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Our patient is a 45-year-old Chinese male who presented with exertional dyspnea for 6 months. He had history of hypertension, diabetes and previous PCI to left circumflex artery in 2015 but defaulted follow up. Of note, history taking revealed alcohol intake of 41 standard units per week.
Clinical examination was unremarkable – examination of the precordium did not reveal any murmurs, there were also no findings suggestive of heart failure clinically.

An echocardiogram showed LVEF of 35% with global hypokinesis and eccentric left ventricular hypertrophy, and no significant valvular disease.
Myocardial perfusion scan showed fixed medium sized perfusion defects in the inferior and lateral segments, consistent with partial thickness infarcts with no superimposed ischemia and moderate retained viability. Significantly, there was a small sized basal to mid anterior perfusion defect which was predominantly reversible, consistent with ischemia.

The coronary angiogram demonstrated angiographically moderate to severe stenosis in left circumflex (LCx) and right coronary artery (RCA) disease with moderate left anterior descending (LAD) disease. 
Left main – free of diseaseLeft anterior descending – proximal LAD 50% stenosis, mid LAD 50% stenosis, distal LAD 50% stenosisLeft circumflex – proximal LCx 60% stenosis, mid LCx 70% stenosisRight coronary artery – mid RCA 70% stenosis, distal RCA 50% and 50% tandem stenosis
iFR NICMP - RCA 1 (1).mp4
iFR NICMP - Cx 2 (1).mp4
iFR NICMP - LAD 2 (1).mp4

We regarded the myocardial perfusion scan findings as somewhat non-diagnostic for the following reasons – (1) the degree of left ventricular dilatation and dysfunction seemed somewhat out of proportion to the extent of the coronary artery disease (2) the “basal anterior ischemia” reported was perhaps artifactual given the fact that isolated basal ischemia is distinctly unusual without concomitant apical ischemia and (3) this patient had other features in his history, including a history of alcoholism as well as non-compliance to medications that compelled additional evidence before revascularization (surgical or PCI) was undertaken.
As such, decision was made to proceed with hemodynamic assessment of all 3 vessels. iFR was chosen instead of FFR in view of significant transient bradycardia at the start of the procedure, limiting use of adenosine. Surprisingly, iFR readings of 0.92 (LAD), 0.96 (LCx) and 0.99 (RCA) indicated hemodynamically insignificant lesions. 
In view of the discordant results between the stress myocardial perfusion scan and invasive hemodynamic assessment findings, a joint decision was made with the patient for a trial of optimal medical therapy and alcohol abstinence.
Cardiac magnetic resonance imaging performed  4 months after demonstrated recovery of left ventricular dysfunction, with no dyskinetic/akinetic segments, late gadolinium enhancement and an ejection fraction of 60%.

Our patient had left ventricular dysfunction, non-invasive functional assessment demonstrating ischemia, and angiographically moderate/severe multi-vessel disease. In a large number of practices this would have led to an “ischemic cardiomyopathy” label followed by revascularization along with optimized medical therapy.  Subsequent improvement in ejection fraction would have erroneously been attributed to revascularization.
In summary, we present a case of cardiomyopathy with coincidental coronary artery disease - treated medically with normalization of structure and function on cardiac MRI. Invasive physiology gave us robust grounds to defer revascularization and optimize medical therapy.