CULPRIT shock at TCT 2017

Culprit-Lesion-Only PCI Compared with Multivessel PCI is Associated with Better Survival in Multivessel Disease, CS, and AMI

November 9, 2017

According to findings from a multicenter trial presented by Dr. Holger Thiele, MD, at TCT 2017 (published simultaneously online at, percutaneous coronary intervention (PCI) of the culprit lesion only is associated with a lower 30-day composite risk for severe renal failure or death compared with multivessel PCI in patients with multivessel disease, cardiogenic shock (CS), and acute myocardial infarction (AMI).1


Investigators of the CULPRIT-SHOCK (Culprit Lesion Only PCI vs Multivessel PCI in Cardiogenic Shock) trial evaluated outcomes of patients with multivessel disease, CS, and AMI who were randomized to either culprit-lesion-only PCI (n = 344) vs immediate multivessel PCI (n = 342). The primary endpoint was comprised of a composite of death or severe renal failure.


The primary endpoint occurred in 45.9% (n = 158) of patients receiving PCI of the culprit lesion only, whereas 55.4% (n = 189) of patients in the multivessel PCI arm met the composite endpoint for death or severe renal failure (relative risk; 0.83; 95% confidence interval [CI], 0.71 to 0.96; P =.01).


Death alone occurred in 43% of the culprit-only patients and 52% in the multivessel arm (P =.03). Relative risk of death for the culprit-lesion-only PCI arm vs the multivessel PCI group was 0.84 (95% CI, 0.72 to 0.98; P =.03). Additionally, the relative risk for severe renal failure resulting in renal replacement therapy was 0.71 among those receiving culprit-lesion-only PCI vs multivessel PCI (95% CI, 0.49 to 1.03; P =.07).

Figure 1: Composite Primary Endpoint for Multivessel vs Culprit-Lesion-Only a
Composite Primary Endpoint for Multivessel vs Culprit-Lesion-Only PCI
aData from Thiele et al1

Investigators observed no significant differences between the 2 groups in regard to recurrent myocardial infarction (1.2% vs 0.9%, P =1.00), stroke (3.5% vs 2.9%, P =.68, or bleeding (16.6% vs 22.0%, P =.07). Additionally, time to hemodynamic stabilization (median 3 vs 3 days, P =.56), duration of ICU stay (median 5 vs 5 days, P =.61), and use of mechanical ventilation (79.4% vs 83.2%, P =.20) were similar between the 2 groups.

Perspectives with regard to use of Mechanical Circulatory Support (MCS) in Cardiogenic Shock

The CULPRIT-SHOCK was not a trial of general MCS use, nor was it focused on the Impella® device specifically. The low rate of use makes forming conclusions about their utility in this data set not possible. In addition, the investigators did not provide data on pre- vs post-Impella device use (or any MCS timing data). Prior studies of multivessel PCI in ST-elevation myocardial infarction (STEMI) show a trend toward benefit in patients without CS. In CULPRIT-SHOCK, the hazard of multivessel PCI was demonstrated. Whether multivessel outcomes with hemodynamic support would result in different outcomes (similar to STEMI without shock) is not known.

Limitations and Conclusion

Considering the nature of PCI, blinding participants and interventionalists was not possible for this study. In addition, crossover occurred in 75 patients from both groups. In part, crossover was due to a lack of hemodynamic improvement, the identification of new lesions following culprit lesion PCI, or plaque shifts.

Due to the observed crossover, the investigators suggest that treatment strategies in this population may “require adaptation to the specific clinical circumstances.”

Dr. William O’Neill, a member of the panel during the CULPRIT-SHOCK presentation at TCT, noted that the data continues to show mortality rates around 50%, which have not improved since the publication of the SHOCK trial in 2009. Also, he mentioned that the lack of improvement since that time requires new approaches to care with better systems for treatment of CS as a means for advancing the field for better patient outcomes.


  1. Thiele H, Akin I, Sandri M, et al. PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock. N Engl J Med [published online October 30, 2017]. doi: 10.1056/NEJMoa1710261.