The advent of DES was spurred by the need to address the Achilles heel of BMS (ie. neointimal hyperplasia). It’s essentially a focal recurrence of “stable CAD” via a different mechanism than atherosclerosis.
Knowing what we know now of stable CAD, it is completely congruent that DES would offer no advantage on hard outcomes over BMS, and that benefits would only accrue to reduction in TLR.
It is interesting that there was no signal of increased stent thrombosis with DES (which is its own Achilles heel) with 9 mos of DAPT, which is generally halfway btw the “recommended” duration for stable CAD PCI (6 mos) vs ACS PCI (12 mos). Perhaps this simply reflects the patient population.
The advent of DES was spurred by the need to address the Achilles heel of BMS (ie. neointimal hyperplasia). It’s essentially a focal recurrence of “stable CAD” via a different mechanism than atherosclerosis.
Knowing what we know now of stable CAD, it is completely congruent that DES would offer no advantage on hard outcomes over BMS, and that benefits would only accrue to reduction in TLR.
It is interesting that there was no signal of increased stent thrombosis with DES (which is its own Achilles heel) with 9 mos of DAPT, which is generally halfway btw the “recommended” duration for stable CAD PCI (6 mos) vs ACS PCI (12 mos). Perhaps this simply reflects the patient population.