6 - Coronary microvascular dysfunction by quantitative stress perfusion mapping: a case

Description of Clinical Presentation: We present the case of a 61 year old female who presented to our outpatient rapid access chest pain clinic upon referral following presentation to the emergency department with intermediate risk chest pain, and a past history of poorly controlled type 1 diabetes mellitus, hypothyroidism and coeliac disease. Examination revealed an elevated resting blood pressure of 150/90 mmHg. Serial high sensitivity troponins were normal.

Diagnostic Techniques and Their Most Important Findings: ECG at rest showed sinus rhythm with no ischaemic features, and during treadmill stress, 1mm of horizontal ST-segment depression in the lateral leads at peak exercise and into late recovery.

Echocardiography at rest showed normal biventricular size and systolic function with no resting wall motion abnormalities or significant valvular disease, and following treadmill stress, no inducible regional wall motion abnormalities.

CMR was performed three days later after 24 hours of caffeine abstinence at 1.5 T (Siemens Aera) using a protocol consisting of cine imaging, adenosine stress and rest inline Gadgetron quantitative perfusion mapping, and late gadolinium enhancement (LGE).

Biventricular cavity size, wall thickness, and global and regional systolic function were normal. Quantitative perfusion mapping (see figure) showed globally reduced subendocardial stress perfusion of 1.9 ml/min/g (normal >2.25 ml/min/g) compared to subepicardial (2.4 ml/min/g), resulting in an averaged globally reduced whole wall stress perfusion of 2.2 ml/min/g, with no segmental perfusion defects corresponding to a coronary artery territory. Global rest myocardial perfusion was 1.2 ml/min/g, yielding a myocardial perfusion reserve of 1.8. No myocardial late gadolinium enhancement was present.

The patient was referred for invasive coronary angiography. No obstructive epicardial coronary artery disease was identified.

A diagnosis of coronary microvascular dysfunction (CMD) was made.

Learning Points from this

Case: CMD is a frequent clinical problem in patients with chest pain and without obstructive coronary disease. Additionally, patients believed to have CMD have a poor prognosis with an increased rate of major adverse cardiovascular events. At present, no clinical guidelines exist to direct treatment. Nevertheless, current practice involves management of underlying cardiovascular risk factors, anti-platelet, lipid-lowering and anti-anginal therapies. Additionally, providing a cardiovascular diagnosis and explanation of their symptoms can be as important to a patient as providing a treatment plan. Our patient was commenced on an anti-hypertensive, aspirin, and a statin. The abnormalities clearly visualised on CMR quantitative stress perfusion mapping also facilitated patient education regarding the diagnosis and engagement with the proposed treatment strategy.