In patients with aortic stenosis, the onset of congestive heart failure symptoms is associated with a significant depression of intrinsic left ventricular contractile function and increased end-diastolic volume and pressure.
HF symptoms in AS associate with LV contractile impairment and elevated filling pressures; leaves open causal sequence, warranting prospective studies.
The contractile capacity of the human ventricle when chronically pressure-overloaded by aortic stenosis remains a subject of major debate.The compensatory mechanisms used to maintain normal resting cardiac output and ejection fraction, and the relation of compensatory mechanisms to symptoms, have not been fully documented.In this report we examined ventricular performance and the relationship of compensatory mechanisms to symptoms in 11 patients with severe aortic stenosis and congestive heart failure symptoms (AS-CHF group), in 10 patients with significant aortic stenosis but no heart failure symptoms (AS-C group), and in 12 normal subjects.Alterations in afterload, preload and wall thickness in aortic stenosis may adversely affect the validity of indexes of contractile function, so we attempted to account for or avoid the effect of such alterations.The natural variations in ventricular volume were used to estimate group ventricular function relationships relating peak systolic wall stress to end-diastolic volume index (Frank-Starling), and to estimate group relationships of end-systolic pressure or stress to end-systolic volume (Sagawa).The slope of the linear regression lines that estimated the Frank-Starling index and the Sagawa index showed statistically significant depression (p < 0.01) of left ventricular contractile function in the AS-CHF patients, while ventricular contractile function was relatively normal in the AS-C patients.End-diastolic volume index and pressure were significantly increased (p < 0.01) only in the AS-CHF group.Peak systolic left ventricular wall stress, ejection fraction, resting cardiac index, and the ratio of ventricular mass to volume were not statistically different from normal in either group.
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Spann et al. (1980) studied this question.
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