title: Systemic hypertension in low-gradient severe aortic stenosis with preserved ejection fraction.
abstract: BACKGROUND
  Low-gradient severe aortic stenosis with preserved ejection fraction is an increasingly recognized entity, and symptomatic patients may benefit from aortic valve replacement. However, systemic hypertension frequently coexists with low-gradient severe aortic stenosis, which itself may cause elevated left ventricular (LV) filling pressures with resultant symptoms of dyspnea.
  
  
  RESULTS
  Symptomatic patients with hypertension (aortic systolic pressure >140 mm Hg) and low-gradient (mean gradient <40 mm Hg) severe aortic stenosis (aortic valve area <1 cm(2)) with preserved ejection fraction (ejection fraction >50%) who underwent invasive hemodynamic catheterization of the left and right sides of the heart received infusion of intravenous sodium nitroprusside to reduce blood pressure and arterial afterload. 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/m(2)). 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 compared with baseline). Aortic valve area (0.86±0.11 to 1.02±0.16 cm(2); P=0.001) and mean gradient (27±5 to 29±6 mm Hg; P=0.02) increased with nitroprusside.
  
  
  CONCLUSIONS
  Systemic hypertension in low-gradient severe aortic stenosis with preserved ejection fraction is associated with elevated LV filling pressures and pulmonary hypertension. Treatment of hypertension with vasodilator therapy results in a lowering of the total LV afterload, with a decrease in LV filling pressures and pulmonary artery pressures. These findings have important implications for the management of patients with low-gradient severe aortic stenosis with preserved ejection fraction and hypertension.
authors: Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic College of Medicine, Rochester, MN.
authors: Mackram F
authors: MF
authors: Eleid
authors: Rick A
authors: RA
authors: Nishimura
authors: Paul
authors: P
authors: Sorajja
authors: Barry A
authors: BA
authors: Borlaug
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000959:Antihypertensive Agents / Q000008:administration & dosage; D001024:Aortic Valve Stenosis / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004417:Dyspnea / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy* / Q000503:physiopathology; D006976:Hypertension, Pulmonary / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D007262:Infusions, Intravenous; D008297:Male; D009599:Nitroprusside / Q000008:administration & dosage*; D011446:Prospective Studies; D011669:Pulmonary Wedge Pressure / Q000187:drug effects / Q000502:physiology; D012720:Severity of Illness Index; D013318:Stroke Volume / Q000187:drug effects* / Q000502:physiology; D017725:Ventricular Pressure / Q000187:drug effects / Q000502:physiology
chemical_list: D000959:Antihypertensive Agents; D009599:Nitroprusside
keywords: aortic valve stenosis; hypertension; stroke volume