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The first descriptions of patients impacted with what has become known as hypertrophic cardiomyopathy occurred roughly 50 years ago.1 2 Careful examination involving both auscultatory and palpatory physical findings and, subsequently, invasive haemodynamics led to the appreciation of dynamic subvalvular obstruction. Thus began an era of intense haemodynamic assessment into this fascinating condition which has come to be appreciated in most cases as a disease of not only left ventricular hypertrophy but also dynamic impedance to left ventricular ejection. There has also been a considerable degree of controversy over the existence of, mechanisms of, and treatments for this unique type of haemodynamic abnormality.
The existence of dynamic left ventricular outflow tract obstruction
There had been considerable debate, prominently featured at the annual sessions of the American Heart Association several decades ago, on whether there is true obstruction as opposed to systolic cavity obliteration.3 4 5 6 Today, we recognise that both situations can exist, but there are clearly many patients who have true obstruction in the left ventricular outflow tract with an open, non-emptied residual ventricular cavity. This obstruction is highly dynamic in that the severity of the obstruction is dramatically impacted by simple haemodynamic manoeuvres such as changing posture or even eating meals. Likewise, simple bedside manoeuvres can significantly change the auscultatory and Doppler echocardiographic findings. Ultimately, the impact of this obstruction for individual patients can be highly variable with some requiring no symptom-directed treatment, while others come to need surgical intervention in order to maintain an acceptable quality of life.7
Proposed mechanisms of outflow tract obstruction
Our understanding of the functional and anatomical determinants of …
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