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Muscular (hypertrophic) subaortic stenosis (hypertrophic obstructive cardiomyopathy): the evidence for true
Insights
The subaortic pressure gradient in hypertrophic obstructive cardiomyopathy is clinically significant. Obstruction to left ventricular outflow, caused by septal hypertrophy and mitral leaflet motion, impacts patient symptoms and requires appropriate therapy.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- The clinical significance of subaortic pressure gradients in hypertrophic obstructive cardiomyopathy (HOCM) remains debated.
- Muscular subaortic stenosis is a key feature of HOCM.
Purpose of the Study:
- To summarize evidence supporting the existence of true left ventricular outflow obstruction in HOCM.
- To elucidate the mechanisms and clinical implications of this obstruction.
Main Methods:
- Review and synthesis of existing clinical and haemodynamic evidence.
- Analysis of the relationship between ventricular septal hypertrophy, mitral leaflet dynamics, and outflow obstruction.
Main Results:
- Ventricular septal hypertrophy narrows the outflow tract, leading to Venturi forces.
- Systolic anterior motion of mitral leaflets causes obstruction and mitral regurgitation.
- The timing and duration of mitral leaflet-septal contact dictate the severity of obstruction, pressure gradient, and regurgitation.
Conclusions:
- Obstructive pressure gradients in HOCM are of significant clinical and haemodynamic importance.
- Patients with obstructive gradients experience more symptoms.
- Denying outflow obstruction hinders appropriate medical and surgical management for HOCM patients.
Abstract:
The clinical and haemodynamic significance of the subaortic pressure gradient in patients with muscular (hypertrophic) subaortic stenosis (hypertrophic obstructive cardiomyopathy) has long been debated. In this report we summarize the evidence which indicates that true obstruction to left ventricular outflow exists in these patients. Rapid left ventricular ejection, through an outflow tract narrowed by ventricular septal hypertrophy, results in Venturi forces causing systolic anterior motion of the anterior (or posterior) mitral leaflets. Mitral leaflet-septal contact results in obstruction to outflow and the accompanying mitral regurgitation. The time of onset of mitral leaflet-septal contact determines the magnitude of the pressure gradient and the severity of the mitral regurgitation, as well as the degree of prolongation of left ventricular ejection time and the percentage of left ventricular stroke volume that is ejected in the presence of an obstructive pressure gradient. Early and prolonged mitral leaflet-septal contact results in a large pressure gradient, significant mitral regurgitation, as well as dramatic prolongation of the ejection time and a large percentage of left ventricular stroke volume being obstructed. Late and short mitral leaflet-septal contact results in little haemodynamic perturbation. Hypertrophic cardiomyopathy patients with obstructive pressure gradients are significantly more symptomatic than those without. Thus the obstructive pressure gradients in hypertrophic cardiomyopathy are of clinical as well as haemodynamic significance. To deny the existence of obstruction to outflow in patients with muscular subaortic stenosis is to deny these patients appropriate medical and surgical therapy.