Attenuated Coronary Collateral Function After Drug-Eluting Stent Implantation

Abstract

Caution has been, and should continue to be, the watchword for coronary artery stent implantation. Astute cardiologists should not be lulled to sleep in the face of the overwhelming everyday success of their expert interventional colleagues' skill in the use of drug-eluting stents (DES). Despite its revolutionary advances, DES implantation has a downside. In addition to the rare complications known to occur during the implantation procedure (extensive dissection, emboli, perforation, side branch occlusion, early abrupt closure, and so on), DES are associated with late subacute thrombosis despite perfect implantation technique and concomitant antiplatelet therapy (1). See page 15In this issue of the Journal, Meier et al.(2) identify a new downside to DES: the late attenuation of collateral function. Recall that the most important, if not the only, role of coronary collaterals is to protect the myocardium from ischemia. The rate and type of collateral recruitment with or without angiogenesis vary greatly and for reasons not completely understood (3). Acute recruitment of collateral flow can be demonstrated in some normal hearts without coronary artery disease (4). However, in most but not all patients with chronic ischemic heart disease, collaterals are recruited slowly, forming gradually over time. Responding to loss of distal coronary perfusion pressure and intermittent ischemia, angiogenic growth factors and other mediators are postulated to promote formation of new capillary pathways, thus improving perfusion to the challenged myocardial bed (5,6). In other patients, for example, some acute myocardial infarction (MI) patients, collaterals are acutely recruited, opening immediately during abrupt arterial occlusion and serving to limit what would otherwise be extensive MI.It is also important to note that collateral function can change after coronary intervention. Opening a chronic totally occluded vessel with percutaneous angioplasty alters the microcirculatory responses (7,8). Abrupt occlusion of a newly recanalized chronic total coronary artery occlusion may result in an MI even though substantial preexisting collaterals protected the myocardium before opening the occlusion. The restored perfusion after percutaneous coronary intervention (PCI) changed the collateral bed responses for the worse (9). Collateral function after stenting. Meier et al. (2) studied 120 patients undergoing repeat PCI 6 months after baremetal stent (BMS, n ϭ 60) and DES (n ϭ 60) implantation, matching patients for clinical and angiographic features including the in-stent stenosis severity. The collateral flow index (CFI ϭ coronary occlusion pressure/aortic pressure Ϫ central venous pressure) was measured during stent implantation using a pressure sensor angioplasty guidewire and invasively determined again at a follow-up catheterization. The functional impact of collaterals was also correlated to ischemic tolerance, as measured by intracoronary electrogram ST-segment elevation (Ն0.1 mV) during ischemia induced by balloon coronary occlu...

Understanding and minimizing late thrombosis of drug-eluting stents.

“…34 Thrombosis may have worse consequences with drug-eluting stents than with bare metal stents, as the former have various inhibitory effects on the production of cytokines, growth factors, and chemotactic proteins, which may impair collateral function. 35,36 If collateral regression has occurred, this phenomenon can lead to more serious cardiac events. 37…”

Coronary Collaterals and Graft Failure

“…They conclude that well developed collaterals to a revascularized region are a risk factor for restenosis of the treated lesion. By the way, other authors have pointed out that recanalization of a chronic total occlusion through PCI with drug-eluting stents is associated with a rapid decline in distal collateral function which may expose the patient to higher risk of adverse cardiac events in case of later restenosis [19,20,21]. Nonetheless, the discussion of the effects of PCI on the distal collateral circulation is beyond the scopes of the present chapter.…”

Prevention of stent thrombosis

“…Smanjenje funkcije kolaterala posle PCI, uz činjenicu da je za nastanak kolaterala u odgovoru na reokluziju arterije potrebno nekoliko nedelja, čini da iznenadna okluzija tokom TS izaziva pojavu velikog infarkta. [13][14] Preporuke za uzimanje i obustavu dvojne anitrombocitne terapije Aspirin posle PCI treba uzimati doživotno, ali za produženo uzimanje klopidogrela nema jasnih stavova.…”