Luminal thrombotic occlusions associated with non-significant atherosclerosis are commonly observed in patients with critical lower limb ischemia, which suggests the possibility of thromboembolic disease as a great contributor to ischemia. This was particularly verifiable in infrapopliteal vessels, thus showing a possible mechanism of progression from peripheral vascular disease to critical ischemia, as well as a possible role for antithrombotic agents.

Arteries from 95 patients (121 amputations) were studied; 75 of these patients had suffered amputations due to critical ischemia, while the remaining had amputations for other reasons. The pathological characteristics were recorded separately for the femoral artery, the popliteal artery, and infrapopliteal arteries.

In the 239 arteries from patients with critical ischemia, atherosclerotic plaques were more frequently found in the femoropopliteal area compared with the infrapopliteal area (67.6% vs. 38.5%; odds ratio [OR]: 5.47; p = 0.003). Among these 239 arteries, 69% presented ≥70% stenosis as a consequence of pathological intimal thickening, fibroatheroma, fibrocalcific lesions, or restenosis. Others were associated with luminal thrombi (23.6%) or thrombi without significant atherosclerotic lesions.

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The presence of chronic luminal thrombi was more frequent in arteries with non-significant atherosclerosis (OR: 16.7; p = 0.002), which was more common in infrapopliteal arteries than in femoropopliteal arteries (p = 0.0041). However, acute thrombotic occlusion was less frequent in arteries with larger diameter.

Conclusion

Thrombotic luminal occlusion is frequently associated with non-significant atherosclerosis and it is usually observed in patients with critical ischemia who required amputation. Thrombosis may be a mechanism of progression from intermittent claudication to critical ischemia, and a possible role for antithrombotic agents is suggested.

Original title: Pathology of Peripheral Artery Disease in Critical Limb Ischemia.

Reference: Navneet Narula et al. J Am Coll Cardiol 2018. Online before print.

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