Immune system activation follows inflammation in unstable angina: pathogenetic implications
Giuseppina Caligiuri, MDa,
Giovanna Liuzzo, MDa,
Luigi M. Biasucci, MD, FACCa and
Attilio Maseri, MD, FACCa
a Department of Cardiology, Catholic University, Rome, Italy
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Figure 1 CRP levels were significantly higher on admission in group A2 (25 mg/L, p < 0.0001) than in group A1 (4.5 mg/L) and groups B1 and B2 (3.3 and 2 mg/L respectively). The high CRP levels significantly decreased in group A2 to 7.8, 0.2 to 32.2 mg/l in sample 2 and to 6.8, 0.2 to 26.5 mg/l in sample 3 (p < 0.0001 vs. sample 1). In control groups B1 and B2, CRP levels were lower than in unstable angina groups (A1 and A2, p < 0.0001) and did not change during the study. The x-axis represents the time of sampling: 1 = admission; 2 = after 7 to 15 days; 3 = after 6 months; A1 = resolving UA, n = 19; A2 = refractory UA, n = 16; B1 = stable angina, Canadian class I to II, n = 20; B2 = stable angina, Canadian class III to IV, n = 15.
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Figure 2 Total IgM serum levels were higher in unstable groups A1 and A2 than in stable angina groups B1 and B2 (p < 0.0001) and showed a transient increase at sample 2 (p < 0.001 vs. sample 1 and p < 0.05 vs. sample 3) that was not detectable in the controls. The increment of IgM was significantly greater in group A1 (favorable outcome) than in group A2 (p < 0.05).
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Figure 3 The proportion of activated T cells (CD3+/DR+) was similar in unstable and stable angina groups on admission (sample 1), but was transiently and significantly increased at sample 2 in group A and not in group B (p < 0.0001). Group A1 (favorable outcome) showed a more dramatic transient increase in activated T cells than group A2 (less favorable outcome): they were 6 (2 to 8) % in sample 1, increased up to 20 (7 to 31) % at sample 2 (p < 0.0001) and returned to 5 (2 to 15) % at sample 3 (p < 0.0001 vs. sample 2, p = NS vs. sample 1). No time variation was detectable in controls. The x-axis represents the time of sampling: 1 = admission; 2 = after 7 to 15 days; 3 = after 6 months; A1 = resolving UA, n = 19; A2 = refractory UA, n = 16; B1 = stable angina, Canadian class I to II, n = 20; B2 = stable angina, Canadian class III to IV, n = 15.
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Figure 4 The increment in CD3+/DR+ (activated T) cells was significantly greater in case of favorable outcome (group A1, median increase 250%) than in case of medical therapy failure in UA (group A2, median increase 30%, p < 0.0001).
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Figure 5 IL-2 levels were similar in unstable and stable angina on admission, but showed a significant and transient increase at sample 2 only in group A (p < 0.001 vs. samples 1 and 3). Such a time variation was absent in groups B. The x-axis represents the time of sampling: 1 = admission; 2 = after 7 to 15 days; 3 = after 6 months; A1 = resolving UA, n = 19; A2 = refractory UA, n = 16; B1 = stable angina, Canadian class I to II, n = 20; B2 = stable angina, Canadian class III to IV, n = 15.
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Figure 6 Scatter plot shows the relation between CRP acute levels (at sample 1) and the percentage increment in CD3+/DR+ (at sample 2 compared to sample 1 in each patient) in UA (group A). Serum levels of CRP in the acute phase of UA were inversely related to the percentage increment of CD3+/DR+ lymphocytes at 7 to 15 days (Spearman’s rank correlation: r = 0.63, p = 0.0003). Patients with a more favorable outcome (group A1, open squares) had lower CRP levels and a higher CD3+/DR+ increment as compared with patients with a less favorable outcome of UA (group A2, solid squares).
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