Nitroglycerin rebound associated with vascular, rather than platelet, hypersensitivity
Daniel Hébert, PhDa and
Jules Y. T. Lam, MD, FACCa
a Department of Medicine, Montreal Heart Institute, University of Montreal Medical School, Montreal, Quebec, Canada
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Figure 1 Mean arterial pressure was monitored at baseline, 3 h and 48 h after continuous nitroglycerin (NTG) treatment and 2 h after withdrawal of NTG therapy. Arterial pressure decreased after 3 h of NTG treatment, with a return to baseline after 48 h consistent with the development of hemodynamic tolerance. However, arterial pressure was significantly increased 2 h after NTG withdrawal consistent with a rebound phenomenon. +p < 0.05 versus baseline.
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Figure 2 Compared with baseline, platelet deposition onto the aortic media was significantly decreased at 3 h and 48 h during nitroglycerin (NTG) therapy and remained decreased 2 h after patch removal. *p < 0.05 versus baseline.
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Figure 3 Platelet aggregation was measured by impedance aggregometry in whole blood and was initiated with the addition of 0.075 U/ml of thrombin. Platelet aggregation was decreased after 48 h of continuous nitroglycerin (NTG) therapy (*p < 0.05 vs. baseline) and remained decreased 2 h after its withdrawal.
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Figure 4 Bolus angiotensin II infusion increased mean arterial pressure. There was a nonsignificant decrease in the efficacy of angiotensin after 3 h of nitroglycerin treatment, while a nonsignificant increase was observed at 48 h when compared with baseline. Two hours after withdrawal of nitroglycerin treatment, there was a supersensitive response with a significant increase in mean arterial pressure. *p < 0.05 versus baseline.
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