Troponin Rise After PCI Signals Higher Mortality Risk

From Heartwire
Sue Hughes

May 17, 2011 (New York, New York) — Troponin elevations following elective PCI are associated with an increase in long-term mortality, according to a new meta-analysis. The authors suggest that more intensive treatment of patients with raised troponin levels post-PCI may lead to improved long-term outcomes.

The meta-analysis, published online May 13, 2011 in Catheterization and Cardiovascular Interventions, was conducted by a team led by Dr Dmitriy N Feldman (Weill Cornell Medical College, New York).

Feldman explained to heartwire that the issue of whether postprocedure troponin rises are associated with worse long-term outcomes has been the subject of controversy for many years.
He noted that troponins are more sensitive and specific markers of myocardial necrosis than creatine kinase and are essential in establishing diagnosis as well as predicting prognosis in patients with suspected ACS.
But their role in predicting prognosis in elective-PCI patients is not so well defined.

The authors point out that while large increases in creatine kinase after elective PCI are associated with an increase in in-hospital adverse cardiac events and reduced long-term survival, the association between troponin elevation after elective PCI and long-term cardiac events is not so well established.

To look at this issue further, they performed a meta-analysis of 22 studies, involving 22 353 patients, reporting on the prognostic impact of cardiac troponin T or troponin I elevation after elective PCI and published between 1998 and 2009.

Results showed that postprocedural troponin T was elevated in 26% of patients and troponin I was increased in 34% of patients. The long-term all-cause mortality in patients with raised troponins was significantly higher when compared with patients without troponin rises. In addition, the combination of all-cause mortality/MI was also higher.

Feldman said the reason for this association is not completely clear, but it is thought that patients who have these increases have a higher plaque burden and there is therefore a greater likelihood of plaque being dislodged during the PCI and traveling downstream to block small arterioles causing myocardial necrosis.
It may also be the result of resistance to aspirin and/or clopidogrel so platelets are more active and lodge in small vessels.

Asked what recommendations he would make on the basis of these new results, Feldman said ideally there should be a study showing that more aggressive treatment in patients with raised troponin levels improved outcomes, but such a study is not planned at present.

He noted that ACC/AHA guidelines recommend routine measurement of cardiac enzymes post-PCI (class 2A recommendation), but not all hospitals do this. Feldman commented to heartwire : "Our results suggest that there is value in measuring postprocedure troponin. This can identify higher-risk patients who need to be followed more closely and treated more aggressively." He added that patients with raised troponin following a previous PCI could be given more aggressive antithrombotic therapy if undergoing a subsequent procedure.