Stent thrombosis accounts for almost 10% of patients undergoing primary PCI, according to a large observational study published online October 10, 2012, ahead of print in the Journal of the American College of Cardiology. The report notes that patients with ST-segment elevation myocardial infarction (STEMI) due to stent thrombosis are more susceptible to reinfarction and repeat stent thrombosis but have mortality comparable to that of patients with STEMI attributable to other etiologies.

Investigators led by Timothy D. Henry, MD, of the Minneapolis Heart Institute Foundation (Minneapolis, MN),  looked at 3,305 consecutive STEMI patients who received primary PCI at the Minneapolis Heart Institute (n = 2,086) or the Cone Heart and Vascular Center (Greensboro, NC; n = 1,219) from 2003 through 2010. Patients treated at the former institution who were transported from long distances were given a half-dose of fibrinolytic therapy before transport.

Overall, 282 cases (8.5%) were determined to be due to definite stent thrombosis, as defined by Academic Research Consortium criteria. Over the study period, the incidence of STEMI with this etiology increased steadily from 6.0% in 2003-2004 to 10.9% in 2009-2010. By the last year, the culprit stent was a DES in more than 60% of patients, and most (95%) were first-generation devices.

Stent Thrombosis Timing Unaffected by Device Type

Depending on how long after stent implantation the stent thrombosis occurred, it was classified as:

• Early (0-30 days): 22%
• Late (31-365 days): 22%
• Very late (> 365 days): 56%

The distribution of events over these periods was similar between BMS and DES.

Overall, compliance with dual antiplatelet therapy at the time of stent thrombosis was 33.5%, with compliance rates of 75.3% for patients with early stent thrombosis, 29.9% for late stent thrombosis, and 11.7% for very late stent thrombosis.

At 30 days, patients with STEMI due to stent thrombosis had a similar rate of mortality but more reinfarction and repeat stent thrombosis than those with STEMI attributable to other etiologies (table 1).

Table 1. Thirty-Day Outcomes Based on STEMI Cause

Mean follow-up was 2.1 years. After adjustment for baseline variables, 4-year Kaplan-Meier estimates showed that, again, the stent thrombosis group had comparable all-cause mortality but higher rates of reinfarction and repeat stent thrombosis (table 2).

Table 2. Cumulative 4-Year Outcomes for STEMI Due to Stent Thrombosis vs. De Novo Occlusion

An important implication of the study is that a significant proportion of all STEMI events can now be linked to the presence of a stent, Dr. Henry told TCTMD in a telephone interview. That is not because the incidence of stent thrombosis is rising, he explained, but because the number of individuals with coronary stents is constantly growing, and all stents carry an ongoing risk of triggering thrombosis.

As more patients receive newer-generation DES, which often carry lower risk for stent thrombosis, the prevalence of STEMI due to this event is likely to decrease, noted Sorin J. Brener, MD, of Weill Cornell Medical College (New York, NY), in a telephone interview with TCTMD. But, he added, whether this type of STEMI also declines as a percentage of all STEMIs remains to be seen, because the number of de novo STEMIs has also fallen dramatically in recent years.

Stent Thrombosis Not as Deadly as Thought

Contrary to the common belief that BMS stent thrombosis is concentrated in the acute period, BMS accounted for almost as many late and very late stent events as DES in the study, Dr. Henry noted. However, he observed, the pathogenesis of later stent thrombosis tends to differ between the stent types. With BMS, new atherosclerosis develops inside the stent over time, eventually leading to plaque rupture, while with DES, restenosis is minimal and thrombosis occurs more abruptly, he explained.

Another important observation was that, overall, STEMI due to stent thrombosis is no more deadly than other STEMIs, Dr. Henry added, noting that mortality rates of up to 50% are sometimes cited.

“We have learned over the past few years that although stent thrombosis is dangerous when it occurs early, for reasons we don’t understand, the mortality of late and very late stent thrombosis is actually quite low,” Dr. Brener said. And that is when most events occur, he added.

Less Is More

When patients present with STEMI due to stent thrombosis, “a strong clinical recommendation is to try to determine why the stent thrombosed,” Eric R. Bates, MD, of the University of Michigan Medical Center (Ann Arbor, MI), told TCTMD in a telephone interview. 

Dr. Brener agreed. “It makes a difference whether the sent thrombosed because it was left unapposed or the patient did not take their antiplatelet medications or perhaps [was] resistant to them,” he said. Drs. Bates and Brener routinely perform IVUS to check for malapposition, but the practice is not widespread, Dr. Brener said, in part because some clinicians worry that the IVUS catheter may push a clot downstream.

“Most of the time we just aspirate and use a balloon to correct malapposition,” Dr. Brener said. “We try to avoid implanting another stent because that just further increases the incidence of recurrent stent thrombosis. The best thing to do is to open up [the vessel] and get out of there.”

Dr. Bates agreed, but added that sometimes another stent, possibly a BMS, is needed if optimal apposition is not achieved or a dissection has occurred.

Other treatment strategies for stent-thrombosis induced STEMI suggested by the authors include increased use of glycoprotein IIb/IIIa inhibitors and prescription of a new, more potent antiplatelet agent after intervention. In addition, they say, “more frequent prophylactic revascularization with bypass surgery may be warranted.”

Dr. Henry noted that the etiology of stent thrombosis is heterogeneous. Beyond the stent itself, causes include interruption of antiplatelet therapy, stent underexpansion, and the presence of a hypercoagulable state. Clearly some of these are more amenable to management than others, he noted, adding that in the future, use of a biodegradable stent might reduce the incidence of repeat stent thrombosis.

Meanwhile, said Dr. Bates, “this study raises a flag that stent thrombosis is not an anecdotal event. Now—at least at these 2 centers—it accounts for at least 10% of their STEMI population. That’s pretty dramatic. It’s a reminder that stent thrombosis remains a limitation of coronary stent implantation.”

Study Details 

Patients with STEMI due to stent thrombosis compared with de novo occlusion had more diabetes, hypertension, prior MI and CABG, lower frequency of TIMI flow grade 2 to 3 on initial angiography, shorter door-to-balloon and -reperfusion times, more frequent use of glycoprotein IIb/IIIa inhibitors, and less frequent use of stents.

The original stent was implanted for off-label indications in 73.6% of patients, including 43.3% with STEMI.

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