TY - JOUR
T1 - Effect of nitroglycerin during hemodynamic estimation of valve orifice in patients with mitral stenosis
AU - Halperin, Jonathan L.
AU - Rrothlauf, Elizabeth B.
AU - Brooks, Kenneth M.
AU - Mindich, Bruce P.
AU - Ambrose, John A.
PY - 1987
Y1 - 1987
N2 - In patients with mitral stenosis, valve orifice calculations using pulmonary capillary wedge pressure as a substitute for left atrial pressure may overestimate the severity of disease. Previous studies have shown that mitral valve area determined from transseptal left atrial pressure measurements exceeds that area derived from pulmonary wedge pressure measurements. This is probably due to pulmonary venoconstriction, which is reversed by nitroglycerin. Nitroglycerin, 0.4 mg, was administered sublingually to 20 patients with mitral valve disease during preoperative cardiac catheterization using the pulmonary capillary wedge pressure as the proximal hydraulic variable. At the time of peak hypotensive effect, 3 to 5 minutes after nitroglycerin administration, the mean pulmonary capillary wedge pressure decreased from 23 ± 2 (mean ± SEM) to 19 ± 2 mm Hg (p < 0.005). The mean diastolic transmitral pressure gradient (12.6 ± 1.2 mm Hg before and 11.5 ± 1.0 mm Hg after nitroglycerin; p = NS) and cardiac output (4.0 ± 0.3 to 4.1 ± 0.3 liters/min; p = NS) did not change significantly. Nevertheless, the hemodynamic mitral orifice area, calculated using the Gorlin formula, increased from 0.8 ± 0.1 to 1.1 ± 0.2 cm2 (p < 0.05). In 12 patients with isolated mitral stenosis, without regurgitation, the mitral valve orifice area after nitroglycerin was 0.4 ± 0.2 cm2 larger than it was before drug administration (p < 0.05). Administration of nitroglycerin during evaluation of mitral stenosis eliminates pulmonary venoconstriction, which raises the pulmonary capillary wedge pressure above the left atrial pressure in some patients. Nitroglycerin may add diagnostic accuracy without transseptal catheterization. Whether this response to nitroglycerin has direct therapeutic value in patients with mitral valve obstruction has yet to be determined.
AB - In patients with mitral stenosis, valve orifice calculations using pulmonary capillary wedge pressure as a substitute for left atrial pressure may overestimate the severity of disease. Previous studies have shown that mitral valve area determined from transseptal left atrial pressure measurements exceeds that area derived from pulmonary wedge pressure measurements. This is probably due to pulmonary venoconstriction, which is reversed by nitroglycerin. Nitroglycerin, 0.4 mg, was administered sublingually to 20 patients with mitral valve disease during preoperative cardiac catheterization using the pulmonary capillary wedge pressure as the proximal hydraulic variable. At the time of peak hypotensive effect, 3 to 5 minutes after nitroglycerin administration, the mean pulmonary capillary wedge pressure decreased from 23 ± 2 (mean ± SEM) to 19 ± 2 mm Hg (p < 0.005). The mean diastolic transmitral pressure gradient (12.6 ± 1.2 mm Hg before and 11.5 ± 1.0 mm Hg after nitroglycerin; p = NS) and cardiac output (4.0 ± 0.3 to 4.1 ± 0.3 liters/min; p = NS) did not change significantly. Nevertheless, the hemodynamic mitral orifice area, calculated using the Gorlin formula, increased from 0.8 ± 0.1 to 1.1 ± 0.2 cm2 (p < 0.05). In 12 patients with isolated mitral stenosis, without regurgitation, the mitral valve orifice area after nitroglycerin was 0.4 ± 0.2 cm2 larger than it was before drug administration (p < 0.05). Administration of nitroglycerin during evaluation of mitral stenosis eliminates pulmonary venoconstriction, which raises the pulmonary capillary wedge pressure above the left atrial pressure in some patients. Nitroglycerin may add diagnostic accuracy without transseptal catheterization. Whether this response to nitroglycerin has direct therapeutic value in patients with mitral valve obstruction has yet to be determined.
UR - http://www.scopus.com/inward/record.url?scp=0023195979&partnerID=8YFLogxK
U2 - 10.1016/S0735-1097(87)80017-7
DO - 10.1016/S0735-1097(87)80017-7
M3 - Article
AN - SCOPUS:0023195979
SN - 0735-1097
VL - 10
SP - 342
EP - 348
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 2
ER -