Ventricular performance, pump function and compensatory mechanisms in patients with aortic stenosis.

Abstract

SUMMARY 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.ISOLATED cardiac muscle and intact animal hearts have shown decreased contractile function in the severely and acutely pressure-overloaded hypertrophied and failing heart.-.' When the pressure overload is less intense and less acute and when heart failure does not develop, ventricular performance is variable.6' 7 In experimental animals, it appears that depression of myocardial function is directly related to the severity of the overload, the presence of congestive failure and, possibly, the duration of the overload. 3,6,7 Despite these experimental studies, ventricular contractile function in patients with chronic pressure overload caused by aortic stenosis is still debated.8 17 From the limited patient studies available, it seems reasonable to postulate that ventricular contractile function is depressed when severe pressure overload has caused congestive failure, but normal when the overload is less severe and failure has not occurred.s9 11,16, 17 In this study, we tested this hypothesis by determining hemodynamic values and quantitative ventricular function measurements in three groups of patients. Patients with severe aortic stenosis and congestive heart failure symptoms were compared with

ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease

“…During this time, the left ventricle adapts to the systolic pressure overload through a hypertrophic process that results in increased LV wall thickness, while a normal chamber volume is maintained (62)(63)(64). The resulting increase in relative wall thickness is usually enough to counter the high intracavitary systolic pressure, and as a result, LV systolic wall stress (afterload) remains within the range of normal.…”

2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease

“…During this time, the left ventricle adapts to the systolic pressure overload through a hypertrophic process that results in increased LV wall thickness, while a normal chamber volume is maintained. [62][63][64] The resulting increase in relative wall thickness is usually enough to counter the high intracavitary systolic pressure, and as a result, LV systolic wall stress (afterload) remains within the range of normal. The inverse relation between systolic wall stress and ejection fraction is maintained; as long as wall stress is normal, the ejection fraction is preserved.…”

Assessment of left ventricular contractility from late systolic stress-volume relations.

“…[6][7][8][9][10][11][12][13][14][15][16][17][18] In animals, the slope of this relation is very sensitive to changes in inotropic state and is unaffected by alterations in preload or afterload.6'@ 14 In man, the linearity of this relationship12-16 and its value in assessing acute10' 12, 18 or chronic10 changes in myocardial contractility have also been established. Nevertheless, practical problems still limit the clinical use of this index.…”