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Left ventricular outflow tract obstruction in hypertrophic cardiomyopathy: past, present and future
  1. S R Ommen1,
  2. P M Shah2,
  3. A J Tajik3
  1. 1
    Mayo Clinic, Rochester, Minnesota, USA
  2. 2
    Hoag Heart Valve Center, Newport Beach, California, USA
  3. 3
    Mayo Clinic, Scottsdale, Arizona, USA
  1. Dr Steve R Ommen, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA; ommen.steve{at}mayo.edu

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Fifty years ago, the first modern reports of what we now recognise as hypertrophic cardiomyopathy (HCM) were written by a surgeon, Sir Russell Brock,1 and a pathologist, Donald Teare.2 These classic papers stimulated an intense and sometimes controversial field of study, focused in large part on the characterisation of left ventricular outflow tract obstruction. Detailed invasive haemodynamic investigations highlighted the extraordinary dynamic nature of this new form of outflow obstruction, and numerous surgical therapies were proposed and abandoned. The introduction of echocardiography allowed investigators to determine the mechanism for obstruction—an adverse interaction between a hypertrophied septum and abnormal movement of the mitral valve towards the septum—but also showed that obstruction was not a universal feature of the disease. The focus of this article is to review the historical controversies surrounding left ventricular outflow tract obstruction in hypertrophic cardiomyopathy, and to discuss the modern approach to its assessment and treatment.

PRESENCE AND PREVALENCE OF OBSTRUCTION

As is the case with many disease processes, initial clinical reports suggested that hypertrophic cardiomyopathy was a rare disorder that was nearly always associated with the need for surgery to relieve obstruction or death at a young age.13 In the late 1950s, master clinicians (see Coats and Hollman4) elucidated the dynamic nature of the muscular, rather than valvular, outflow tract obstruction utilising bedside manoeuvres.5 Thus, physical signs of outflow obstruction, responsive to manipulation of ventricular preload and afterload, in the absence of radiographic evidence of aortic valve calcification, were the key to premortem diagnosis. In the years that followed, pharmacological manipulations during invasive haemodynamic assessment furthered the understanding of the physiological determinants of obstruction, and suggested options for its treatment (table 1).610

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Table 1 Clinical modulators of dynamic left ventricular outflow tract obstruction

In spite of this work, the very existence of impedence to left ventricular ejection was vigorously contended in …

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