Stable angina and acute coronary syndromes are associated with nitric oxide resistance in platelets
Yuliy Y. Chirkov, PhDa,
Andrew S. Holmes, BSc, Honsa,
Scott R. Willoughby, PhDa,
Simon Stewart, PhDa,
Ronald D. Wuttke, BSca,
Peter R. Sage, MBBSa and
John D. Horowitz, PhDa
a Department of Cardiology, The Queen Elizabeth Hospital, University of Adelaide, Adelaide, Australia
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Figure 1 Representative tracings for inhibition of ADP (1 µmol/liter)-induced aggregation by nitroglycerin (NTG) (100 µmol/liter) and sodium nitroprusside (SNP) (10 µmol/liter) in a whole blood sample obtained from a normal male subject.
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Figure 2 Inhibition of adenosine diphosphate-induced platelet aggregation by nitroglycerin (NTG) (100 µmol/liter) and sodium nitroprusside (SNP) (10 µmol/liter) in whole blood samples obtained from normal subjects, nonischemic patients (NIP), patients with stable angina pectoris (SAP), and patients with acute coronary syndromes (ACS). Number of subjects indicated within bars. *p < 0.01 for patients vs. normals and NIP.
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Figure 3 Univariate analyses: interactions of coronary risk factors and pharmacotherapy with inhibition of adenosine diphosphate-induced platelet aggregation by sodium nitroprusside (10 µmol/liter) in whole blood samples obtained from patients with stable angina pectoris and acute coronary syndromes. ACE inh = angiotensin-converting enzyme inhibitors; ASA = aspirin; CaA = calcium antagonists; H. Chol = high cholesterol; HT = hypertension; Pex = perhexiline; SH = sulphydryl. ;*>p < 0.05. ;**>p < 0.01.
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