Approximately 40-65% of patients with ST-elevation acute myocardial infarction (STEMI) have multivessel coronary artery disease, which is associated with worse outcomes compared with single-vessel disease. Proper management of non-culprit lesions in STEMI is a controversial topic. Current guidelines recommend only treating the culprit lesion unless the patient has cardiogenic shock1,2; however, there is no consensus about the best treatment strategy for this clinical syndrome3,4.
Treating the culprit and non-culprit lesions together during STEMI has the following potential advantages: 1) acute multivessel PCI eliminates the need for a secondary procedure; 2) plaque instability may include non-culprit lesions, potentially triggering recurrent ischaemic events5; 3) complete coronary revascularisation is associated with improved cardiac function and better long-term prognosis6; and, 4) acute multivessel PCI may reduce treatment costs by diminishing the need for future hospitalisations and subsequent procedures.
In contrast, acute multivessel PCI may contribute to a higher risk of complications for the following reasons: 1) the increased thrombotic and inflammatory burden in STEMI is partly related to an increased incidence of stent thrombosis among patients treated with this strategy7,8; 2) the severity of non-culprit lesions in STEMI is frequently overestimated, resulting in unnecessary intervention of functionally insignificant lesions9; 3) greater radio-contrast is used, which may be poorly tolerated in STEMI, increasing the risk of contrast-induced nephropathy and worse prognosis10; and, 4) deferred treatment of non-culprit lesions allows further discussion of treatment options by the heart team based on the angiogram and non-invasive tests.
Multiple studies have addressed this topic and were recently reviewed11; here we will only mention a few studies. We previously reported on the results of culprit-vessel-only versus multivessel PCI during STEMI, from a post hoc analysis of the HORIZONS-AMI (Harmonising Outcomes with Revascularisation and Stents in Acute Myocardial Infarction) trial12. At one-year post-STEMI, patients undergoing multivessel PCI versus staged PCI (e.g., culprit-only PCI with later non-culprit intervention) had significantly greater rates of all-cause mortality (9.2% vs. 2.3%, p<0.0001) and cardiac mortality (6.2% vs. 2.0%, p=0.005). Additionally, acute multivessel PCI was associated with more stent thrombosis events. We found no outcome parameter in favour of acute multivessel PCI. Multivariable analysis showed that staged versus multivessel PCI strategy was independently associated with lower all-cause mortality at one-month and one-year post-STEMI. The 3-year extended outcomes of this study confirmed the prognostic superiority of staged PCI vs. one-time multivessel intervention during long-term follow-up13.
Vlaar et al confirmed our results in their meta-analysis of four prospective and 14 retrospective studies involving more than 40,000 patients with STEMI14. Staged PCI aimed at completing the revascularisation was associated with lower short-term mortality rates compared with the culprit-vessel-alone PCI (odds ratio [OR]=3.03, p=0.005), and with the multivessel PCI group (OR=5.31, p=0.0001). Lower mortality rates were also associated with culprit-vessel-only versus multivessel PCI (OR=0.66, p=0.007). Lower long-term mortality rates were recorded in the staged PCI group. The rank-probability of the three therapeutic strategies was also investigated for short- and long-term mortality; staged PCI was the better strategy followed by culprit-vessel-only PCI (without subsequent revascularisation) and by multivessel PCI. However, the meta-analysis included studies that seemed to be in disagreement, and none of the prospective studies were large enough to show a significant between-group mortality difference. Hannan et al addressed the same topic retrospectively in a cohort of 4,024 STEMI patients with multivessel disease15. They found significantly lower in-hospital and long-term (42-month follow-up) mortality rates following culprit-vessel-only PCI group compared with acute multivessel PCI. At follow-up, mortality rates of staged multivessel PCI were lower than in the culprit-vessel-only PCI group, supporting completion of subsequent revascularisation in infarcted patients with multivessel coronary disease. Jensen et al retrospectively examined mortality according to timing of multivessel PCI in STEMI: acute procedure, staged procedures during the index hospitalisation or staged procedures performed within 60 days16. The study cohort consisted of 5,944 patients, of whom 4,770 had single-vessel disease and 1,174 had multivessel PCI within 60 days. For 354 (30.2%) patients with acute multivessel PCI, 194 (16.5%) patients with multivessel PCI during the index hospitalisation, and 626 (53.3%) patients with multivessel PCI within 60 days after the index hospitalisation, the adjusted hazards ratios (HRs) for one-year mortality were statistically significant at 1.53, 0.60, and 0.28, respectively, compared to patients with single-vessel disease. The investigators concluded that acute multivessel PCI in patients with STEMI was associated with increased mortality. Such cases should be treated in a staged fashion to complete the revascularisation, rather than at all at once.
Despite these data, I believe that a final conclusion cannot yet be drawn in this field of investigation. Most data addressing this question were derived from retrospective investigations or post hoc analyses. I was unable to find a properly designed and/or powered prospective randomised trial that examined multivessel PCI during STEMI; none were powered to explore all-cause mortality or cardiac mortality treatment effect as a primary endpoint. Furthermore, most reports described significant baseline differences between the two analysed groups, which may have influenced the clinical outcomes; age, pre-TIMI grades of flow and impaired left ventricular function sometimes differed between groups. Moreover, lesion and flow characteristics of non-culprit lesions were never described or specified. Thus, it is possible that patients treated with acute multivessel PCI were sicker and at greater cardiac risk regardless of the treatment strategy. More complex and lengthy procedures performed in tougher cases were likely associated with more periprocedural complications –such as contrast nephropathy, cardiac enzyme leaks, heart failure, and need to treat multiple culprit lesions.
Although some trials have attempted to correct for baseline differences using propensity controlled analysis, given the risk of residual confounding, a randomised trial is required to definitively address this issue. Until such a study is available, it can be argued that the results may be biased. The available studies lacked information about the operators’ reasons for choosing one strategy over another; therefore, a potential bias in therapeutic decision might have influenced the observations. Additionally, the angiographic diagnosis of culprit versus non-culprit lesion in STEMI might sometimes be ambiguous, owing to the documented tendency to overestimate coronary artery disease severity in the context of STEMI due to coronary spasm and systemic vasoconstriction. Such a phenomenon may result in PCI treatment of non-significant\non-culprit lesions, adversely influencing the obtained results.
In summary, the results of the presently available studies strongly suggest that acute multivessel PCI in patients with STEMI may be associated with a greater risk of mortality compared to staged PCI. Furthermore, complete staged revascularisation remains the best therapeutic strategy in STEMI patients. Thus, pending the results of a properly designed randomised trial, a deferred angioplasty strategy of non-culprit lesions should remain the standard approach in patients with multivessel coronary artery disease and STEMI.
Conflict of interest statement
The author has no conflicts of interest to declare.
