Elevated B-type natriuretic peptide levels in patients undergoing coronary stenting

Release of B-type natriuretic peptide (BNP) may be triggered by tissue hypoxia even in the absence of left ventricular (LV) dysfunction, generating interest in studying changes in levels following percutaneous coronary intervention (PCI). Though the prognostic role of natriuretic peptides following elective PCI has been documented, most studies only assessed single pre-procedural levels. Previous studies assessing BNP rise following balloon angioplasty or coronary stenting have reported conflicting results; most of these studies excluded patients with recent acute coronary syndrome (ACS).

We studied the changes in BNP following coronary stenting in 100 patients across the entire spectrum of ACS and observed a significant rise in BNP following stenting. Baseline BNP levels > 100 pg/ml were observed in 31% of patients; following PCI, 45% of patients were noted to have BNP > 100 pg/ml. In patients with baseline BNP < 100 pg/ml, 20% had post-procedure BNP levels > 100 pg/ml. Post-PCI BNP levels were significantly higher in patients with recent ACS (versus those with stable angina), those with LV dysfunction, high baseline troponin I, visible angiographic thrombus and those with post-PCI TIMI 1-2 flow. Patients with post-PCI BNP levels > 100 pg/ml had a trend toward more frequent occurrence of TIMI no reflow following PCI (9.3 versus 1.7%; p = 0.07).

Recent ACS, raised basal troponin, LV dysfunction, and presence of angiographic thrombus were all associated with high baseline and post-PCI BNP levels. Though recent ACS was the strongest predictor of elevated BNP levels, BNP levels rose following PCI even in patients with chronic stable angina.