Antithrombotic properties of transdermal nitroglycerin in stable angina pectoris

https://doi.org/10.1016/0002-9149(94)90283-6Get rights and content

Abstract

Nitroglycerin provides an external source of nitric oxide which stimulates guanylate cyclase and produces vasodilatation and inhibition of platelet function. The antithrombotic effects of intravenous nitroglycerin were recently documented in various experimental models and in patients with unstable angina. This protocol was designed to evaluate whether these effects could also be detected with transdermal nitroglycerin in patients with stable angina. In a randomized, double-blind, controlled parallel trial, 22 patients received transdermal nitroglycerin, 0.6 mg/hour (11 patients), or placebo (11 patients). Platelet aggregation to adenosine diphosphate (ADP) and to thrombin was measured in whole blood. Thrombus formation was assessed on porcine aortic media exposed to the patient's venous blood for 3 minutes at shear rates of 2,546 and 754 s−1. Platelet aggregation to ADP decreased from 7.7 ± 0.8 to 5.3 ± 0.8 ohms (p < 0.05) with nitroglycerin, and to thrombin from 15.6 ± 1.2 to 12 ± 1.2 ohms (p < 0.05). Thrombus size at the high-shear rate decreased from 2.8 ± 0.7 to 1.0 ± 0.3 μm2 (p < 0.05), and at the low-shear rate from 2.5 ± 0.5 to 1.0 ± 0.2 μm2 (p < 0.05). Placebo had no significant effect on platelet aggregation and platelet thrombus deposition. These parameters were all reduced by ≥ 20% in 8 patients taking nitroglycerin but only in 3 patients taking placebo (p < 0.05). Transdermal nitroglycerin significantly inhibits platelet aggregation and mural thrombus formation in patients with angina pectoris.

References (20)

There are more references available in the full text version of this article.

Cited by (31)

  • Concomitant nitrates enhance clopidogrel response during dual anti-platelet therapy

    2016, International Journal of Cardiology
    Citation Excerpt :

    Whether or not this association is due to synergic anti-platelet potency requires randomized study of a large sample size, although our preliminary data seems important, despite lacking mechanistic explanation. Originally, nitrates are known to inhibit platelet function, which have been consistently shown in numerous studies, moreover, nitrates are commonly prescribed during and post-PCI mostly due to vasodilatation effects (e.g. [6–9,19]). Nitrates are known to activate guanylyl cyclase, and increase cellular cyclic guanosine monophosphates in smooth muscle and platelet [20].

  • Stable Ischemic Heart Disease

    2016, Heart Failure Clinics
    Citation Excerpt :

    NO also inhibits potassium channels to hyperpolarize muscle membranes and activates light chain phosphatase, both effecting relaxation, accounting for more vasodilatation. NO increases cGMP in platelets to reduce calcium and suppress platelet activation.23 In modest doses, nitrates reduce preload; in higher doses, they lower afterload.

  • Stable ischemic heart disease

    2014, Cardiology Clinics
  • The Effects of Medications on Myocardial Perfusion

    2008, Journal of the American College of Cardiology
    Citation Excerpt :

    The anti-ischemic effect of nitroglycerin might also be attributable to the redistribution of coronary flow from normal to ischemic myocardium through dilation of collateral vessels (10,11,18). Nitroglycerin may also preserve myocardial perfusion through the inhibition of platelet thrombus formation (19–22). Nitric oxide is capable of activating soluble guanylyl cyclase in platelets.

  • Acute and delayed antithrombotic effects of alcohol in humans

    2001, American Journal of Cardiology
    Citation Excerpt :

    There is also excellent reproducibility (r = 0.95, p = 0.0001) between measurements performed 1 week apart.8,9 Repeat studies on the same morning in 11 patients taking a placebo agent showed no serial change in platelet thrombus size as assessed by this technique.11 Repeat studies in 17 stable patients at a mean of 2.1 and 7.6 months also showed no significant serial changes in platelet thrombus size.8,9

View all citing articles on Scopus
View full text