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

Abstract Background Inflammation plays important roles in the pathogenesis of both de novo and restenotic lesions in coronary artery disease (CAD). Case Summary 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 ischemia-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: 1) ischemia-driven (least-necessary) and restricted (least-invasive) PCI, which relieved severe anginal symptoms; 2) immunosuppressive therapy, which was associated with delayed progression and even partial regression of the coronary lesions, as well as reduced need for further ischemia-driven hospitalization and/or revascularization during a 40-month follow-up. Discussion We propose to use inflammation-associated rapidly progressive coronary artery disease (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 ischemia-driven and restricted PCI (to relieve severe myocardial ischemia and avoid unnecessary vascular mechanical injury) might be crucial to the treatment of IR-CAD.