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PRAMI study

Immediate multivessel PCI in patients with acute STEMI – results oft he PRAMI trial in perspective

Acute Coronary Syndromes (ACS)

In patients with STEMI treated with primary PCI multivessel disease is present in about 40-50 % of hemodynamically stable patients and about 70-80 % of patients with cardiogenic shock.
Current ESC guidelines recommend culprit lesion only PCI in stable patients and immediate multivessel PCI in patients with cardiogenic shock.
Just recently the results of the PRAMI trial have been published.
Here patients with STEMI with multivessel disease and successful primary PCI of the culprit lesion were randomized to additional immediate PCI of all lesions with > 50 % stenosis or conservative therapy.
The trial intended to enrol 600 patients and was powered to detect a reduction  of the primary combined endpoint of cardiovascular death, recurrent myocardial infarction and refractory angina from 20% to 14 % per year.
It was stopped prematurely after the inclusion of 465 patients because of a significant advantage of immediate multivessel PCI of 9% versus 23 %, p=0.001.
Should we now adopt this strategy for our patients with STEMI and multivessel disease in clinical practice ?
I do not think so, because PRAMI has a number of limitations.
The patients in the conservative group did not undergo a staged PCI or even a test for ischemia, a strategy recommeded in ESC guidelines.
So the patients in the conservative group were treated not optimal and not to current clinical standards. PCI of all lesions > 50% without any proof of t he hemodynamic significance of the lesion e.g. by FRR will certainly lead to interventions in a number of insignificant stenosis.
Interestingly the mean stent diameter in non-infarcted arteries was 3.1 mm, implying a selection bias of patients , because usually this diameter is smaller. Nothing is mentioned in the manuscript about the success and completeness of multivessel PCI.
Another problem is the premature termination of the trial, which usually means that results between the groups are frozen at the moment of the highest difference. There are a number of examples that such great differences diminished during the course of t he trial or results went even in the opposite direction.
In addition, the differences between multivessel PCI and culprit PCI in mortality are greater than between reperfusion and no reperfusion or between primary PCI and fibrinolysis  in large clinical trials, which is highly unlikely.


Therefore a play of chance finding can not be ruled out, despite the fact that all endpoints hinted in the same direction. The results of PRAMI are in sharp contrast to the results of the much larger COURAGE trial, in which PCI of stable lesions despite proof a ischemia was not associated with an improved outcome compared to optimal medical therapy.
Before we adapt immediate multivessel PCI as routine treatment in our daily clinical practice, a second larger trial confirming the surprising results of PRAMI is necessary.
This trial named COMPLETE ( is currently underway and will enroll 3900 patients. The primary endpoint is the combination of cardiovascular death or myocardial infarction during 4-year follow-up.
Until then, culprit lesion PCI with subsequent staged PCI of lesions after proof of hemodynamic relevance with FFR or a stress test should remain the standard of care.


Prof Uwe Zeymer,
Klinikum Ludwigshafen and Institut für Herzinfarktforschung Ludwigshafen, Germany