ADAMTS4 level in patients with stable coronary artery disease and acute coronary syndromes
Yanping Zha1, Yong Chen, Fayun Xu
1Department of Cardiology, Provincial Hospital, Shandong University, Jinan, China.
Insights
Plasma levels of ADAMTS4, a marker for acute coronary syndromes (ACS), increase with coronary artery disease (CAD) severity. Serial changes in ADAMTS4 may indicate plaque destabilization in ACS patients.
Area of Science:
- Cardiovascular Research
- Biomarker Discovery
- Atherosclerosis Research
Background:
- ADAMTS4 (a disintegrin and metalloprotease with thrombospondin motifs 4) is implicated in atherosclerosis.
- Expression in atherosclerotic plaques suggests a role in acute coronary syndromes (ACS).
Purpose of the Study:
- To compare ADAMTS4 levels across the spectrum of coronary artery disease (CAD).
- To investigate temporal profiles of ADAMTS4 in ACS.
Main Methods:
- Plasma ADAMTS4 levels measured via enzyme immunoassay in patients with stable effort angina pectoris (SAP), ACS, and controls.
- Serial blood sampling in ACS patients over 7 days post-admission.
Main Results:
- Significantly higher plasma ADAMTS4 in cases vs. controls (P<0.001).
- ADAMTS4 levels increased with CAD progression (SAP to STEMI) (P<0.001).
- Elevated ADAMTS4 associated with ACS (ROC AUC 0.753, P<0.001); distinct temporal patterns observed.
Conclusions:
- Serial plasma ADAMTS4 changes documented in ACS patients.
- ADAMTS4 may serve as a marker for plaque destabilization in ACS.
Objective:
A recent study indicates that ADAMTS4 (a disintegrin and metalloprotease with thrombospondin motifs 4) was expressed in macrophage rich areas of human atherosclerotic carotid plaques and coronary unstable plaques suggesting a pathogenic role in the development of acute coronary syndromes (ACS). The aim of the study was to compare ADAMTS4 across the entire spectrum of coronary artery disease (CAD) and to investigate the temporal profiles of ADAMTS4.
Methods:
Plasma levels of ADAMTS4 were measured in patients with stable effort angina pectoris (SAP), ACS and in controls. Venous blood was sampled upon admission before angiography and drug administration. In patients with ACS who underwent medical treatment, serial blood samples were also collected on days 1, 2, 3, 5 and 7 after admission. ADAMTS4 was measured using an enzyme immunoassay.
Results:
Plasma ADAMTS4 level in cases was significantly greater than in controls (P<0.001). Higher levels of ADAMTS4 were found with progression of CAD from SAP to unstable angina pectoris (UAP) to non-ST-segment elevation acute myocardial infarction (NSTEMI) and to ST-segment elevation acute myocardial infarction (STEMI) (P<0.001). Elevated ADAMTS4 level was associated with ACS with an area under receiver operating characteristic (ROC) curve of 0.753 (95% CI 0.654-0.851; P<0.001). The pattern of ADAMTS4 release observed was clearly different in various forms of ACS. ADAMTS4 showed a weak correlation with high-sensitivity C-reactive protein (hs-CRP); however, no significant correlation was found between ADAMTS4 and troponin T (TnT) in ACS patients.
Conclusions:
Serial changes in plasma ADAMTS4 were documented in patients with ACS and may serve as a marker of plaque destabilization.
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