe multi-vessel myocardial ischaemia from pharmacological under-stress. It has clear value pre chemotherapy for risk stratification, guiding clinical decision making both of cancer and cardiovascular treatments. In this case, the severity of the ischaemia warranted urgent coronary intervention to be prioritised over cancer therapy and guided cancer treatment choice.