Fourteen patients with critical aortic stenosis (valve area 0.4 cm2/m2), a history of advanced congestive heart failure, left ventricular ejection fraction less than 0.45 (mean 0.28 d 0.03) and no other valvular lesions or obstructive coronary artery disease were studied to assess prognosis with aortic valve replacement. Eleven of 14 (79%) survived surgery; 10 of these 11 showed major clinical improvement postoperatively and form group 1. The three patients who died and the patient who did not improve form group 2. Although group 2 had higher preoperative values for aortic valve area and left ventricular end-diastolic volume and lower ejection fraction and cardiac output than group 1, none of these factors alone reliably predicted outcome. The mean systolic gradient was an important predictor of outcome: No patient with a mean systolic gradient 30 mm Hg had a good outcome, irrespective of valve area or other hemodynamic variables.Ejection fraction was plotted against left ventricular wall stress for both groups. For group 1, there was a close linear relation that could be extrapolated back to normal wall stress and normal ejection fraction. This suggested afterload mismatch as a major cause for this group's depressed ejection fraction. In group 2 ejection fraction was lower for any given wall stress, suggesting depressed contractility, rather than afterload mismatch, as the cause of the left ventricular dysfunction. Thus, either afterload mismatch or depressed contractility may result in depressed ejection fraction in patients with aortic stenosis; which one predominates may have major prognostic importance.

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Chronic volume overload hypertrophy as seen in mitral regurgitation in humans eventually may cause left ventricular dysfunction. Longitudinal study of the mechanisms leading to such dysfunction is difficult in humans and more easily performed in an animal model. In this study, we describe a canine model of volume overload hypertrophy produced by mitral regurgitation. An arterially placed grasping forceps was used to disrupt mitral chordae or leaflets; thus mitral regurgitation was produced without the need for thoracotomy. Eleven of 22 dogs had severe mitral regurgitation (regurgitant fraction greater than 0.50) and survived for greater than or equal to 3 mo (average 9.2 +/- 6 mo) after the production of mitral regurgitation. At 3 mo, end-diastolic volume increased from 48 +/- 9 to 85 +/- 19 ml, P less than 0.01. Left ventricular mass increased from 71 +/- 13 to 90 +/- 10 g, P less than 0.01. Left ventricular end-diastolic pressure increased from 9 +/- 3 to 19 +/- 6 mmHg, P less than 0.01. Cardiac output decreased from 2.3 +/- 0.61 to 1.80 +/- 0.64 l/min, P less than 0.05. The mass-to-volume ratio decreased from 1.44 +/- 0.17 to 1.09 +/- 0.13, P less than 0.01. We conclude that this closed-chest model of chronic mitral regurgitation produces significant eccentric cardiac hypertrophy. Despite a doubling of end-diastolic volume, there was a fall in cardiac output and a rise in left ventricular end-diastolic pressure, suggesting cardiac decompensation.

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