Prediction of coronary artery disease by left ventricular regional wall motion abnormalities in patients with stenosis of the aortic valve.

To identify predictive factors for coronary artery disease in patients with stenosis of the aortic valve the clinical histories, haemodynamic measurements, biplane contrast left ventriculograms, and coronary angiograms of 83 consecutively catheterised patients with valvar aortic stenosis were examined retrospectively. The mean (SD) age was 66.4 (9.1) years and 78% were men. Fifty five patients had significant coronary artery disease (greater than or equal to 50% diameter narrowing). Forty five (82%) of 55 patients with and 23 (82%) of 28 patients without coronary disease had angina. Heart failure occurred in a third of the patients; these patients were on average older, were more likely to be female, and had lower ejection fractions and cardiac outputs than patients in whom failure did not occur. Calculated valve area, transvalvar gradient, and left ventricular end diastolic pressure did not discriminate between patients with and without coronary disease. Syncope was less common than angina and heart failure and was associated with significantly lower valve areas and higher gradients than those found in patients without syncope. Left ventricular regional wall motion abnormalities were equally common in the groups with and without angina and predicted coronary artery disease with 94% accuracy. The absence of regional wall motion abnormality was an insensitive marker of normal coronary arteries as 45% of such patients had coronary disease. Five of the 83 patients had significant coronary disease without angina or regional wall motion abnormality. In patients with aortic stenosis angina did not predict the presence of coronary artery disease; therefore, it is advisable to have the results of coronary angiography before aortic valve replacement in a population such as this. Two of the patients with heart failure and severe aortic stenosis had regional wall motion abnormality with normal coronary arteries. Thus in some patients left ventricular failure produced by increased afterload may itself be a cause of left ventricular regional wall motion abnormality.