Figure legends
Figure 1: Inhibition of ADP-induced platelet aggregation by SNP (10µM) in whole blood samples from healthy control subjects and patients in chronic phase of coronary artery spasm (CAS). Comparisons between coronary slow flow phenomenon (SCFP) and Prinzmetal’s angina (PA) subgroups of patients are also shown.
Figure 2: Comparison of the inhibitory effects of SNP (10µM) on ADP-induced platelet aggregation during acute exacerbations of CAS, compared by paired analysis with the chronic state. There is a trend towards further impairment of SNP responses (p = 0.06) in the acute phase.
Figure 3: (A) Plasma concentrations of SD-1, evaluated in control subjects, and CAS patients in acute and chronic phases. (B ) Ratios of individual plasma tryptase concentrations in acute phase, compared with those in chronic phase (p = 0.03).
Figure 4: Comparison of platelet-derived microparticle (PMP) counts between CAS patients (during acute and chronic phases) and control subjects. ANOVA: p = 0.03; Bonferroni test (acute versus chronic phases): p = 0.02.
Figure 5: Impact of infusion of NTG/NAC in acutely symptomatic patients:- (A) Impact on ex vivo platelet response to SNP. (B) Impact on plasma SD-1 concentrations
Figure 6: In vitro effects of increasing concentrations of NAC and of the H2S donor NaHS on anti-aggregatory responses to SNP (10µM) in blood samples from patients in chronic phase of CAS. ANOVA: p < 0.01 for both concentration-response relationships and effect of NaHS versus that of NAC.
Figure 7: Impacts of co-incubation in vitro with inhibitors of H2S formation [PAG (3.3mM) and AOAA (0.5mM)] on anti-aggregatory responses to SNP (10µM)/NAC (100µM) in blood samples from patients in chronic phase of CAS.
Table: Demographics and treatment regimens at time of assessment of coronary artery spasm patients and control subjects recruited (p values are for control subjects vs chronic CAS patients).