Abstract
The hemodynamic effect of a large dose of nitroglycerin (NTG) (90 mg) given transdermally using a reservoir system was studied in 10 patients with severe, long-standing congestive heart failure. Serial hemodynamic measurements over 24 hours revealed a mild decrease in mean pulmonary artery wedge pressure. However, the change from baseline was significant only at 2 hours (19 ± 9 vs 27 ± 6 mm Hg). Mean right atrial pressure fell 1 hour after initiation of therapy, from 12 ± 7 to 8 ± 5 mm Hg. However, the change from control was not statistically significant. No significant changes were noted in heart rate, mean blood pressure, cardiac index, and systemic and pulmonary vascular resistance. Individual analysis of the effect of transdermal NTG on pulmonary artery wedge pressure demonstrated at 20% or greater reduction in 8 of 10 patients. However, persistent effect (longer than 8 hours) was seen in only 4 patients. Removal of NTG patches at 24 hours did not result in hemodynamic rebound. Serum catecholamine levels and renin concentration did not change 2 hours and 24 hours after initiation of NTG therapy or after removal of NTG patches. Thus, a large dose (90 mg) of transdermal NTG using a reservoir system results in mild and mostly statistically insignificant hemodynamic effect in patients with chronic severe congestive heart failure. Although a reduction in pulmonary artery wedge pressure is seen in most patients, rapid attenuation of this response is found in many patients and the effect only rarely lasts for 24 hours. The lack of hemodynamic rebound after discontinuation of therapy in addition to the absence of changes in serum catecholamine levels and renin concentration suggest that hemodynamic attenuation is not a result of activation of vasoconstrictive mechanisms during continuous NTG therapy.
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