Somewhat analogous to the use of dobutamine to clarify pseudo versus truly severe AS in patients with a small AVA, low gradient, and a preserved EF, 15 they demonstrate that nitroprusside can increase flow and provide insight into the true severity of the AS. However, cut points for determining truly severe AS based on a change in AVA and gradient with pharmacological intervention are not uniform across studies and require further investigation. 15,16 Even so, the current data provide further support for the concept that systemic HTN can influence the evaluation of AS severity.
17
Clinical ImplicationsIn managing patients with AS, it is important to recognize the high prevalence of coexistent systemic HTN, its harmful effects on LV remodeling and function, and its adverse impact on clinical outcomes. Moreover, when determining the severity of AS and making decisions about the timing of valve replacement, it is important to recognize that systemic HTN can influence the assessment of AS severity (generally causing overestimation of severity; Figure).17 After valve replacement is performed, there may be a greater tendency toward systemic HTN because of the increased flow from the relief of valvular afterload, which may mitigate the expected favorable effects of LV unloading with valve replacement and limit symptomatic improvement. For all these reasons, both before and after valve replacement, treatment of systemic HTN should be an important objective of medical therapy.When managing a symptomatic patient with uncontrolled systemic HTN (at the time of the echocardiogram) and a small AVA, low gradient, and preserved EF, it is reasonable to redo the echocardiogram when the patient is normotensive, particularly if the measurements of AS severity are borderline between moderate and severe. It also is prudent to reassess symptoms once the patient is consistently normotensive. When managing an asymptomatic patient with uncontrolled systemic HTN and a small AVA, low gradient, and preserved EF, effective HTN treatment may mitigate the deleterious effects on the LV of increased systemic vascular load and potentially delay symptom onset. Although LV outflow obstruction at the level of the valve is the sine qua non of AS, increased systemic vascular load-identified most readily as systemic HTN-is often coexistent with AS and contributes to the pressure overload, hypertrophic remodeling, and dysfunction of the LV, which underlies much of the morbidity and mortality of the disease. As such, we must remember to treat the patient (including HTN and other cardiovascular comorbidities) and not have a myopic focus on the valve alone to provide the best clinical outcomes.
Sources of FundingDr Lindman was supported by K23 HL116660 from the NIH.
DisclosuresNone.
References