Perioperative Management After Coronary Stenting
No-reflow in the context of extensive microembolization is dependent on coronary thrombus load, which itself is prevented from build-up by the presence of residual flow to the occluded artery. Is the probability of residual flow different in the context of a gradual chronic total occlusion (CTO) in comparison with the sudden total occlusion occurring with stent thrombosis? There are several arguments in favor of a systematically diminished residual, that is, collateral blood supply to the area at risk for infarction in the presence of a stent thrombosis as opposed to CTO, which may occur entirely unnoticed (Figure 3). Coronary collateral function in the presence of CTO without or with myocardial infarction is significantly higher than in the context of a less severe coronary atherosclerotic lesion (approximately 35% of normal flow during vessel patency versus 20%, respectively); in fact, there is a direct correlation between the degree of stenosis and collateral function. As a consequence, treatment of a stenotic lesion by PCI (i.e., the event preceding that of stent thrombosis) leads to a decrease, although incomplete elimination of collateral function from the mentioned average value of 20–15% of collateral, relative to normal flow during vessel patency. The amount of post-PCI collateral function reduction is greater following DES than BMS implantation (Figure 4), the fact of which has been interpreted related to the anti-inflammatory action of DES, which counteracts monocyte function, which is crucial in the pathogenesis of collateral growth. This collateral function pruning following PCI together with the fact that collateral artery growth in response to reocclusion takes several weeks to fully occur, renders the sudden total occlusion during stent thrombosis prone to devastating effects in the sense of large infarcts despite often only short occlusion times. In addition, the sudden total coronary occlusion in stent thrombosis is unique, because ischemic preconditioning with repetitive episodes of ischemia before total occlusion and coronary collateral recruitment does not take place as in chronic CAD (Figure 5). Considering the relatively low overall incidence of stent thrombosis of 0.5–1% per year and the prospect that newer generation DES may tend to have a lower incidence than earlier DES and than BMS (0.8 vs 1.7% per 5 years; p = 0.21), clinical practice of DES and BMS implantation should not be altered based on the abovementioned mechanisms related to the prognostic impact of stent thrombosis.
(Enlarge Image)
Figure 3.
Collateralized, occluded left anterior descending artery.
(A–C) Angiograms of the left coronary artery (anteroposterior, cranial projection) showing total occlusion of the LAD (black arrow). The systolic left ventricular function in this patient was entirely normal (left ventricular angiogram during diastole and during systole; right anterior oblique projection). (D) Angiogram of the RCA in the same patient with total retrograde contrast filling of the LAD via a branch collateral artery (white arrow).
LAD: Left anterior descending artery; RCA: Right coronary artery.
(Enlarge Image)
Figure 4.
Collateral flow index in patients 6 months following a bare metal stent or drug-eluting stent implantation.
Reproduced with permission from [15].
(Enlarge Image)
Figure 5.
Simultaneous recording of an intracoronary ECG, mean aortic and mean distal coronary occlusive pressure during three consecutive 2-min coronary balloon occlusions.
The ECG ST-segment shift decreases during the third versus the first and second occlusion, while Poccl relative to Paoincreases.
ic.: Intracoronary; Pao: Mean aortic pressure; Poccl: Mean distal coronary occlusive pressure.
Reproduced with permission from [15].
Possible Mechanism(s) Related to the Prognosis of Stent Thrombosis
No-reflow in the context of extensive microembolization is dependent on coronary thrombus load, which itself is prevented from build-up by the presence of residual flow to the occluded artery. Is the probability of residual flow different in the context of a gradual chronic total occlusion (CTO) in comparison with the sudden total occlusion occurring with stent thrombosis? There are several arguments in favor of a systematically diminished residual, that is, collateral blood supply to the area at risk for infarction in the presence of a stent thrombosis as opposed to CTO, which may occur entirely unnoticed (Figure 3). Coronary collateral function in the presence of CTO without or with myocardial infarction is significantly higher than in the context of a less severe coronary atherosclerotic lesion (approximately 35% of normal flow during vessel patency versus 20%, respectively); in fact, there is a direct correlation between the degree of stenosis and collateral function. As a consequence, treatment of a stenotic lesion by PCI (i.e., the event preceding that of stent thrombosis) leads to a decrease, although incomplete elimination of collateral function from the mentioned average value of 20–15% of collateral, relative to normal flow during vessel patency. The amount of post-PCI collateral function reduction is greater following DES than BMS implantation (Figure 4), the fact of which has been interpreted related to the anti-inflammatory action of DES, which counteracts monocyte function, which is crucial in the pathogenesis of collateral growth. This collateral function pruning following PCI together with the fact that collateral artery growth in response to reocclusion takes several weeks to fully occur, renders the sudden total occlusion during stent thrombosis prone to devastating effects in the sense of large infarcts despite often only short occlusion times. In addition, the sudden total coronary occlusion in stent thrombosis is unique, because ischemic preconditioning with repetitive episodes of ischemia before total occlusion and coronary collateral recruitment does not take place as in chronic CAD (Figure 5). Considering the relatively low overall incidence of stent thrombosis of 0.5–1% per year and the prospect that newer generation DES may tend to have a lower incidence than earlier DES and than BMS (0.8 vs 1.7% per 5 years; p = 0.21), clinical practice of DES and BMS implantation should not be altered based on the abovementioned mechanisms related to the prognostic impact of stent thrombosis.
(Enlarge Image)
Figure 3.
Collateralized, occluded left anterior descending artery.
(A–C) Angiograms of the left coronary artery (anteroposterior, cranial projection) showing total occlusion of the LAD (black arrow). The systolic left ventricular function in this patient was entirely normal (left ventricular angiogram during diastole and during systole; right anterior oblique projection). (D) Angiogram of the RCA in the same patient with total retrograde contrast filling of the LAD via a branch collateral artery (white arrow).
LAD: Left anterior descending artery; RCA: Right coronary artery.
(Enlarge Image)
Figure 4.
Collateral flow index in patients 6 months following a bare metal stent or drug-eluting stent implantation.
Reproduced with permission from [15].
(Enlarge Image)
Figure 5.
Simultaneous recording of an intracoronary ECG, mean aortic and mean distal coronary occlusive pressure during three consecutive 2-min coronary balloon occlusions.
The ECG ST-segment shift decreases during the third versus the first and second occlusion, while Poccl relative to Paoincreases.
ic.: Intracoronary; Pao: Mean aortic pressure; Poccl: Mean distal coronary occlusive pressure.
Reproduced with permission from [15].
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