Complete PCI in STEMI: An interventional paradigm shift

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By Eliano P Navarese


In a new focused update, the American College of Cardiology (ACC)/American Heart Association (AHA)/Society for Cardiovascular Angiography and Interventions (SCAI) now recommend that complete percutaneous coronary intervention (PCI) is acceptable in some patients with ST-segment elevation myocardial infarction (STEMI) with multivessel disease. Eliano P Navarese reviews the evidence base for complete PCI compared with culprit-artery
only PCI.

A sizable number of patients with STEMI present with obstructive lesions (≥50% stenosis) in non-culprit arteries.1 The 2009 ACC/AHA/SCAI guidelines recommended that in such patients—in the absence of cardiogenic shock—only the culprit vessel should be treated during the index procedure with the remaining lesions revascularised at a later date.2 The rationale for these guidelines was driven by concerns about the potential risks of performing complete revascularisation in a highly prothrombotic and proinflammatory environment and having a longer intervention time. Also, as few randomised controlled trials on complete PCI have been performed, the recommendations were mainly based on observational data.


In 2011, Navarese et al3 (pooling evidence from randomised controlled trials and observational studies) published the first meta-analysis on complete PCI and found that complete revascularisation was associated with significantly reduced revascularisation rates compared with culprit-only PCI. The recent PRAMI (Preventive angioplasty in acute myocardial infarction)4 and  CvLPRIT (Complete versus lesion-only primary PCI trial)5 studies have further added to the debate about the benefits of complete PCI compared with culprit-only PCI. The former showed that complete PCI was associated with a significant 65% reduction in the risk of a combined endpoint of cardiac death, non-fatal myocardial infarction, over 23 months of follow-up, compared with culprit-only PCI, and the latter found that it was associated with a 55% reduction in major adverse cardiac events (MACE) at 12 months. Furthermore, a meta-analysis6 (which included both PRAMI and CvLPRIT) published last year indicated that complete PCI reduces MACE by 41%, which is driven by a 52% reduction in recurrent myocardial infarction and a 49% reduction in repeat revascularisation. This meta-analysis underscores the need to revascularise—with stents—other non-culprit coronary plaques, in STEMI patients with multivessel disease. It also supports the assertion that non-culprit lesions can serve as prothrombotic milieu during the acute phase and, if untreated, present as a new myocardial infarction—becoming culprit themselves, eventually leading to increased ischaemic burden and worse clinical outcomes. The PROSPECT (Providing regional observations to study predictors of events in the coronary tree) study,7 which enrolled patients with acute coronary syndrome and used virtual histology intravascular ultrasound to detect lesions at higher risk of progression, showed that almost half of clinical events indeed cluster in the non-culprit vulnerable plaques.


Based on the recent trial findings, in October 2015, the ACC, AHA, and SCAI published a focused update to their guidelines for primary PCI in STEMI patients.8 The update states that PCI of a non-culprit artery is now acceptable for some STEMI patients with multivessel disease. It states that PCI of a non-culprit artery—either during the index PCI procedure or as a planned staged procedure—can be considered in patients who are haemodynamically stable (class IIb recommendation). This change from the 2009 guidelines, which gave complete PCI a class III recommendation (harm) represent a real paradigm shift.


However, an unsolved issue is the optimal timing of the revascularisation of the non-culprit vessels: should it be during the same session or some days after the PCI for the culprit artery? The PRAMI trial adopted a “tout court” approach with the revascularisation of the non-culprit vessel done during index procedure, but the recent DANAMI-3—PRIMULTI9 (Complete revascularisation versus treatment of the culprit lesion only in patients with STEMI and multivessel disease) trial showed the feasibility and efficacy of a staged approach with the haemodynamic severity of the lesion evaluation by fractional flow reserve (FFR) measurement two days after initial PCI. In this study, completed PCI (guided by FFR) was associated with a significant reduction in future events compared with culprit-only PCI (with no further intervention). Both approaches can be reasonable based on a case-to case basis (eg. critical lesion in a non-culprit vessel vs. moderate-significant lesion at angiography requiring further evaluation by FFR).


Another issue regarding complete PCI is the revascularisation of chronic total occlusions, which can be discovered at angiography in the remaining vessels during PCI for STEMI.Whether the revascularisation of chronic total occlusions in the setting of STEMI is associated with an acceptable risk, remains uncertain given the lack of randomised controlled trials addressing this question.


Simultaneous and in-hospital complete revascularisation in the setting of STEMI appears to be safe and effective if based on careful judgement of the lesion and patient clinical status. However until further data are available, the optimal timing of complete intervention should be decided in light of several clinical and procedural variables including procedural and lesion complexity as well patient clinical risk profile and concomitant comorbidities (eg. chronic kidney disease). The interventional cardiologist should always strike the balance of the risk/benefit ratio before tackling a non-culprit lesion.


References


1.Muller et al. Am Heart J 1991; 121: 1042–49.

2.Kushner et al.  J Am Coll Cardiol 2009; 54: 2205–41.

3.Navarese et al. J Thromb Thrombolysis 2011; 31: 217–25.

4.Wald et al. N Engl J Med 2013; 369: 1115–23.

5.Gershlick et al. J Am Coll Cardiol 2015; 65: 963–72.

6.Kowalewski et al. Heart 2015; 101: 1309–17.

7.Stone et al. N Engl J Med 2011; 364(3): 226–35.

8.Levine et al. J Am Coll Cardiol. 2015; Epub

9.Engstrøm et al. Lancet 2015; 386: 665–71.


Eliano P Navarese is at Systematic Investigation and Research on Interventions and Outcomes (SIRIO) MEDICINE research network and Department of Internal Medicine, Division of Cardiology, Pulmonology and Vascular Medicine, Heinrich-Heine-University, Düsseldorf, Germany