Relationship between left ventriculoarterial coupling and damage stage in severe aortic stenosis

Abstract

Abstract Background In patients with severe aortic stenosis (AS), an anatomic and functional staging classification has been proposed to assess extent of cardiac chambers damage to improve the decision of aortic valve replacement based only in symptoms or ejection fraction (EF) <50%. This staging relies on the concept that left ventricular (LV) afterload secondary to AS induce LV dysfunction with progression to LV and right ventricular damage. However, afterload has valvular and vascular components, and the latter is not evaluated by the classification of stages. Characteristics of arterial vasculature can impact on LV function through the alteration in LV-VA coupling which is the relationship between effective arterial elastance (Ea) and LV end-systolic elastance (Emax). Objective To evaluate the relationship between LV-VA coupling and the different stages of cardiac damage in severe AS. Methods We studied 205 patients, age average 70±11 years, 117 men, with severe AS (AVA <1 cm2) with Doppler echocardiography. Measurements of cardiac chambers were made according to ASE/EACVI Guidelines. Ea was calculated as end-systolic pressure divided by stroke volume. End-systolic pressure was obtained from tonometry of carotid pulse. Emax was estimated by the method of Senzaki (1) as an index of LV contractility. Ea / Emax ratio was used to assess LV-VA coupling. Patients were divided in five groups according to the classification of staging cardiac damage proposed by Tasted (2): stage 0, no valvular cardiac damage; stage 1, LV damage (EF <60%); stage 2, left atrial or mitral valve damage; stage 3, pulmonary vasculature or tricuspid valve damage and stage 4, right ventricular damage, or subclinical heart failure (LV stroke volume index <30 ml/m2). Results Mean ± standard deviation (see Table 1). No patient was in stage 0. Symptoms was present in 40% of stage 1, 85% of stage 2 and 100% of stage 3 and 4. Ea increases from stage 2 to stage 4 while Emax did not change in those groups but decreased from stage 1 to 2. Consequently, LV-VA coupling progressively decreased from stage 1 to 4. Conclusions Worsening of LV-VA coupling increase with staging cardiac damage. The alteration of LV-VA coupling from stage 2 to 4 is due to an increase in Ea without significant changes in level of contractility (Emax). The progression of cardiac damage appears to be related not only to valve disease but also to the characteristics of arterial vasculature. Funding Acknowledgement Type of funding sources: None.