Key result
Unstable angina pectoris was associated with significantly increased big ET-1 levels (2.6 +/- 1.5 fmol/ml) compared to normal values (0.52 +/- 0.07 fmol/ml; p < 0.03).
Why the study?
Are circulating ET-1 and big ET-1 levels altered in patients with unstable angina pectoris compared to stable angina and healthy controls?
Observational
Are circulating ET-1 and big ET-1 levels altered in patients with unstable angina pectoris compared to stable angina and healthy controls?
Big ET-1 levels are significantly elevated during the acute stage of unstable angina pectoris, reflecting a transient general activation of the endothelium that recovers after 5 days of stabilization.
Answers are grounded in this paper and cite their sources.
Big ET-1 elevation in unstable angina may signal transient endothelial activation; leaves open its prognostic or therapeutic utility in prospective studies.
The pathophysiologic meaning of elevated circulating endothelin-1 (ET-1) levels in various cardiovascular diseases is not understood. The aim of this study was to measure ET-1 and big ET-1 levels in patients with unstable angina pectoris (UAP) and within 5 days after stabilization. These values were compared to those of patients with stable angina pectoris (SAP) and to healthy controls (Co). In addition, a venous occlusion test was performed as an endothelial provocation test to characterize endothelial function. Big ET-1 levels were increased to 2.6 +/- 1.5 fmol/ml during unstable angina pectoris compared to normal values of 0.52 +/- 0.07 fmol/ml (p < 0.03; n = 14). After stabilization, big ET-1 decreased to 1.5 +/- 0.4 fmol/ml within 5 days (n.s.). ET-1 levels were not increased during UAP and after stabilization. ET-1 and big ET-1 levels from patients with SAP did not differ from those of healthy controls. The venous occlusion test resulted in an increase of ET-1 levels (0.3 +/- 0.02 to 0.46 +/- 0.02 fmol/mg, p = 0.008; SAP 0.3 +/- 0.04 to 0.39 +/- 0.05 fmol/ml, p = 0.009) in healthy controls and in patients with SAP. In contrast, patients with UAP showed no significant increase in ET-1 with this test. After stabilization for 5 days, the provocation test induced an increase in circulating ET-1 in patients with UAP comparable to that of controls (0.62 +/- 0.18 fmol/mg vs. 0.95 +/- 0.25 fmol/mg; p < 0.02). In summary, during UAP big ET-1 values are significantly increased and ET-1 values tend to be elevated. In an endothelial provocation test, ET-1 values did not increase. This might reflect a general activation of the endothelium in UAP during the acute stage, because the normal response is recovered 5 days later.
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Brehm et al. (1998) conducted an observational in Unstable angina pectoris. Unstable angina pectoris vs. Stable angina pectoris and healthy controls was evaluated on Big ET-1 levels (p=< 0.03). Unstable angina pectoris was associated with significantly increased big ET-1 levels (2.6 +/- 1.5 fmol/ml) compared to normal values (0.52 +/- 0.07 fmol/ml; p < 0.03).
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