Trained at Cambridge and Oxford Universities. Consultant Cardiologist and Executive Director of the Barts Heart Centre at Barts Health NHS Trust. Honorary Professor at the William Harvey Research Institute, QMUL. Has served as Honorary Secretary of the British Cardiovascular Society, Associate Editor of Heart and Chair of the London Cardiology Speciality Training Committee. Member of the Cardiology SAC and the BCS training committee.
Professor of Interventional Cardiology, St George's, University of London, London, UKIn acute ST-elevation myocardial infarction (STEMI), coronary reperfusion with percutaneous coronary intervention (PCI) to treat the culprit lesion responsible for infarction improves clinical outcomes in nearly all patients. Complete revascularization and treatment of non-infarct vessels with significant stenoses remains controversial.
Is culprit lesion only or multivessel PCI the optimal management strategy for patients with STEMI? Two randomized clinical trials have attempted to answer this question.
The CvLPRIT (Complete versus Lesion-only Primary PCI) trial compared complete revascularization at index admission with treatment of the infarct-related artery (IRA) only (1). The primary endpoint of all-cause death, recurrent myocardial infarction (MI), heart failure and ischaemia-driven revascularization within 12 months occurred in 10% of the complete revascularization group versus 21.2% of the IRA only revascularization group (HR 0.45; 95% CI 0.24-0.84; p=0.009). However there was no significant reduction in death or MI.
The PRAMI (Preventative Angioplasty in Myocardial Infarction) trial compared preventative PCI with no preventative PCI (2). This was stopped early by the data and safety monitoring committee after the primary endpoint of death from cardiac causes, nonfatal MI or refractory angina occurred in 9 per 100 patients assigned to preventative PCI versus 23 per 100 patients assigned to no preventative PCI (HR 0.35; 95% CI 0.21-0.58; p<0.001). This risk reduction was driven by decreases in non fatal MI and refractory angina rather than mortality.
Analysis of registry data has produced conflicting results. Real world comparison of culprit vessel intervention (CVI) versus multivessel intervention at the time of the index intervention demonstrated reduced in-hospital major adverse cardiovascular events (MACE) and increased 30 day and one year survival in patients treated using CVI (3). Propensity scoring was used to reduce confounding and bias. One year mortality in patients undergoing CVI was 7.4% versus 10.1% in patients undergoing the multivessel approach (HR 0.64; 95% CI 0.45-0.90; p=0.01). These data support the current European Society of Cardiology guidelines that recommend culprit lesion PCI in STEMI patients.
REFERENCES:
- Gershlick AH, Khan JN, Kelly DJ et al. Randomised trial of complete versus lesion-only revascularization in patients undergoing primary percutaneous coronary intervention for STEMI and multivessel disease: the CvPRIT trial. J Am Coll Cardiol. 2015;65(10):963-72.
- Wald DS, Morris JK, Wald NJ, et al. Randomized trial of preventative angioplasty in myocardial infarction. N Engl J Med. 2013;369(12):1115-23.
- Iqbal MB, Ilsley C, Kabir T, et al. Culprit vessel versus multivessel intervention at the time of primary percutaneous coronary intervention in patients with ST-segment-elevation myocardial infarction and multivessel disease: real-world analysis of 3984 patients in London. Circ Cardiovasc Qual Outcomes. 2014;7(6):936-43.
The issue of whether one should treat non-culprit lesions at the same time as the culprit lesion during primary PCI is both important and contentious. The question is difficult to answer as the results of randomised trials and registry studies can both be compromised by selection bias. As indicated in this note, registry data tends to show that patients undergoing multi-vessel intervention seem to do worse. This is in contrast to data from randomised trials which point in the opposite direction – PRAMI showing a clear mortality advantage and CvLPRIT showing no mortality benefit but reduced ischaemic endpoints. The investigators of both the PRAMI and CvLPRIT studies should be congratulated on providing much needed evidence but for the time being the jury is still out and operators need to be guided by their common sense and skill on a case-by-case basis according to the clinical scenario with which they are confronted in the catheter laboratory.
Approximately 50% of patients with ST-elevation myocardial infarction (STEMI) have non-culprit stenoses of ≥50%. The optimal revascularisation strategy in these patients with multivessel disease remains to be established. Current European guidelines recommend that primary PCI should be limited to the culprit vessels, except in patients with cardiogenic shock or persistent ischemia after culprit vessel intervention.
The recent publication of the PRAMI and CvLPRIT trials has stimulated intense interest in the management of non-culprit disease in STEMI. However, both trials are limited by their relatively small sample size and should be regarded as “proof of concept” studies. A larger trial is ongoing that will provide a more detailed analysis of subject. The optimal timing of preventive revascularisation (i.e. at the time of primary PCI versus delayed); and what constitutes a clinically significant non-culprit lesion for the purpose of preventive revascularisation is unknown. Thus, while the PRAMI and CvLPRIT trials demonstrate feasibility and are compelling, it is premature to change practice exclusively on the basis their results. A measured approach, that incorporates assessment of the success of the culprit lesion intervention, non-culprit lesion location/severity/complexity, left ventricular function, hemodynamic status, renal function, operator fatigue, and time of day/night, is advisable when determining the need and timing of preventive revascularisation in STEMI.
