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Dynamic obstruction to left ventricular outflow: the case for its existence in hypertrophic cardiomyopathy
1Cardiology Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland.
Insights
In hypertrophic cardiomyopathy (HCM), a mechanical impediment to blood flow, known as left ventricular outflow obstruction, demonstrably exists. This obstruction leads to elevated pressures detrimental to the heart, supporting surgical intervention for severe cases.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- The hemodynamics of obstruction and left ventricular ejection in hypertrophic cardiomyopathy (HCM) have been debated for decades.
- Disagreement persists regarding the existence and significance of left ventricular outflow obstruction in HCM patients.
Purpose of the Study:
- To unequivocally support the concept of true obstruction to left ventricular outflow in HCM patients with measured gradients and systolic anterior motion (SAM).
- To highlight the critical clinical implications of these gradients, specifically elevated intraventricular systolic pressures.
Main Methods:
- Review and interpretation of available clinical data and catheterization measurements.
- Analysis of the physiological consequences of elevated intraventricular systolic pressures.
Main Results:
- Data unequivocally support the existence of a mechanical impediment (obstruction) to forward flow in HCM patients with left ventricular outflow gradients and SAM.
- Markedly elevated intraventricular systolic pressures are associated with these gradients, increasing systolic myocardial wall stress and oxygen demand.
Conclusions:
- The presence of obstruction and associated elevated pressures in HCM has critical clinical implications.
- Surgical intervention to abolish obstruction and normalize pressures is a rational therapeutic objective for severely symptomatic HCM patients refractory to drug therapy.
Abstract:
The debate and controversy over the hemodynamics of obstruction and left ventricular ejection in HCM is an interesting and complex one in which periodic disagreement has appeared during the last 20 years. We believe that the available data unequivocally support the concept that in those patients with HCM who have left ventricular outflow gradients measured at catheterization (and who have associated marked SAM) a mechanical impediment to forward flow, and thus true obstruction to left ventricular outflow, does exist. Most importantly, the gradient has critical clinical implications by virtue of the markedly elevated intraventricular systolic pressures associated with it. These chronically elevated pressures are potentially detrimental to the left ventricle (a view held even by investigators opposed to the term "obstruction"), by virtue of increasing systolic myocardial wall stress and myocardial oxygen demand. Therefore, surgical abolition of the obstruction and normalization of these pressures remains an important and rational therapeutic objective in those severely symptomatic patients who have obstruction to left ventricular outflow and who have failed to benefit from drug therapy.
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