Effect Of Systemic Pressure On Pressure Gradient And Valve Area Estimates In Aortic Stenosis

Effect Of Systemic Pressure On Pressure Gradient And Valve Area Estimates In Aortic Stenosis
Prof. Dr. Ahmed Kamal Motaweih
M.Sc.Medicine&Cardiology- M.D Cardioloy & Vasc.Dis
Porf.& Hed Of Cardio - Vasc.Medicine Dept
Faculty Of Medicine Azhar Univ. F.E.S.C & F.A.C.C.
Aortic stenosis (AS) is a highly prevalent disease in industrialized countries affecting between 2 and 7% of elderly population. 1,2
Up to 50% of AS patients have been reported to suffer from additional systemic hypertension. 3,4 Although this combination is so frequent, the possible effect of blood pressure changes on the assessment of AS has gained little attention while the impact of flow has extensively been studied. 5-7 Few clinical studies, which evaluated the association between blood pressure and estimated pressure gradients and valve areas, have yielded varying results. 6,8-10 Clinical data are, however, difficult to interpret since the Interventions used to induce blood pressure changes cause a complex combination of changes of peripheral resistance, ejection fraction and transvalvular flow rate. Thus, in human it is almost impossible to study changes exclusively caused by variation of systemic pressure. An experimental setting appears more appropriate to evaluate this question, however, only two experimental studies on the topic were carried out 11,12 and they have yielded opposite results. While Kadem et al.11 recently reported that hypertension may lead to a decrease of pressure gradients in AS in an
experimental animal model, another study showed a linear increase of pressure gradients with rising systemic pressure. 12
Thus, the important question whether variation in blood pressure itself influences pressure gradient and valve area measurements independently of secondary flow changes and whether blood pressure has therefore to be considered in the assessment of AS still remains unclear.
Systemic hypertension is a very common disease, and also affects up to 50% of patients with AS.1,3,4 Because the frequency of this combination has grossly been underestimated in the past, the impact of hypertension on the assessment ofAS has gained little attention. More recently, several clinical, animal, and in vitro studies on this topic have been carried out 6,8-11 and it has been postulated that systemic hypertension indeed influences the assessment of AS independently of afterload-related flow changes. 10
Clinical studies on the issue 6,8-10 are difficult to interpret, because changes of blood pressure cause various physiological changes of peripheral resistance, ejection fraction, and transvalvular flow rate. Two of the studies showed an increase of mean pressure gradients mediated by the administration of nitroprus-side 6
and ACE (angiotensin-converting enzyme) inhibitors 8 while calculated valve areas remained unchanged. In the study by Khot et aI.6 a concomitant increase of SV was also documented. In the work by Chockalingam et al.9 ACE inhibitors caused an increase of ejection fraction while pressure gradients as well as valve areas remained unchanged.
However, from these clinical data it cannot be clarified, whether blood pressure may still impact on pressure gradient and estimated valve area in AS apart from flow-mediated changes. This appears even more uncertain as results from experimental studies were contradictory 11,12
The more recent publication by Kadem et al.11 postulates that the severity of AS may partially be masked in the presence of hypertension since increasing systemic pressure caused a decrease of pressure gradients and increase in valve area. This conclusion was drawn from a study on pigs with supravalvular AS, modeled by banding of the ascending aorta. However, although average cardiac output remained constant in this study, . mean systolic flow rates significantly decreased when hypertension was induced. This decrease of systolic flow could explain the decrease of pressure
gradients. The increase of the simultaneously estimated orifice area with increasing pressure is more difficult to explain. As (AS) was created by banding of the ascending aorta, pressure induced extension of the band may have caused increasing anatomic and effective orifice areas. Thus, limitations of the animal model might explain the discrepancy with the findings of the present study. In contrast to these data, the in vitro study by Razzolini et al.12 demonstrated a small but linear increase of pressure gradients across a 21 mm porcine
bioprothesis with rising systemic pressure. The authors do not offer an explanation for this observation. An increase in gradient without increase of flow would require a decrease in effective orifice area, which is however not supported by fluid dynamics theory.
Taking all these previous studies together, it remains unclear whether hypertension can independently affect the assessment of AS severity apart from secondary changes in flow rate caused by afterload~related changes in ejection fraction.
The results of the present in
vitro studies suggest that the blood pressure does not directly influence invasive or non-invasive pressure gradient and valve area estimates in AS independently of secondary flow changes. Therefore, variation of estimated valve area and pressure gradient with changing blood pressure, when observed in vivo, are most likely due to afterload-dependent changes inflow rate. Thus, changes in blood pressure should not bias the assessment of AS severity as long as valve area, pressure gradient, and flow rate are taken into consideration.a