Dual chamber pacing for hypertrophic obstructive cardiomyopathy: has its time come?

Editorial Dual chamber pacing for hypertrophic obstructive cardiomyopathy: Has its time come? Hypertrophic cardiomyopathy, a fascinating and controversial disease,' 2 iS characterised by massive hypertrophy of the myocardium and is associated with various presentations ranging from complete absence of symptoms to sudden, unexpected death. There is a subgroup of patients who present with severe limiting symptoms of dyspnoea, angina, and syncope related partly to obstruction of the left ventricular outflow tract. Previously, the established therapy for these patients was a trial of ,B blockers, calcium channel blockers, and disopyramide administered in high doses, followed by septal myectomy for those intolerant of or unresponsive to medications.' 2 Recent reports have documented significant symptomatic improvement in many patients with dual chamber pacing ,34 and the question has arisen whether permanent pacemakers should be considered in all patients with hypertrophic obstructive cardiomyopathy who have severe limiting symptoms despite medical treatment. It is important to understand the complex pathophysio-logical processes that contribute to dyspnoea, angina, and syncope in order to direct treatment for patients with hypertrophic cardiomyopathy. Impaired diastolic filling of the left or right ventricle in this condition has long been recognised as a major contributor to the symptoms. 56 Though the documented increase in left ventric-ular end diastolic pressure was initially believed to be due to increased chamber stiffness caused by the "hypertro-phied inelastic muscle"78 recent insight into the process of ventricular relaxation9 has led to the conclusion that impaired relaxation may be of greater importance than increased chamber stiffness in explaining abnormalities of diastolic filling.'56 Myocardial relaxation is much impaired in hypertrophic cardiomyopathy and this impairment is believed to be caused by (a) abnormalities of calcium metabolism that lead to abnormal inactivation of the contractile elements, (b) a high systolic contraction load, (c) non-uniformity of relaxation, and (d) myocardial ischaemia.' 5 6 In addition to having severe abnormalities of diastolic function, many patients also have a dynamic left ventric-ular outflow gradient.' 2 Whether this gradient represents true obstruction or is merely a manifestation of rapid early emptying of the hyperdynamic left ventricle has been questioned.'01' Non-invasive Doppler studies have shown true obstruction to outflow.'6 The mechanism of obstruction is said to be the combination of a Venturi effect that draws the anterior mitral leaflet into a narrowed outflow tract'6 and an anatomical anterior displacement of the mitral valve tensor apparatus.'2 The obstruction causes symptoms by placing a systolic overload on the …