Hypertrophic cardiomyopathy (HCM) is the com monest hereditary cardiac disease and the most frequently found cardiomyopathy. However, diagnosis and management remains very challenging. This condition is very heterogeneous with respect to genotypic and phenotypic expression, natural history, prognosis, and overall the treatment strategy remains contentious [1]. Despite the varying degrees and patterns of hypertrophy, ventricular systolic and diastolic dysfunction, dynamic intraventricular pressure gradients and microvascular ischemia, the key challenge is to accurately identify which patients will develop symptoms and which patients will respond to therapy. The same issues apply to the stratification of individual risk for sudden cardiac death (SCD), as debate continues over whether a single risk factor for SCD is enough to justify implantation of a cardioverter-defribillator (ICD), for primary prevention alone [2]. The definition of hypertrophy for diagnosis of HCM is currently arbitrary. Despite the conventional 15 mm diastolic septal wall thickness diagnostic threshold, HCM can present with milder degrees of septal hypertrophy [1, 3]. Clear recognition of this condition is crucial, not only from the point of view of clinical management and SCD risk stratification for the individual concerned, but also as screening of first-degree relatives has now extended into routine practice. One form of HCM that is commonly misdiagnosed is the apical variant, with hypertrophy predominantly involving the left ventricular apex and varying degrees of extension basally. Although uncommon is the Western world [4], it is common in Japanese and Chinese populations, accounting for up to 40% in these areas [5, 6]. Typical features include giant negative T waves on electrocardiogram (ECG), a spade-like configuration of the left ventricle, absence of an intraventricular pressure gradient, mild symptoms, and a generally more benign course with lower mortality rates than other forms of HCM [4–8]. Despite being a well-described entity, the diagnosis of apical HCM may be frequently missed by conventional imaging techniques. In this issue of the Journal, Duygu and co-workers studied a group of patients with suspected coronary disease who were subsequently referred for coronary angiography, and found to have the characteristic ‘‘ace of spades’’ appearance typical of apical HCM on contrast ventriculography [9]. Notably, although almost all patients were referred reportedly with anginal chest pain, none of them had significant coronary artery disease. Myocardial ischemia is common and multifactorial in HCM. Major causes may include small vessel disease, myocardial bridging, and impaired F. Alpendurada (&) S. K. Prasad CMR Unit, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK e-mail: f.alpendurada@rbht.nhs.uk