Mechanisms Predictors of Elevated Troponin Levels After PCI

The pathophysiological mechanism for elevated cardiac troponin levels after PCI is unclear. Potential mechanisms include myocardial necrosis or ischemia from prolonged balloon inflations, transient abrupt closure, distal embolization, and side-branch occlusion.

Prolonged Balloon Inflations

In two series of patients undergoing PCI, elevated postprocedural levels of troponin correlated closely with long balloon-inflation times (13,14). Katoh et al. (15) studied 16 patients undergoing PCI with measurements of coronary sinus troponin T immediately after and 4, 8, and 12 h after PCI. Despite inflations up to 64 s associated with chest pain

2hrs 4hrs 6hrs 12to20hrs

Time of blood draw after PCI Fig. 1. Proportion of patients with increased concentration of troponin T (cTnT) with serial measurement after elective PCI (n = 52). (Data from ref. 11.)

2hrs 4hrs 6hrs 12to20hrs

Time of blood draw after PCI Fig. 1. Proportion of patients with increased concentration of troponin T (cTnT) with serial measurement after elective PCI (n = 52). (Data from ref. 11.)

and ST-segment changes in all patients, the concentration of troponin T in samples from the femoral vein and coronary sinus remained within normal limits in all patients over the 12-h period. It therefore seems unlikely that balloon inflation alone leads to troponin release in the absence of distal embolization, side-branch occlusion, or other procedural complications.

Side-Branch Occlusion, Abrupt Closure, and Other Procedural Complications

In several small series, troponin elevation was found to occur mostly or exclusively when procedural complications, particularly side-branch occlusion, occurred (16,17). In multivariable models, side-branch occlusion and other procedural complications are identified as independent predictors of troponin elevation (10,18,19). More than 80% of patients with elevated troponin post-PCI have no identifiable procedural or angiographic complications (10,20). However, distal embolization may not be angiographically apparent, and occlusion of very small side branches is easily missed. Patients with acute coronary syndromes (ACS) who have elevated levels oftroponin I post-PCI are significantly more likely to have evidence of impaired tissue-level perfusion T(m) (thrombolysis in myocardial infarction) myocardial perfusion grade 0/1 and reduced perfusion on myocardial contrast echocardiogram than patients without postprocedural troponin I elevation (Fig. 2) (21).

Stenting vs Balloon Angioplasty

Several observational studies have documented higher rates oftroponin elevation following coronary stenting compared with balloon angioplasty alone (18,22-24). However, in other studies, there were no significant differences in levels of troponin with stenting vs angioplasty alone (13,19,20). Coronary stents may increase the frequency of minor myonecrosis by occlusion of small side branches or increased distal embolization. Alternatively, the difference may be related to the more frequent use of stents in more complex vessels and lesions. In two studies, the use of stents was no longer associated with troponin elevation after adjusting for confounding variables in a multivariable model (18,25). The use of multiple stents has been shown to be an independent predictor of troponin

Table 1

Incidence of Elevated Troponin After PCI

Table 1

Incidence of Elevated Troponin After PCI

Reference/

No. of

Troponin

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