Inflammation-associated rapidly progressive coronary artery disease: a case report

Inflammation plays important roles in the pathogenesis of both de novo and restenotic lesions in coronary artery disease (CAD).

This patient was a middle-aged female who had few risk factors for atherosclerotic CAD (AS-CAD) but prior history of psoriasis and elevated erythrocyte sedimentation rate. The patient experienced four ischaemia-driven hospitalizations and/or percutaneous coronary interventions (PCIs) within 18 months due to new-onset or worsened coronary de novo and/or restenotic lesions, especially recurrent restenosis at the same vessel segment, despite optimal PCI and strict secondary prevention for AS-CAD. The patient received: (i) ischaemia-driven (least-necessary) and restricted (least-invasive) PCI, which relieved severe anginal symptoms and (ii) immunosuppressive therapy, which was associated with delayed progression and even partial regression of the coronary lesions, as well as reduced need for further ischaemia-driven hospitalization and/or revascularization during a 40-month follow-up.

We propose to use inflammation-associated rapidly progressive CAD (IR-CAD) to define the disease entity of this patient. Both systemic inflammation and local vascular inflammation secondary to local vascular mechanical injury, such as that induced by PCI per se, might contribute to the pathogenesis of IR-CAD. Immunosuppressive therapy (to control inflammation) together with ischaemia-driven and restricted PCI (to relieve severe myocardial ischaemia and avoid unnecessary vascular mechanical injury) might be crucial to the treatment of IR-CAD.