May 2020 Br J Cardiol 2020;27:64–6 doi:10.5837/bjc.2020.011
Yuen W Liao, James Redfern, John D Somauroo, Robert M Cooper
Introduction Hypertrophic cardiomyopathy (HCM) predominantly results from genetic variants that affect cardiac sarcomeres. The result is a heterogeneous condition characterised by ventricular hypertrophy that cannot be explained by increased afterload (i.e. arterial hypertension, aortic stenosis). Various hypothesised mechanisms were potentially responsible for a perceived increased risk of arrhythmia during exercise in patients with HCM: dynamic left ventricular outflow tract obstruction (LVOTO) increasing left ventricular pressure and strain; sympathetic vagal imbalance; microvascular ischaemia and metabolic acidosis.1 Subsequent internatio
July 2017 Br J Cardiol 2017;24:118–9 doi:http://doi.org/10.5837/bjc.2017.016 Online First
Deidre F Waterhouse, Theodore M Murphy, Charles McCreery, Rory O’Hanlon
Figure 1. Electrocardiogram demonstrating deep T-wave inversion in leads 1, aVL, and V2 through to V6 The CMR demonstrated marked asymmetrical hypertrophy of the anterior and anteroseptal walls at basal and mid-ventricular level. The peak basal wall thickness was 25 mm. The reference wall thickness was 7–9 mm. There was also apical circumferential hypertrophy with a peak apical wall thickness of 11 mm and systolic obliteration from distal left ventricle (LV) through to the apex. Perfusion was performed with regadenosine stress. There was severe microvascular ischaemia in a near circumferential pattern basally, and marked ischaemia in the ma
March 2015 Br J Cardiol 2015;22:31–3 doi:10.5837/bjc.2015.009
Pierre Le Page, Hamish MacLachlan, Lisa Anderson, Lee-Ann Penn, Angela Moss, Andrew R J Mitchell; from the Jersey International Centre for Advanced Studies
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January 2006 Br J Cardiol 2006;13:58-61
Elliot J Smith, Ajay K Jain, Charles J Knight
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September 2002 Br J Cardiol 2002;9:449-59
Sami Firoozi, Julia Rahman, William J McKenna
No content available
February 2002 Br J Cardiol 2002;9:120-21
Suneel Talwar, Khalid Khan
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