• Cardiology Clinical Trials
• Interventional Techniques & Devices
• Myocardial Infarction

• Cardiology Clinical Trials
• Interventional Techniques & Devices
• Cardiology & Cardiovascular Medicine
• Myocardial Infarction

Management of antiplatelet therapy in the treatment of patients with ST segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI) has many decision points. Using evidence-based findings, Marcus St. John, MD, Miami Cardiac and Vascular Institute, Miami, Florida, USA, described the decisions made to treat a 44-year-old man who presented with severe substernal chest pain (Canadian Cardiovascular Society class IV angina). He had a history of hypertension, diabetes, and dyslipidemia, and he was a smoker. There was no history of stroke or bleeding. An electrocardiogram revealed inferior ST elevations and depressions in leads 1 and L. His vital signs were normal, and there were no signs of congestive heart failure.

The patient received aspirin and heparin in the emergency department. While there, he suffered an episode of hematemesis, which may have influenced his clinical course. The first decision point in his treatment was deciding which antiplatelet therapy to use. The decision was based on the 2013 American College of Cardiology/American Heart Association STEMI guidelines [O'Gara PT et al. Circulation 2013]. Aspirin (162 to 325 mg) and a loading dose of a P2Y₁₂ inhibitor were given to the patient. The choices for P2Y₁₂ were clopidogrel (600 mg), prasugrel (60 mg), or ticagrelor (180 mg). Ticagrelor was chosen based on the PLATO study, which reported that patients with acute coronary syndrome treated with it had significantly fewer deaths, myocardial infarctions (MIs), or strokes (9.8% vs 11.7%; p < .001 for the composite end point) at 1 year, with an acceptable bleeding profile, when compared with clopidogrel [Wallentin L et al. N Engl J Med 2009].

The next decision point was to initiate bivalirudin in the catheterization laboratory. This decision was based on the ACUITY study, which showed that bivalirudin monotherapy was associated with similar rates of ischemia (8.8% vs 8.2%; p = .45), significantly lower rates of bleeding (3.5% vs 6.8%; p < .001), and improved net clinical outcome (11.6% vs 13.3%, p < .057) when compared with heparin plus glycoprotein (GP) IIb/IIIa inhibitors [Stone GW et al. N Engl J Med 2006].

Note, however, that a more recent and somewhat controversial HEAT PCI trial reported that major adverse ischemic cardiac events were significantly more common with bivalirudin (8.7%) than heparin (5.7%; p = .01) [Shahzad A et al. Lancet 2014. This difference was driven by a 4-fold increase in the rate of stent thrombosis observed with bivalirudin (3.4%) therapy versus heparin (.9%; p = .001). There was no difference in the rate of major bleeding, which may be explained by the high proportion of patients treated by radial access. In addition, it has been suggested that in the hands of experienced operators, PCI patients have better outcomes with radial versus femoral access [Mehta SR et al. J Am Coll Cardiol 2012]. Therefore, the use of bivalirudin in this setting has been questioned, as highlighted by results of a recent meta-analysis (Cavander LANCET).

The patient received a bare metal stent along with manual aspiration thrombectomy. Specifically, a bare metal stent was chosen relative to a drug-eluting stent to reduce the risk of stent thrombosis if his adenosine diphosphate receptor blocker needed to be discontinued because of bleeding before 1 year. New data, however, suggest that later-generation drug-eluting stents have lower rates of stent thrombosis compared to early-generation drug-eluting stents. In particular, cobalt-chromium everolimus-eluting stents appear to be associated with significantly lower rates of stent thrombosis within 2 years of implantation compared with bare metal stents [Palmerini T et al. Lancet 2012].

Another decision point was reached when the patient complained of recurrent chest pain and had signs of inferior ST elevations 30 minutes after the procedure. Another angiogram was performed. The patient was given a double bolus of eptifibatide, and bivalirudin drip was resumed. Fetch thrombectomy revealed a red thrombus in aspirate. After further balloon dilation, intravascular ultrasound revealed adequate stent apposition. Postprocedure coronary blood flow was normal (TIMI 3), and there was good myocardial blush. Dr. St. John speculated that secondary problems in this patient may have increased the risk of stent thrombosis, such as lack of absorption of antiplatelet therapy in the setting of vomiting and the very quick time from door to balloon. This was based on a study that showed that among patients with STEMI undergoing primary PCI, antiplatelet action by ticagrelor (46% of platelets still active) was significantly delayed at 2 hours [Alexopoulos D et al. Circ Cardiovasc Interv 2012]. In addition and as noted, this patient received bivalirudin, which has been associated with increased rates of acute stent thrombosis relative to heparin.

The patient was admitted to the intensive care unit, placed on beta-blockers, angiotensin-converting enzyme I, and statins. He was discharged 4 days later and subsequently lost to follow-up.

Dr. St. John's key message was that there are many decision points along the way from door to balloon and decisions should be made according to evidence-based medicine. Platelet inhibition with newer agents is rapid but not instantaneous. Depending on time to PCI and risk factors for poor absorption (cardiogenic shock, vomiting), physicians should consider adjunctive treatment with a GP IIb/IIIa receptor antagonist IIb/IIIa as a “bridge” to adequate platelet inhibition with oral agents.

An additional lesson in this case is the importance of systems to maximize patient follow-up. This patient's risk of recurrent event is highest in the first year after his MI, particularly in the first 30 days. Compliance with evidence-based medications, including aspirin, ticagrelor (twice daily), statin therapy, and beta-blocker therapy, is critical; however, he was lost to follow-up after discharge. Should he remain stable for 1 year after his MI the next decision point with regard to antiplatelet therapy will be whether to continue his ticagrelor beyond 1 year. Currently, there are no data to answer this question. Nonetheless, the DAPT trial is anticipated to report in 2014 and the PEGASUS-TIMI 54 trial in 2015, and these will provide important evidence to support clinical decision making.

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