Percutaneous coronary intervention in the context of systemic inflammation: more injury and worse outcome

Abstract

Minor myocardial injury (MMI), identified by elevated serum levels of cardiac markers, is not uncommon after successful, uncomplicated elective percutaneous coronary intervention (PCI) in patients with stable angina. Serum cardiac troponin, especially cardiac troponin I (cTnI), are more sensitive than serum creatine kinase - MB in detecting MMI. Occlusion of small side-branch vessels, visualized by angiography, may explain the mechanism of the MMI in some, but not all patients. Occlusion of small intramyocardial vessels, not visualized by angiography, might be the mechanism of MMI in these patients. Recent reports have shown that cardiac troponin I elevation after successful, uncomplicated elective PCI in patients with stable angina may be a marker of adverse long-term outcome. Also, it has recently been reported that increased serum C-Reactive protein (CRP) is common in patients with stable angina and is a significant and independent determinant of MMI after uncomplicated elective PCI, indicating involvement of the systemic inflammatory state in the etiology of this periprocedural myocardial injury. An intense inflammatory response is expected following PCI in patients with increased baseline CRP levels, which can cause small vessel occlusion and/or microembolization that will lead to troponin elevation. With these findings in mind, and with the observation that increased risk associated with systemic inflammation can be reduced with certain preventive therapies, CRP may help to identify those who would benefit most from these pharmacological therapies before coronary interventions.