Primary coronary microvascular dysfunction and poor coronary collaterals predict post-percutaneous coronary intervention cardiac necrosis

Abstract

An elevation in cardiac troponin-I (cTnI) after elective percutaneous coronary intervention (PCI) is because of cardiac necrosis and has prognostic implications. Primary microvascular dysfunction, evident before PCI, and paucity of coronary collaterals at baseline may influence cTnI. We selected 22 patients awaiting elective PCI for a single-vessel, type-A coronary stenosis, with normal left ventricular function and a normal preprocedure cTnI. Intracoronary pressure and Doppler flow were measured during coronary balloon occlusion to derive microvascular resistance: Rp=[Pd(occl)-Pv]/APVoccl and collateral resistance: Rcoll=[Pa-Pd(occl)]/APVoccl, at each stage of PCI, where Pa is mean aortic pressure, Pv is central venous pressure, Pd(occl) is mean distal pressure, Rp is coronary microvascular resistance, Rcoll is coronary collateral resistance, and APVoccl is average peak velocity during coronary balloon occlusion. The resistance indices were compared with postprocedural cTnI levels measured at 24 h. There was a relationship between baseline Rp before PCI and elevated plasma cTnI levels at 24 h. Mean (SEM) Rp (mmHg/cm/s) increased for each cTnI tertile: T1 (mean cTnI 0.04 ng/ml): 1.3 (0.3), T2 (mean cTnI 0.13 ng/ml): 3.1 (0.4), and T3 (mean cTnI 2.5 ng/ml): 4.6 (0.7) (P=0.002). Baseline Rcoll (mmHg/cm/s) was similarly related to cTnI result and mean values showed an increasing trend: T1: 11.1 (1.9), T2: 14.5 (2.3), and T3: 19.5 (3.4) (P=0.12). Serial coronary balloon occlusions did not significantly alter Rp (P=0.82) or recruit coronary collaterals (P=0.69). Primary coronary microvascular dysfunction and poor collaterals at baseline are associated with post-PCI necrosis.