Our ambulances are equipped with r-tPA or similar (there is a tendency to avoid streptokinase as rural/indigenous populations have high exposure to streptococcus/hx rheumatic fever and therefore high risk of added complications) and in the event of STEMIs can be administered en route to ED. Similarly many peripheral sites will administer tenecteplase or similar in Emergency Departments as there are almost no sites that are set up to perform out-of-hours angioplasty once you are out of the major cities; even less chance for neuro-radiological intervention, I think there are only 6 or 7 sites in the country and they are all in major cities.
If his research does bear fruit, I could see it immediately becoming the standard of care in Australia outside of major centres
I worked with stroke centers, doctors, etc in building stroke access systems, and that doesn't fly with reality.
Number 1, is that its hard for patients to recognize they are having a stroke. so "If called promptly" is a bit of unrealistic idealism.
Although they say 4 hours, tPA administered after 1 hour has lost most of its benefit, and places that can do thrombectomy 24/7 (in US dedicated stroke centers) is not numerous. You are losing a lot of that hour just for time for the helicopter to warm up, find a spot, and land + your ambulance time getting to /stabilizing the patient.
I'm sure the patients on your beat had suitable access, but that's a bit of selectivity bias no? In the US, although the majority of the population is within the golden hour, there are still a ton of population that does not have access to a stroke center. I find it extremely hard to believe that this is not the case in Australia - where I have heard stories of people getting a finger cut off and having to drive 3 hours to the nearest hospital.
Unfortunately I don't quite know what to make of the recurring phrase "mismatch between clinical deficit and infarct". Could anyone enlighten me, please?
When you look at the area of brain that should be downstream of a clot and therefore nonfunctional, that’s the “infarct volume”. It’s the volume of brain that we believe is infarcted.
The “mismatch” is when we do a CT, find that, say, the chunk of your brain that moves your right hand is downstream from the infarct, but your right hand is still working. This suggests that that part of your brain has enough blood coming to it from other, less salient, arteries that it’s dying slowly instead of fast.
That “mismatch” area is the one that, if we can go in and surgically pull out the clot, we can save.
Once a clot has matured they tend to be useless, which is part of why there’s a solid upper cap on time to administration. You cross a line where any clot they’re likely to bust isn’t one you want to bust. So, a window of a couple of hours. Urokinase doesn’t change that, to my knowledge.
Surgical removal of the clot, on the other hand, has recently been shown to offer enormous benefit to at-risk tissue (tissue not yet dead but in the watershed area) 24 hours later, without risk of hitting the wrong clot. It’s no miracle either, but evidence is piling up that it’s got more Pros and fewer Cons.
Thus, no one really following armchair hypotheses (one old non RCT trial not withstanding) about combining two increasingly undesirable drugs.
I respect the guy’s thought and effort, and have to admit he might be right about their combined effectiveness, but this article leaves out a lot of the context as to -why- this isn’t getting attention. Writing a hagiography-by-omission is below what I’ve come to expect from statnews.