Prevention of Elevated Troponin Levels After PCI

A number of pharmacological agents have been shown to reduce the frequency and/or severity of periprocedural myonecrosis as measured by postprocedural levels of troponin. Because microembolization of thrombus is believed to be one of the primary causes of periprocedural myonecrosis, it is not surprising that more potent antiplatelet agents, such as the thienopyridines and the iv glycoprotein IIb/IIIa receptor inhibitors, and more potent inhibitors of thrombin reduce the frequency of this complication.

In one retrospective, nonrandomized analysis, patients pretreated with ticlopidine prior to coronary stenting had lower frequency and magnitude of increase in the concentration of troponin T compared with patients who started taking ticlopidine the day of the procedure (37). A small randomized trial of clopidogrel vs ticlodipidine started on the day of PCI showed less troponin T elevation and lower mean troponin T values after PCI with clopidogrel (38).

0-12 hrs 0-24 hrs 0-48hrs

Fig. 6. Proportion of patients with elevated cTnT after PCI when treated with adjunctive tirofiban vs control. (Data from ref. 17.)

0-12 hrs 0-24 hrs 0-48hrs

Fig. 6. Proportion of patients with elevated cTnT after PCI when treated with adjunctive tirofiban vs control. (Data from ref. 17.)

Tirofiban started prior to the first balloon inflation and continued for 18 h post-PCI was shown in a randomized, placebo-controlled trial to reduce the frequency of troponin T elevation at 24 h (48 vs 69%;p < 0.05), although the difference at 48 h was no longer statistically significant (Fig. 6). The reduced frequency of troponin and CK-MB elevations post-PCI with the use of glycoprotein Ilb/IIIa inhibitor is thought to be related to reduced periprocedural myonecrosis, rather than an interaction between this class of drugs and the cardiac marker assays (39). Kini et al. (40) performed a randomized trial of eptifibatide, tirofiban, or abiciximab during PCI, with additional half boluses of the study drug given 10 min later if <90% inhibition of platelet aggregation was achieved. There was no difference in the incidence of troponin I elevation >2.0 ng/mL post-PCI between the different glycoprotein IIb/IIIa receptor inhibitors.

In a randomized trial of patients with unstable angina undergoing PCI that compared hirudin, a direct thrombin inhibitor, with heparin, both doses of hirudin used were more effective than heparin in preventing troponin T elevations >0.2 ng/mL post-PCI (24 vs 58%; p = 0.01) (41).

The use of other classes of drugs has also been examined in relation to the incidence of post-PCI troponin elevation. Intravenous nitroglycerine started immediately after PCI and continued for 12 h was shown to be superior to placebo in reducing the frequency of troponin I elevation >0.1 pg/L at 12 h post-PCI (5 vs 19%; p = 0.036) (42). This finding may be related to the improved coronary blood flow and myocardial perfusion that occur with iv nitroglycerine. Interventions that induce ischemic preconditioning, such as nico-randil, may also reduce the frequency of minor myocardial damage during PCI (43). A randomized, placebo-controlled trial of atorvastatin (40 mg/d) started 7 d prior to PCI demonstrated a marked reduction in troponin I elevation (20 vs 48%; p = 0.0004) in the first 24 h after PCI (27). Given the effect of atorvastatin on reducing CRP levels and the association of CRP with elevated troponin post-PCI (26), it has been postulated that atorvastatin prevents periprocedural myonecrosis through its anti-inflammatory properties.

A number of mechanical approaches reduce periprocedural MI, as assessed by CK-MB, including the use of distal embolization protection devices for saphenous vein graft interventions (44), and direct stenting without predilation (45). The impact of these strategies on troponin release post-PCI has not been studied.

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