90% of these patients were on inotropes (unsurprisingly, they had shock). Could the presence of an inotrope be expected to alter the results?
Is mortality the best endpoint for this study? Should infarct size or ejection fraction have been considered in the 30 day survival group?
What does this patient sample tell us about our patients? Only 1/3 of them were smokers for example. Just how well does a sample need to fit with your population for results to be meaningful?
They all had lesions at angiography, and in only 3.2% was revascularisation not completed – does this mean all MI patients with shock should go to the cath lab?
This group excluded those patients in coma (why do you think this might be? – remember the presumption is that patients in this study died of cardiogenic shock). NICE guidelines for acute STEMI specifically point out that coma should not be used as a contraindication to PCI (see the recommendations section). Do you agree with NICE?
The conclusions mention a trend towards increased VAD use. This phrase (a trend towards) is used quite a bit. Is a p value of 0.07 any more meaningful when looking for a difference than one of 0.12?
On a similar note is it appropriate to calculate relative risks when there is not a significant difference?
Is early revascularisation such a confounding feature that IABP, or any other therapy, becomes insignificant i.e. is your fate determined by the PCI and nothing else?
Should we bin the IABP in the cath lab?
Will the pressure waveform for the IABP ever stop being an exam favourite (like the PA catheter trace)?!
As always you don’t have to base your response on these questions – these are just some of the things I thought about when reading the paper. I look forward to reading your thoughts.