Comparison of ADAMTS-1, -4 and -5 expression in culprit plaques between acute myocardial infarction and stable angina

ADAMTS (a disintegrin and metalloproteinase with thrombospondin type 1 motifs) proteases might contribute to plaque destabilisation by weakening the fibrous cap. However, little is known about the expression of ADAMTS proteases in coronary atherosclerotic plaques.

To examine the expression of ADAMTS proteases in coronary atherectomy samples obtained from patients with acute myocardial infarction (AMI) or stable angina.

Atherectomy specimens were obtained from 34 patients with AMI (n=23) or stable angina (n=11) who underwent directional coronary atherectomy. The specimens were stained with H&E and analysed immunohistochemically using antibodies specific to ADAMTS-1, -4 and -5; versican cleavage products; and markers for endothelial cells, macrophages and smooth muscle cells.

Baseline characteristics were similar between the two groups. The proportion of CD31 and CD68 immunopositive areas did not differ between the two groups, but the area immunopositive for smooth muscle α-actin was smaller in the AMI group. The relative area immunopositive for ADAMTS-1 in AMI (1.04% (IQR 0.59-2.09%)) was significantly greater than that in stable angina (0.24% (0.15-0.39%); p<0.001). In contrast, the proportion of areas immunopositive for ADAMTS-4 or -5 was similar in the two groups. Areas that stained for ADAMTS-1 largely overlapped with those positive for CD68 and versican cleavage products. The areas immunopositive for ADAMTS-1 were significantly correlated with CD68 immunostained areas (r=0.50, p=0.003).

ADAMTS-1, -4 and -5 were present in human coronary atherosclerotic plaques, and ADATS-1 was more strongly expressed in AMI plaques than in stable plaques. ADAMTS-1 may play a role in plaque instability.