Understanding the pathophysiology of aortic valve dysfunction using advantage CMR techniques: 4D flow in aortic valve disease

Aortic valve disease is common with early valve thickening (known as aortic sclerosis, ASC) affecting around 30% of those over 65 years of age, and nearly 3% of the population over 75 years old having haemodynamically significant aortic stenosis. During clinical follow up of aortic stenosis, little distinction has been made between those with congenitally bicuspid aortic valve disease (2% of the population) (BAV AS) and those with acquired degenerative disease (TAV AS), although these contribute roughly equal proportions of aortic valve surgery. I demonstrated that ASC is more common than previously thought with a prevalence of 38.5% in the over 65 year old general population and was strongly related with age, hypertension and a history of ischaemic heart disease (all p<0.05). In an age matched population without pre-existing hypertension but with ASC, I found those with ASC have a statistically significantly higher blood pressure than those without ASC (mean systolic blood pressure difference of 4.4mmHg; p=0.004). However, in a population with known hypertension and ASC, no prescribing differences in antihypertensive agents exist and no differences in the absolute level of hypertension were found. In a CMR sub study, markers of aortic stiffness were more impaired in both ASC and established tricuspid AS disease to a similar degree, suggesting a fully expressed vascular phenotype exists before progression to valvular AS, when compared with control and BAV AS. However, there was a mean age difference of about 8 years between ASC and BAV AS and control groups, which confounds the result. After age adjustment, a faster pulse wave velocity between ASC and controls remained (19.02 m/s compared with 14.4 m/s, p=0.028). TAV and BAV AS have distinct differences in aortic dimensions and turbulent kinetic energy formation was greater in BAV AS, implying irreversible pressure loss (p<0.0001). Turbulent kinetic energy correlated to valve area (r=0.53, p=0.001) and very strongly to LV mass in a BAV AS population (r=0.83; p=0.0001), implying greater LV work may be required to compensate for the higher turbulent kinetic energy, particularly in the BAV group. The patterns of wall shear stress (WSS) on the aorta did not differ in intensity but did have differences in peak sites of the aortic wall in TAV and BAV AS. Impaired distensibility in the aorta was seen in both TAV and BAV AS, which appears to be more regional (confined to the ascending aorta) in BAV AS. Turbulent kinetic energy emerged as a novel and interesting marker in AS, especially in BAV AS, showing moderate or strong correlation with LV mass, volumes, longitudinal strain and stroke work, and may go some way to explain the previously noted weaker than expected correlations between LV mass and valve area in AS. Future longitudinal studies to relate turbulent kinetic energy more precisely to LV function and outcome are warranted.