Circulation, Vol 64, 1089-1097, Copyright © 1981 by American Heart Association
BG Brown, E Bolson, RB Petersen, CD Pierce and HT Dodge
The effect of sublingual or intracoronary nitroglycerin (NTG) on luminal
caliber in normal and diseased portions of epicardial coronary arteries was
determined in 85 lesions from 57 typical patients with ischemic heart
disease. Measurements were made from coronary angiograms, using a
computer-assisted method and a carefully blinded protocol for analysis of
the pre- and post- NTG angiograms. Luminal area in the "normal" portion of
the diseased segment and at its maximum constriction and an estimate of
flow resistance in the stenosis were computed. Luminal area increased 1.27
mm2 (p less than 0.001) in the "normal" regions, an average increase of 18%
over the control area. Dilation with NTG depended strongly on vessel size;
area increased 35% in normal vessels of 1.6-2.3 mm luminal diameter and
only 9% in vessels 4.0-5.0 mm in diameter. Lesions were grouped into four
levels of severity by percent stenosis. Minimum luminal area increased 0.35
mm2 (p less than 0.01) at the narrowest point in moderate lesions, a 22%
area increase, and 0.14 mm2 (p less than 0.001) in severe lesions, a 36%
area increase. Stenosis dilation resulted in an average 25% reduction (p
less than 0.01) in estimated stenosis flow resistance in moderate lesions
and a 38% reduction (p less than 0.001) in severe lesions. A statistically
significant resistance reduction of greater than 20% occurred in 15 to 20
severe stenoses; only two of 20 showed no measurable dilation. We reviewed
recent literature on hemodynamic responses to NTG and determined that
changes of this magnitude are among the largest reported. We conclude that
vasodilation of epicardial coronary stenosis is usually a major component
of the beneficial response to NTG. We support that conclusion by
demonstrating a striking improvement in ischemic left ventricular
compliance abnormalities after low-dose intracoronary NTG.
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The mechanisms of nitroglycerin action: stenosis vasodilatation as a major component of the drug response
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