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As an Edinburgh medical student in the 1970s, George Sutherland was puzzled by the observation that sudden cardiac death occurred most commonly in the morning and was seasonally related, being more frequent during colder weather. SCD in the young has also been related to conditions such as hypertrophic cardiomyopathy and other genetic abnormalities of the heart, but these do not account for the majority of cases, which remain unexplained, even in autopsy series.
‘Before retiring I wanted to investigate whether acute blood pressure changes alone, or in combination with a substrate, could act as a trigger for sudden death,’ says Sutherland, who in today’s Rene Laennec Clinical Cardiology lecture will propose a possible new paradigm for SCD linking everyday changes in blood pressure to electromechanical changes within the heart which are pro-arrhythmic.
Sutherland has had a distinguished career as a cardiologist whose main interest was the development of cardiac imaging, and has held chairs in cardiology/cardiac imaging in the UK, Sweden, Holland and Belgium. Over the last 40 years, his research achievements have included the use of 2D echocardiography to describe congenital heart defects for the first time, the development of aspects of adult and paediatric transoesophageal echocardiography and the introduction of strain and strain-rate imaging into echocardiography. During his career his distinguished mentors have included Jane Somerville, JRTC Roelandt, Liv Hatle, Bengt Wranne and Bart Bijnens.
On the subject of his lecture today, Sutherland and his colleagues, Piet Claus and Peter Hamers, in a series of studies at the University of Leuven, Belgium, simulated every day short-lived physiologic blood pressure using short-lived descending aortic balloon inflations in a pig model.
They found that a balloon inflation for 5/10 beats inducing a 30 mmHg pressure change in the aorta led to marked shape changes in the left ventricle and caused a striking dissociation of mechanical and electrical events within the left ventricle. This challenge opened a ‘window’ of electrical instability which frequently resulted in the production of premature ventricular beats. ‘Interestingly, it was acute pressure fall which was related per beat to the induction of the arrhythmia and not pressure rise,’ says Sutherland.
The potential mechanisms underlying this phenomenon will be discussed during the lecture and Sutherland will postulate that the acute induced ventricular premature beats, which are a result of the release of stretch within the left ventricular myocardium, act as a ‘trigger’ which interacts with a subclinical/clinical substrate within either right or left ventricle to produce a fatal ventricular arrhythmia. Such a mechanism, he will suggest, could underlie the relatively large cohort of SCD which is currently unexplained.
Rene Laennec Lecture on Clinical Cardiology, 30 Aug 16:30-17:10, Regents Park - The Hub
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