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Should we dilate the non-infarct related arteries in patients with multi-vessel disease?

Should we dilate the non-infarct related arteries in patients with multi-vessel disease?. Carma Karam, MD Cardiologist AIHP, ACCA, FACC Clinique Médicale du Ring. Since 1980, we know that AMI is related to coronary occlusion and therefore the preferred therapy is to open the IRA.

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Should we dilate the non-infarct related arteries in patients with multi-vessel disease?

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  1. Should we dilate the non-infarct related arteries in patients with multi-vessel disease? Carma Karam, MD Cardiologist AIHP, ACCA, FACC Clinique Médicale du Ring

  2. Since 1980, we know that AMI is related to coronary occlusion and therefore the preferred therapy is to open the IRA Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. DeWood MA, et al N Engl J Med. 1980 Oct 16;303(16):897-902.

  3. Decreased prevalence of late potentials with mechanical versus thrombolysis-induced reperfusion in acute myocardial infarction Karam C, JLG, PGS, et alHôpital Bichat, France Many authors have shown that reperfusion obtained by angioplasty is superior to reperfusion obtained with thrombolytics J Am Coll Cardiol, 1996; 27:1343-1348

  4. Should we dilate the non-infarct related arteries in patients with MVD?

  5. Di Mario et al. assigned 69 STEMI patients with multivessel disease to unbalanced randomization with culprit lesion treatment only (n = 17) versus complete multivessel intervention (n = 52). The multivessel intervention group required longer procedures and larger amounts of contrast, but only had a trend for lower revascularization requirements at 12 months. Di Mario C, Mara S, Flavio A, et al. (HELP-AMI) study Int J Cardiovasc Interv 2004;6:128-133

  6. Politi et al. : 214 STEMI pts with MVD culprit vessel PCI alone (n = 84), simultaneous treatment of nonculprit (n = 65), or culprit only + staged revascularization (n = 65). In-hospital mortality, unplanned rehospitalization, and repeat revascularization more frequent in the culprit-vessel-only (all p < 0.05). Requirement for repeat revascularization in the culprit-only strategy should not be considered a major adverse event, but rather interpreted within a global strategy in which closer clinical follow-up is needed. The sample size of these studies was grossly underpowered to detect differences in death or recurrent MI. Politi L, Sgura F, Rossi R, et al. Heart 2009Sep 23

  7. Multivessel intervention during primary PCIFew studiesSmall number of patients Trend but no statistically significant differenceQuestionable endpointsUnderpowered sample sizeRandomization bias?

  8. Possible selection biasSuccessful culprit vessel stenting readily accomplished during a smooth procedure, leading to TIMI coronary flow grade 3 and nearly complete ST-segment resolution. If another easy/attractive target is identified in this patient, the temptation to finish the procedure achieving complete revascularization might be high. Conversely, a complex, prolonged procedure required to open the culprit lesion will likely discourage the operator from further attempts in other vessels.

  9. Fortunately, a recent study published in 2010 helps answer the questions concerning culprit vessel only versus multivessel intervention during primary PCI

  10. Culprit Vessel Percutaneous Coronary Intervention Versus Multivessel and Staged Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction Patients With Multivessel Disease Edward L. Hannan, Zaza Samadashvili, Gary Walford, David R. Holmes, Jr, Alice K. Jacobs, Nicholas J.Stamato, Ferdinand J. Venditti, Samin Sharma, Spencer B. King, III JACC Cardiovasc Interv 2010;3:22-31.

  11. ObjectivesThe purpose of this study was to examine the differences in in-hospital and longer-term mortality for STEMI pts with MVD as a function of whether they underwent single-vessel (culprit vessel) percutaneous coronary interventions or multivessel PCI JACC Cardiovasc Interv 2010;3:22-31.

  12. What is the best time to intervene on nonculprit vessels ?New York between January 2003, and June 20061-Pts who underwent culprit vessel PCI only 2-Pts who underwent multivessel PCI during the index procedure3-Pts undergoing nonculprit vessel PCI during the index admission4-Pts undergoing staged PCI to the nonculprit vessel within 60 days of admission JACC Cardiovasc Interv 2010;3:22-31.

  13. MethodsTotal of 4,024 pts3,521 pts (87.5%) culprit vessel PCI only Staged PCI during the index admission in 259 pts (6.43%) 538 pts staged PCI within 60 days (13.37%). JACC Cardiovasc Interv 2010;3:22-31.

  14. ResultsPts without hemodynamic compromise :Culprit vessel PCI lower in-hospital mortality than multivessel PCI during the index procedure (0.9% vs. 2.4%, p = 0.04). Culprit vessel only vs nonculprit vessel during the same hospitalization : No difference in outcome. Staged multivessel PCI within 60 days : lower 12-mth mortality than culprit vessel PCI only (1.3% vs. 3.3%, p = 0.04). JACC Cardiovasc Interv 2010;3:22-31.

  15. Conclusion of the study A strategy of culprit vessel PCI only at the time of STEMI is associated with the best outcome in pts with MVD.Multicenter population-based study The only one that examines long-term outcomes and the use of multivessel PCI after discharge as well as during the index admission.

  16. Current ACC/AHA guidelines recommend culprit vessel PCI only in pts undergoing primary PCI (unless there is hemodynamic compromise) This study corroborates these findings Since there are no data to the contrary, culprit vessel PCI only should remain the preferred revascularization strategy, and if there is an indication for PCI of a nonculprit vessel, such a procedure should be performed in a staged fashion The optimal timing of such a staged procedure, however, remains unclear

  17. Non culprit vessels primary intervention may lead to: Prolonged interventions

  18. Non culprit vessels primary intervention may lead to: Contrast overload

  19. Non culprit vessels primary interventionmay lead to: Renal impairment and Heart Failure

  20. Nonculprit lesion severity may be exaggerated as the result of circulating catecholamine-mediated vasoconstriction, and precise evaluation of revascularization requirements may be hampered.

  21. Non culprit vessels primary interventionmay lead to: Jeopardizing myocardial territory that would be of special concern in the acute phase

  22. Non culprit vessels primary interventionmay lead to: High financial costs

  23. Non culprit vessels primarystenting might be associated with higher rates of periprocedural MI, and with increased rates of late revascularizations secondary to restenosis.

  24. Hypothetic favorable effects of primary non-culprit vessels PCI Ensuring adequate, complete, early revascularization NOT PROVEN Lower requirement of repeated procedures NOT PROVEN Improvement of left ventricular function NOT PROVEN Reduction of hospital stay NOT PROVEN Reduction in hospital costsNOT PROVEN Improving long-term clinical outcomeNOT PROVEN

  25. Conclusion: Staged procedures for multivessel disease post culprit primary PCI

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