Aortic valve sclerosis without haemodynamically significant obstruction has been related to cardiovascular morbidity and mortality. However, do the underlying mechanisms also implicate systolic and diastolic left ventricular function, even in the absence of morphological changes?
A recent article in the European Journal of Preventive Cardiology , attempted to address this. Specifically, Yuriko Yoshida et al., using data from the Subclinical Cardiac Dysfunction in General Population (SCADGP) study, demonstrated a high prevalence, of about 20%, of aortic valve sclerosis (AVS) in the general population, which was associated with subclinical left ventricular systolic/diastolic dysfunction. The authors examined 962 individuals (50% men) free from cardiovascular disease and with normal LV geometry, defined as LV mass index £ 115 g/m2 for men and £ 95 g/m2 7 for women, and relative wall thickness £ 0.42, according to the current guidelines.
The enrolled participants presented with no AVS (79.7%), aortic valve thickening (7.7%), calcification on one leaflet (9.0%), and calcification on ³ 2 leaflets (3.5%). Age, B-type natriuretic peptide values, LV mass and the classical CVD risk factors (i.e., arterial hypertension, hypercholesterolaemia, diabetes mellitus), were more dominant in all AVS groups compared to no AVS. Using Doppler echocardiography to evaluate LV diastolic function and speckle tracking for LVGLS, the researchers revealed that AVS, as well as AV thickening, were significantly associated with subclinical LV diastolic impairment, independently of age, sex, as well as history of hypertension, hypercholesterolaemia, diabetes, current smoking, and body mass index.
Although this study has some major limitations due to the cross-sectional design that cannot confirm causality and the lack of using cardiac computed tomography to assess aortic calcification, it reveals an important message for further research. Specifically, one should not wait to see LV hypertrophy as an indicator of LV remodeling, which can be a late and partially irreversible condition, but try to detect and even quantify early myocardial damage, even when LV ejection fraction is within normal limits, in order to reverse the clinical course of those patients. A potential explanation is that symptomatic status merely depends on diastolic function and modestly on systolic function especially as evaluated by LV ejection fraction, while the clinical status may depend not only on the myocardial response, but also on the aortic valve, highlighting the concept of valvular reserve.
AVS is thought to be related to atherosclerosis in terms of pathogenesis, which is one of the primary causes of arterial stiffening imposing an increased load on left ventricular function through multiple mechanisms [2, 3]. The force of contraction required to achieve expansion of the stiffened arteries and accommodation of the ejected blood can be elevated. Blood flow circulation, in the coronary circuit, can be reduced, while increased pulse wave velocity imposes a greater load to left ventricle. Thus, among several echocardiographic techniques, GLS measurements appears to be a more robust parameter in the assessment of subclinical left ventricular dysfunction, along with natriuretic peptides secretion. Additionally, it is therefore conceivable that, because the detrimental effects of AVS are due to deteriorating left ventricular function, an index incorporating both sources of left ventricle afterload, valvular and arterial, like aorto-ventricular coupling, might be more clinically relevant.