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Non-Infarct Related Artery Intervention in St-Elevation Myocardial Infarc-
184 tion With Multivessel Disease: MultiVessel PCI in STEMI:
Timing of Intervention?

Fig.3: Various strategies for PCI in MVD-STEMI

Evidence - Post 2011:
Proponents of aggressive approach argue that in STEMI heightened inflammation is not limited to the culprit
plaque, there is a Pan-inflammation leading to multiple plaque disruptions[9]. So multivessel PCI would afford
protection against plaque rupture of these lesions and prevent recurrent MI/ischemia and death. Also critical
stenosis in non-culprit vessel causes ‘ischeamia at distance’ which hampers the compensatory contractility of
remote myocardial segments, so multivessel PCI leads to faster improvement in LV function[10]. Also the evo-
lution of PCI with high penetration of latest-generation drug-eluting stents, better hardware and optimisation
of antithrombotic and Antiplatelet strategy, outcomes of PCI have improved significantly in the last decade.
PRAMI (Preventive Angioplasty in Acute Myocardial Infarction) study, patients with STEMI and MVD were
randomised to an aggressive approach designated as “preventive angioplasty” with non-culprit PCI imme-
diately following p-PCI, and a conservative approach with staged non-culprit PCI only in case of refractory
symptoms[11]. This was a open-label, single-blind study with small sample size and slow recruitment (465
patients enrolled over 5years from 5 high volume centres in UK, each performing >300 pPCI per year). Ran-
domisation in this trial was done after pPCI and there was high selection bias (2428 patients screened and
465 patients were enrolled). The “preventive angioplasty” strategy was proved to be superior with a significant
65% relative reduction in the combined primary endpoint of cardiovascular death, non-fatal MI and refractory
angina. Results were driven by a 65% reduction in refractory angina and a 68% reduction in non-fatal MI,
although a trend towards a reduction in mortality (p=0.07) was also documented. In this trial obstructive CAD
was defined only by angiographic criteria which led to overestimation of the non-culprit lesion and overtreat-
ment in “preventive angioplasty” arm. Moreover no information was provided about non-culprit lesions such
as QCA, TIMI flow or lesion characteristics. Because of highly selected patients, it is difficult to extrapolate
a concept of “preventive angioplasty” to an all-comer STEMI population. Very few interventionalist follow
the PRAMI trial as the real clinical questions about non-culprit lesions- “should we do it?” and “when to do
it?” remain partially unanswered after the PRAMI study. The PRAMI study probably suggests that non-culprit
lesions could be treated in specific cases according to both patient and anatomy, but does not address the
optimal timing for these patients.
CvLPRIT (Complete Versus Lesion-Only Primary PCI trial)[12] was multicentre, open randomised trial compar-
ing culprit lesion only with complete intervention in patients presenting with STEMI and evidence of multives-
sel disease. Complete revascularization was performed either at the time of P-PCI (two thirds of complete
revascularisation group) or before hospital discharge. As with PRAMI, this was also a small study with slow
recruitment (850 patients were screened over 48 months and 296 were enrolled from 7 centres in UK); but
randomisation was done prior to pPCI. The primary endpoint (composite of all-cause death, recurrent myocar-

GCDC 2017