Performing PCI in comatose survivors of cardiac arrest

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Marko Noc

Because of a significant improvement in the prehospital treatment of patients with out-of-hospital cardiac arrest, an increasing number of resuscitated, comatose patients are being admitted to hospitals. Of those who are subsequently diagnosed with ST-segment elevation myocardial infarction (STEMI), up to 90% will have acute thrombotic lesions. However, about 30% of patients without STEMI, on early post resuscitation electrocardiogram, may also have obstructive coronary lesions. In this commentary, Marko Noc explores when percutaneous coronary intervention (PCI) should be used to treat survivors of cardiac arrest.

Despite the absence of randomised trials for immediate coronary angiography and PCI, interventional cardiologists at “24/7 STEMI centres” are increasingly being asked to perform PCI in patients who have survived an out-of-hospital cardiac arrest. According to the European Association of Percutaneous Cardiovascular Interventions/Stent for Life consensus document,1 comatose survivors of out-of-hospital cardiac arrest with STEMI should be put into the “STEMI fast track” and go directly to the catheterisation laboratory. However, the approach is different for patients without STEMI.

Although coronary artery disease is likely to be the cause of an out-of-hospital cardiac arrest, there are many other possible causes that need to be ruled out. Therefore, time should be spent in the emergency department to exclude non-coronary causes such as respiratory failure, cerebrovascular event, pulmonary embolism, intoxication, and other non-cardiogenic aetiologies. In the absence of an obvious non-coronary cause, coronary angiography should be performed within two hours—this is particularly important in haemodynamically unstable patients and in patients with recurrent malignant ventricular arrhythmias.

Coronary angiography after a resuscitated out-of-hospital cardiac arrest may reveal heterogeneous findings, including angiographically normal coronary arteries, non-obstructive disease (<50% diameter stenosis), intermediate disease (50–70%), obstructive disease with angiographically stable appearance, or the presence of typical culprit “acute coronary syndrome” lesions. The aim of percutaneous coronary intervention (PCI) is to reduce the incidence of recurrent cardiac arrest, infarct size in case of an acute occlusion and, thereby, improve the haemodynamic status. This may improve the likelihood of a possible neurological recovery during the following days.

At our centre, we believe that the decision-making process for PCI should incorporate angiographic characteristics of a lesion, its cause-effect relationship to the cardiac arrest, the haemodynamic status and likelihood of neurological recovery of the patient to obtain the maximal benefit and avoid futility. Index PCI should be directed primarily to treating the acute culprit lesions, leaving other obstructive lesions for possible staged intervention if the patient wakes up from the coma. Contemporary drug-eluting stents should be used. Stenting is, of course, associated with the need for anticoagulation and antiplatelet therapy to prevent stent thrombosis—the risk of which in comatose patients is significantly increased (>4%) compared with those with acute coronary syndrome or those with stable disease undergoing PCI (1–2%). On the other hand, comatose patients are often at high risk for bleeding due to chest compression and intubation on the field.

At our centre, we use intravenous acetylsalicylic acid and unfractioned heparin (UFH). Since P2Y12 inhibitors are available only in tablet form—and comatose survivors are intubated and mechanically ventilated—our only option is to crush them and administer them via a nasogastric tube. We recently demonstrated that ticagrelor (Brilinta, AstraZeneca) provides much faster and more effective platelet inhibition than clopidogrel.2 In cases with a high thrombotic burden, complex stenting, or bailout situations, a bolus of GP llb/llla inhibitor (such as eptifibatide) may also be considered. In this context, a new intravenous reversible P2Y12 inhibitor, cangrelor (Kengreal, Chiesi Company), may represent an attractive solution but it has not been systematically tested in out-of-hospital cardiac arrest patients. Again, profound platelet inhibition should always be weighed against the increased risk of bleeding. As 30–40% of patients will develop post-resuscitation cardiogenic shock, temporary invasive haemodynamic support—including intra-aortic balloon pump (IABP), percutaneous left ventricular assist (Impella, Abiomed), or veno-arterial extra-corporeal membrane oxygenation—should be considered although its role in comatose survivors of out-of-hospital cardiac arrest has not been specifically studied.

References

  1. Noc et al. Eurointervention 2014; 10(1): 31–37.
  2. Steblovnik et al. Circulation 2016; 134: 2128–30.

Marko Noc, MD, PhD, University Medical Center, Ljubljana-Slovenia