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Obstruction is unimportant in the pathophysiology of hypertrophic cardiomyopathy
Insights
Intracavitary pressure gradients in hypertrophic cardiomyopathy (HCM) may not be caused by obstruction. Research suggests these gradients and related phenomena are due to rapid ventricular emptying, not impeded outflow.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Hypertrophic cardiomyopathy (HCM) is often associated with intracavitary pressure gradients.
- These gradients have historically been attributed to left ventricular outflow tract obstruction.
Purpose of the Study:
- To re-evaluate the significance of intracavitary pressure gradients in HCM.
- To challenge the traditional 'obstruction' hypothesis and explore alternative explanations for observed phenomena.
Main Methods:
- Review of historical and contemporary understanding of HCM pathophysiology.
- Analysis of evidence challenging the concept of left ventricular outflow tract obstruction.
- Consideration of alternative explanations for pressure gradients and related symptoms, such as cavitary obliteration.
Main Results:
- The concept of a fixed muscular obstruction has evolved to systolic anterior motion (SAM) of the mitral valve.
- Evidence suggests that provoked gradients lead to more rapid and complete ventricular emptying, not impeded outflow.
- Phenomena previously attributed to obstruction can be explained by rapid ventricular emptying (cavitary obliteration).
Conclusions:
- The 'obstruction' model in HCM may be less significant than previously assumed.
- Abnormal diastolic function and life-threatening arrhythmias are likely more critical in HCM pathophysiology.
- Focus should shift from relieving perceived obstruction to managing diastolic dysfunction and arrhythmias.
Abstract:
There has been a longstanding controversy about the significance of intracavitary pressure gradients in hypertrophic cardiomyopathy (HCM). It has been generally assumed that the gradient is the result of an 'obstruction' that impedes left ventricular outflow and which can be relieved by operative intervention. In the first decade after the discovery of HCM (1957-66), the site of 'obstruction' was thought to be a muscular sphincter or contraction ring in the submitral region of the left ventricle, and operations designed to emulate pyloromyectomy (for hypertrophic pyloric stenosis) were developed. Following a challenge to the existence of the 'contraction ring' and an alternative non-obstructive explanation of the pressure gradient, the site of 'obstruction' was translocated to a point of apposition between the anterior mitral leaflet and the interventricular septum, a result of systolic anterior motion (SAM) of the mitral valve. Despite the translocation of the site and mechanism of 'obstruction', the operation for 'relief of obstruction' has not changed significantly. The newer site of 'obstruction' has been challenged on the grounds that the ventricle is not demonstrably impeded in its emptying; when a gradient is provoked, the ventricle empties more rapidly and more completely than it does without a gradient. In addition to a non-obstructive explanation of the gradient, other phenomena thought to be indicative of 'obstruction' can be explained by rapid and complete emptying of the ventricle (cavitary obliteration). Since the morbidity and mortality of symptomatic HCM patients without pressure gradients may exceed that of patients with pressure gradients, it is suggested that 'obstruction' may be unimportant in the pathophysiology of HCM and attention should be focused on abnormal diastolic function and life threatening arrhythmias.