Effect of NO Donors on LV Diastolic Function in Patients With Severe Pressure-Overload Hypertrophy
Key result
Intracoronary NO donors significantly decreased LV end-diastolic pressure from 23 to 14 mm Hg (-39%; P<0.0001) in patients with severe aortic stenosis, improving diastolic function.
Why the study?
Do intracoronary NO donors improve LV diastolic function in patients with severe pressure-overload hypertrophy due to severe aortic stenosis?
Population
17 patients with severe aortic stenosis and severe pressure-overload hypertrophy with diastolic dysfunction
Comparison
Intracoronary NO donors vs Baseline measurements prior to NO donor…
Design
Case_series
Follow-up
Immediate (during procedure)
Authors
Discussion
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Member takes
Implication
Should not change practice in severe aortic stenosis; hypothesis-generating for NO modulation of diastolic function.
Structured PICO
Do intracoronary NO donors improve LV diastolic function in patients with severe pressure-overload hypertrophy due to severe aortic stenosis?
P
Population
17 patients with severe aortic stenosis and severe pressure-overload hypertrophy with diastolic dysfunction
I
Intervention
Intracoronary NO donors (nitroglycerin 30, 90, and 150 microg in n=11; sodium nitroprusside 1, 2, and 4 microg/min in n=6)
C
Comparator
Baseline measurements prior to NO donor administration
O
Outcome
Left ventricular (LV) hemodynamics including LV end-diastolic pressure and LV peak systolic pressuresurrogate
Main Result
Effect estimate: -39%
Absolute Event Rate: 14% vs 23%
p-value: p=<0.0001
Intracoronary NO donors significantly improve diastolic function by reducing LV end-diastolic pressure and chamber stiffness in patients with severe pressure-overload hypertrophy from aortic stenosis.
Cite This Study
Matter et al. (1999) studied Severe aortic stenosis with pressure-overload hypertrophy (n=17). Intracoronary NO donors (nitroglycerin or sodium nitroprusside) vs. Baseline was evaluated on Left ventricular end-diastolic pressure (-39%, p=<0.0001). Intracoronary NO donors significantly decreased LV end-diastolic pressure from 23 to 14 mm Hg (-39%; P<0.0001) in patients with severe aortic stenosis, improving diastolic function.