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Hypertrophic cardiomyopathy (HCM) is an inherited disorder of heart muscle characterised by myocardial hypertrophy in the absence of abnormal loading conditions.1 It occurs in about 1 in 500 people and is an important cause of sudden cardiac death in young people. Progression to an end-stage, or “burnt-out” phase occurs in 2–15% of patients every year and is associated with a mortality rate of up to 11% a year.2–4
Left ventricular outflow tract obstruction, caused by contact between one or both leaflets of the mitral valve and the interventricular septum during ventricular systole is present at rest in approximately 25% of patients. In some people, obstruction varies spontaneously (labile obstruction) and in others is present only during physical or pharmacological manoeuvres that change loading conditions or increase contractility (latent obstruction).5
Left ventricular outflow tract obstruction is associated with an increased incidence of sudden death and progression to heart failure.6 7 In this issue of the journal, Dimitrow and colleagues report an association between left ventricular outflow tract obstruction and markers of thrombin generation and platelet activation (specifically, thrombin–antithrombin complex, prothrombin fragment (1+2), …
Competing interests: None.