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A 75-year-old South-East Asian man presented with exertional chest pain. Risk factors for coronary disease included hypertension, diabetes mellitus, hyperlipidaemia, and family history. High sensitivity Troponin was normal. An electrocardiogram (ECG) showed sinus rhythm with deep T wave inversion in leads I, aVL, V4– V6 (Figure 1). Coronary angiography showed diffuse, non-obstructive disease (Figure 2). Rubidium-82 positron-emission tomography (PET) imaging demonstrated increased tracer uptake at rest, suggestive of left ventricular (LV) hypertrophy. There was adenosine stress-induced LV cavity dilation with reversible hypoperfusion in a left anterior descending artery territory (Figure 3A). The global myocardial perfusion reserve (MPR) was reduced at 1.22 ml/g/min (Figure 3B). In view of the resting ECG abnormality, high tracer uptake at rest and reduced global in the context of nonobstructed coronaries, cardiac magnetic resonance (CMR) imaging (3T Skyra) was performed to exclude a cardiomyopathy. This demonstrated marked regional variability in heart muscle thickness with a maximal wall thickness of 19 mm in the mid inferoseptum (Figure 4A). Left ventricular ejection fraction was supranormal (82%) with apical systolic cavity obliteration (see on-line Video A). Although there was only minimal late gadolinium enhancement seen involving the superior right ventricular insertion point (image not shown), native T1 was elevated at 1276 ms consistent with diffuse fibrosis (mid septum, normal range 1052 ± 23 ms; Figure 4B). Adenosine stress imaging demonstrated a circumferential epicardial-endocardial signal intensity gradient, most pronounced in areas of maximal myocardial thickness (Figure 4C, arrows; online Video B).

journal of nuclear cardiology

Coronary microvascular dysfunction in hypertrophic cardiomyopathy detected by Rubidium-82 positron emission tomography and cardiac magnetic resonance imaging