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Commentary

SINC or Swim (Should We Intervene in Non-Culprit Vessels During STEMI?)

Patrick Antoun, MD and Jeffrey A. Breall, MD, PhD

January 2014

Our current practice guidelines1 discourage interventionalists from attempting to open a non-infarct artery at the time of an ST-elevation myocardial infarction (STEMI). What could possibly be the rationale for this? To some experienced cardiologists, this recommendation seems “too extreme” and is criticized as being only based upon few meta-analyses in the literature.2-5 No large randomized trial has supported these guidelines as they currently stand. Thus, it is somewhat peculiar to label such an intervention a class III indication simply based upon only meta-analyses and subgroup analyses. As such, many authors have challenged this recommendation (some even presenting their own data on the subject).6,7 A recent meta-analysis comparing a conservative approach of intervening on a culprit infarct artery only to that of intervening upon both the infarct and non-infarct artery (as adjunct to primary percutaneous coronary intervention [PCI]), found that the difference in outcomes did not persist after exclusion of shock patients which, not surprisingly, are generally found more in patients undergoing non-infarct related interventions.8 A more provocative trial published recently in the New England Journal of Medicine by Wald et al showed actual improvement in outcomes on those patients receiving preventive PCI in non-infarct coronary arteries with major stenoses in the setting of STEMI.9

It has previously been suggested that incomplete revascularization leads to worse outcomes.10 Wouldn’t it be counterintuitive then to leave a source of ischemia untreated in an already stressed heart? This might be even more true in patients who are already in shock. 

One might argue that excessive percutaneous manipulation in the same setting as infarct-related PCI may lead to more inflammation and chemokine release. This in turn might adversely affect myocardial recovery. Others have argued that any complication in a non-infarct related territory may lead to worse outcomes, including possible cardiogenic shock and death. This has yet to be born out, however, in any randomized trial. 

Conversely, leaving an additional vascular bed untreated may be suboptimal, when, in the setting of acute infarct, the cardiac output is relying on every non-ischemic myocardial cell. The obvious question is at what level of stenosis should we intervene in a non-infarct artery (if any)? Should we intervene when it is 50% occluded? 70%? 90%? Perhaps we should routinely perform fractional flow reserve (FFR) prior to any non-infarct artery intervention in order to help us decide what to do, similar to a FAME II strategy. The extreme of a severe coronary stenosis in a non-infarcted related artery is a chronic total occlusion (CTO). Patients with such a concomitant condition tend to fare much worse during acute ST-segment elevation myocardial infarction.11,12 This has been attributed to the “double jeopardy” phenomenon, whereby a greater amount of myocardium is potentially at risk. Treating that CTO as soon as possible after a STEMI could potentially help hibernating or ischemic myocardial cells recover quicker, thus improving myocardial function and overall recovery.

The study by Mozid et al13 in this month’s Journal of Invasive Cardiology would again appear to support a change in the guidelines. The practice of CTO intervention in addition to infarct-related artery intervention appeared to fare better overall. Any experienced interventionalist knows that CTO interventions are among the most difficult procedures we perform. Unlike other difficult type-C lesions, the “downside” from lack of success is often minimal.In other studies where non-infarct related artery intervention was performed (on vessels other than CTOs), we do not know the difficulty factor, ie, calcification, tortuosity, etc. Culprit versus culprit plus non-infract STEMI studies have not clearly specified in the past the lesion difficulty factor (type A-C) of the non-infarct related artery. Similarly, not all CTOs are alike and we do not clearly know the details of the CTOs in this study (ie, what were the negative predictors of the CTOs for each case?). Nevertheless, it is clear that the study by Mozid et al as well as other studies conflict with current guideline recommendations. Intuitively, we should always strive for complete revascularization in patients with multivessel disease where stenoses are functionally significant. The STEMI setting makes the latter more challenging given the multitude of confounders that could affect the results of a multivessel intervention strategy. Perhaps it is time to reevaluate the recommendations in light of the most current studies. A reasonable compromise might be PCI of non-culprit favorable CTOs and/or severe type-A lesions at the time of STEMI, provided the procedure length has been relatively short and a paucity of contrast has been used. Clearly, more clever and stimulating studies like that by Mozid et al are needed.

References

  1. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: a report of the American College of Cardiology Foundation/American Heart Association. Circulation. 2013;127(4):e362-e425.
  2. Hannan EL, Samadashvili Z, Walford G, et al. Culprit vessel percutaneous coronary intervention versus multivessel and staged percutaneous coronary intervention for ST-segment elevation myocardial infarction patients with multivessel disease. JACC Cardiovasc Interv. 2010;3(1):22-31.
  3. Toma M, Buller CE, Westerhout CM, et al. Non-culprit coronary artery percutaneous coronary intervention during acute ST-segment elevation myocardial infarction: insights from the APEX-AMI trial. Eur Heart J. 2010;31(14):1701-1707.
  4. Vlaar PJ, Mahmoud KD, Holmes DR Jr, et al. Culprit vessel only versus multivessel and staged percutaneous coronary intervention for multivessel disease in patients presenting with ST-segment elevation myocardial infarction: a pairwise and network meta-analysis. J Am Coll Cardiol. 2011;58(7):692-703.
  5. Sethi A, Bahekar A, Bhuriya R, Singh S, Ahmed A, Khosla S. Complete versus culprit only revascularization in acute ST-elevation myocardial infarction: a meta-analysis. Catheter Cardiovasc Interv. 2011;77(2):163-170.
  6. Navarese EP, De Servi S, Buffon A, et al. Clinical impact of simultaneous complete revascularization vs. culprit only primary angioplasty in patients with ST-elevation myocardial infarction and multivessel disease: a meta-analysis. J Thromb Thrombolysis. 2011;31(2):217-225.
  7. Bangalore S, Kumar S, Poddar KL, et al. Meta-analysis of multivessel coronary artery revascularization versus culprit-only revascularization in patients with ST-segment elevation myocardial infarction and multivessel disease. Am J Cardiol. 2011;107(9):1300-1310.
  8. Bagai A, Thavendiranathan P, Sharieff W, Al Lawati HA, Cheema AN. Non-infarct-related artery revascularization during primary percutaneous coronary intervention for ST-segment elevation myocardial infarction: a systematic review and meta-analysis. Am Heart J. 2013;166(4):684-693.e1. (Epub 2013 Sep 20).
  9. Wald DS, Morris JK, Wald NJ, et al; PRAMI Investigators. Randomized trial of preventive angioplasty in myocardial infarction. N Engl J Med. 2013;369(12):1115-1123. (Epub 2013 Sep 1).
  10. Garcia S, Sandoval Y, Roukoz H, et al. Outcomes after complete versus incomplete revascularization of patients with multivessel coronary artery disease: a meta-analysis of 89,883 patients enrolled in randomized clinical trials and observational studies. J Am Coll Cardiol. 2013;62(16):1421-1431. (Epub 2013 Jun 7).
  11. Bataille Y, Déry JP, Larose É, et al. Incidence and clinical impact of concurrent chronic total occlusion according to gender in ST-elevation myocardial infarction. Catheter Cardiovasc Interv. 2013;82(1):19-26(Epub 2013 Feb 26).
  12. Lexis CP, van der Horst IC, Rahel BM, et al. Impact of chronic total occlusions on markers of reperfusion, infarct size, and long-term mortality: a substudy from the TAPAS-trial. Catheter Cardiovasc Interv. 2011;77(4):484-491.
  13. Mozid AM, Mohdnazri S, Mannakkara NN, et al. Impact of a chronic total occlusion following primary percutaneous intervention in acute ST-elevation myocardial infarction. J Invasive Cardiol. 2014;26(1):13-16.
  14. De Bruyne B, Pijls NH, Kalesan B, et al; FAME 2 Trial Investigators. Fractional flow reserve-guided PCI versus medical therapy in stable coronary disease. N Engl J Med. 2012;367(11):991-1001 (Epub 2012 Aug 27).

________________________

From the Krannert Institute of Cardiology and Indiana University Health, Indianapolis, Indiana.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Address for correspondence: Jeffrey A. Breall, MD, PhD, Krannert Institute of Cardiology and Indiana University Health, 1800 N. Capitol Avenue, #E-490, Indianapolis, IN 46202. Email: jbreall@iu.edu


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