Systemic Hypertension in Low Gradient Severe Aortic Stenosis With Preserved Ejection Fraction

Study Questions:

What are the acute hemodynamic effects of afterload-reduction with nitroprusside among patients with low-flow, low-gradient (LF LG) severe aortic stenosis (AS) with preserved left ventricular ejection fraction (LVEF) and incompletely treated systemic hypertension?


The study population was 18 consecutive symptomatic patients with hypertension (aortic systolic pressure >140 mm Hg) and LG (mean gradient <40 mm Hg) severe AS (echocardiographic aortic valve area <1.0 cm2 or aortic valve area index <0.6 cm2/m2) with preserved EF (echo EF >50%) who were referred for invasive hemodynamic left and right heart catheterization and who received infusion of intravenous sodium nitroprusside to reduce blood pressure and arterial afterload. Nitroprusside was administered during left/right heart catheterization, and hemodynamics were assessed invasively.


At baseline, patients had severe hypertension (aortic systolic pressure 176 ± 26 mm Hg), pulmonary hypertension (mean pressure 39 ± 12 mm Hg), elevated LV end-diastolic pressure (19 ± 5 mm Hg), and reduced stroke volume (33 ± 8 ml/m2). All measures of afterload were reduced with nitroprusside (p < 0.001 for all). Nitroprusside reduced mean pulmonary artery pressure (25 ± 10 mm Hg) and LV end-diastolic pressure (11 ± 5 mm Hg) (p < 0.001 for both, as compared to baseline). Aortic valve area (0.86 ± 0.11 to 1.02 ± 0.16 cm2, p = 0.001) and mean gradient (27 ± 5 to 29 ± 6 mm Hg, p = 0.02) increased with nitroprusside.


Systemic hypertension in LG severe AS with preserved EF is associated with elevated LV filling pressures and pulmonary hypertension. Treatment of hypertension with vasodilator therapy resulted in lower total LV afterload, with a decrease in LV filling pressures and pulmonary artery pressures. The authors concluded that these findings have important implications for the management of hypertensive patients with LG severe AS with preserved EF.


The management of patients with LF LG severe AS and preserved LVEF is challenging. Some patients clearly have very severe AS, but a low stroke volume (often mediated by concentric LV hypertrophy and a very small LV cavity) results in low cardiac output and LF LG truly severe AS; whereas other patients likely have only moderate AS, but an effective orifice area that suggests more severe AS. This fascinating paper helps further unravel the puzzle of LF LG severe AS with paradoxical normal LVEF. Among patients with incompletely treated systemic hypertension (the population studied here), most patients did not have truly severe AS—when afterload was reduced pharmacologically, gradients increased only modestly, but valve area increased, and in most patients, no longer suggested severe AS. This has very important clinical implications. First, as the authors noted, symptoms of dyspnea among such patients could be attributable to high LV filling pressures, suggesting that (even if AS was severe) intervention might not be indicated. Second, and perhaps most importantly, the severity of AS probably cannot be reliably assessed invasively or noninvasively in the setting of incompletely treated systemic hypertension.

Clinical Topics: Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Prevention, Interventions and Imaging, Echocardiography/Ultrasound, Hypertension

Keywords: Cardiac Catheterization, Blood Pressure, Angioplasty, Pulmonary Artery, Dyspnea, Vasodilator Agents, Hemodynamics, Cardiology, Stroke Volume, Ventricular Function, Hypertrophy, Hypertension, Echocardiography

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