Background and aim of the study: Symptomatic status in aortic stenosis is not always related to hemodynamic severity as estimated by the aortic valve effective orifice area (AVA), and other factors may be involved. It has been seen previously that, whilst ejection fraction is preserved, left ventricular (LV) longitudinal shortening may be selectively decreased in aortic stenosis, and hypothesized that this might be a marker of subendocardial ischemia as subendocardial myocardial fibers are oriented longitudinally. The present study examined the possible relationship between LV longitudinal shortening and symptoms in patients with aortic stenosis.
Methods: Relevant clinical and echocardiographic variables, including the percentage of LV longitudinal shortening, were measured in 131 consecutive patients with at least moderate aortic stenosis (AVA <1.5 cm2).
Results: Symptoms were found in 106 patients (exertional dyspnea 93%, resting dyspnea 25%, angina 57%, syncope 27%). Compared with asymptomatic patients, symptomatic patients had a smaller AVA (0.91 +/- 0.27 versus 1.13 +/- 0.20 cm2; p < 0.001), a lower LV longitudinal shortening (19 +/- 13 versus 28 +/- 9%; p = 0.01), and higher incidence of coronary artery disease (52 versus 20%, p < 0.008). Other variables significantly associated with symptoms included age, previous myocardial infarction, obesity, indexed AVA, LV mass index, LV ejection fraction, cardiac index, energy loss index, and valvular resistance. However, in multivariate analysis, the only variables independently associated with symptomatic status were patient age (p = 0.03), indexed AVA (p = 0.006), and LV longitudinal shortening (p = 0.04). The combination of indexed AVA with LV longitudinal shortening resulted in an improvement of the performance for the prediction of symptoms.
Conclusion: These results show that LV longitudinal shortening is more closely associated with changes in symptomatic status than other currently used indices of LV systolic function. As such, it probably more closely reflects alterations in subendocardial myocardial function.