Introduction: Nonspecific latent inflammation plays a significant role in the development of atherosclerosis and coronary heart disease (CHD) and its exacerbation can cause the atherosclerotic plaque damage and the appearance of atherothrombotic complications. It is considered that the earliest stage of typical for atherosclerosis inflammation is the monocytes adhesion to activated endothelial cells due to hyperexpression of vascular cell adhesion molecules (VCAM). Endothelial adhesion molecules by contacting with blood monocytes and lymphocytes promote their migration into the subendothelial blood vessels space influenced by matrix metalloproteinases (MMP) and cytokines. MMP destroy the collagen and elastin of extracellular matrix and facilitate the damage of atherosclerotic plaque capsule. Pregnancy-associated plasma protein A (PAPP-A) relates to zinc-containing MMP. It is believed that the levels of soluble adhesion molecules (sVCAM) and PAPP-A, which are the criteria of nonspecific inflammation in the vascular wall, can reflect the processes of atherosclerotic plaque destabilization.
Purpose: Identification of coronary heart disease destabilization by measuring the blood levels of sVCAM and PAPP-A in patients with different variants of CHD.
Methods: 173 CHD patients were examined (the average age was 57.24±5.12 years): 92 patients with stable angina and 81 patients with acute coronary syndromes (ACS) (43 – with unstable angina (UA) and 38 – with acute myocardial infarction (MI)). The study excluded patients with chronic heart failure, liver and kidney dysfunction, acute or chronic inflammatory diseases, decompensated diabetes mellitus, severe obesity, infectious diseases. 30 healthy subjects (average age was 55.37±4.82 years) were included in the control group. Levels of sVCAM and PAPP-A were determined by ELISA using the test-systems of Bender MedSystems (Austria) and DRG (Germany).
Results: Rise of sVCAM level occurred in 126 of 173 (72.8%) patients. sVCAM levels in stable patients increased with an increase in disease severity. The most severe changes of both sVCAM and PAPP-A were in patients with ACS, although differences between patients with UA and MI were not significant. PAPP-A levels in patients with II FC did not significantly differ from the norm, and were moderately elevated in 45% patients with III FC. PAPP-A level increase was combined with the rise of C-reactive protein (CRP) and sVCAM, which might indicate a moderate exacerbation of nonspecific inflammation without clinical manifestation. Significant relationships were between levels of both PAPP-A and sVCAM with CRP, but were absent between levels of both PAPP-A and sVCAM with both creatine kinase MB and troponins T and I.
Conclusion: Elevated levels of sVCAM and PAPP-A in blood of the CHD patients are both the reflection of the lowest gradation of vascular inflammation and the indicator of atherosclerotic plaque instability and the possibility of ACS development.