Data on PHT due to significant aortic regurgitation (AR) has up to now been much scarcer, with one study finding severe PHT in 16% of cases of severe AR.
The chronic pressure overload generated by AS and pressure/volume overload caused by AR result in differential patterns of left ventricular (LV) remodeling, with more often a thick-walled, concentric remodeled LV in AS, and a dilated, eccentrically hypertrophied LV in AR. Both types of LV remodeling become maladaptive during the AS/AR progression and initiate the same pathway of elevated LV end-diastolic pressure and consequently elevated left atrial pressure. The high pressure is further on transmitted backwards to the pulmonary veins, causing over time isolated postcapillary PHT. In advanced disease stages, due to pulmonary vascular remodeling and increasing pulmonary vascular resistance, a combined precapillary and postcapillary PHT might develop.
By echocardiography and using eSPAP >60 mm Hg as a surrogate of severe PHT, previous studies have documented higher mortality risk in patients with combined severe AS–PHT.3 5 The prevalence of milder degrees of PHT and their prognostic importance have however been less clear, particularly in patients with moderate AS or with AR.
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