This article is mostly a story about tenecteplase, but, effectively, it’s also a scathing indictment of alteplase – you know, the miraculous “clot-buster” we’ve been using for the past 23 years.
Because, despite rumors to the contrary, it doesn’t actually bust clots.
This isn’t news to anyone who actually follows the stroke literature closely. Indeed, the entire endovascular/thrombectomy industry is constructed upon this edifice of failure. And, as we see in this 202-patient study comparing recanalization rates after large-vessel occlusion, tenecteplase appears to be more efficacious than alteplase – 22% vs. 10%.
That is to say, in a population of 24 ICA occlusions, 3 basilar occlusions, 60 M1 occlusions, and 14 M2 occlusions, alteplase successfully “busted the clot” in 10. Most of the difference in recanalization was driven by the M1 and M2 patients, where tenecteplase had a 26% success rate and alteplase languished at 8%. These rates for alteplase are a little lower than most prior literature, so it is reasonable to be suspicious of the superiority margin associated with tenecteplase.
But, regardless, as you can see, both are dismal – and, for the past 20+ years, prior to the advent of even limited endovascular availability, we’ve just been pushing alteplase on these large vessels to no beneficial effect – except to Genentech and their shareholders.
“Tenecteplase versus Alteplase before Thrombectomy
for Ischemic Stroke”
https://www.nejm.org/doi/full/10.1056/NEJMoa1716405
Well written as always and to the point. Just had a basilar artery stroke / locked-in syndrome and gave tPa as the gateway drug to getting acceptance for endovascular therapy at the tertiary stroke center. Two questions come up – any evidence for EVT without tPa? And how good are outcomes for basilar stroke with EVT? A devastating condition, this guy had.
I’m not familiar with basilar strokes having much promise, regardless. There just isn’t any “collateral” circulation to speak of – reperfusion is useless if there’s no living brain remaining.