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Recent Evidence about Coronary Stent Technology
Introduction
Coronary Heart Disease is still leading cause of death in developed nations, and also causing lot of morbidity and long term complications such as heart failure, impaired daily activity, etc. Because of that, cardiovascular disease is one of the major concern of the modern medicine. Many technology and knowledge have been developed recently about cardiovascular.
One of the technology is coronary stenting procedure. A coronary stent is a tube placed in the coronary arteries that supply the heart, to keep the arteries open in the treatment of coronary heart disease. It is used in a procedure called percutaneous coronary intervention (PCI). This technique and device is developed in order to substitute the invasive procedure (surgery).
Since its invention coronary stent has been widely used in treatment of myocard ischemia, and extended to be used in other vascular problems such as peripheral artery ischemia, and carotid stenting. One of the innovation of the stent technology is the drug-eluting stent (DES). DES is a stent that contain the drug that can block cell proliferation. This prevents fibrosis that, together with clots (thrombus), could otherwise block the stented artery, a process called restenosis.
Drug-eluting stents in current clinical use were approved by the FDA after clinical trials showed they were statistically superior to bare-metal stents (BMS) for the treatment of native coronary artery narrowings, having lower rates of major adverse cardiac events (MACE) (usually defined as a composite clinical endpoint of death myocardial infarction repeat intervention because of restenosis).
Recent Evidence
On March 4 2011, scientist published their study in Journal of American College of Cardiology. The present study suggests that neoatherosclerosis or the new thickening of vessel walls occurs in both Bare Metal Stent and DES, however, for DES implants, it is observed more frequently and at an earlier time point (median 420 days) as compared with BMS (median 2,160 days). This is an interesting data since previous evidence showed that DES is superior than Bare Metal Stent.
For stent-related deaths, in-stent neoatherosclerosis incidence was similar for BMS and DES (18% vs. 20%). However, for nonstent-related death, the incidence of neoatherosclerosis was more frequent for DES than BMS (42% vs. 20%). Moreover, neoatherosclerosis in DES shows unstable characteristics by 2 years after implant, whereas similar features in BMS occur at relatively later times (average implant duration 6 years). These observations raise the question whether neoatherosclerosis seen within DES as well as BMS at follow-up may in part be responsible for some late thrombotic events. The implications of current findings may be of practical importance as the usage of DES implants continues to increase worldwide. The occurrence of uncovered struts complicated by a dysfunctional endothelium remains the primary cause of stent thrombosis in DES; nevertheless, the present study adds another risk factor, namely, in-stent plaque rupture, although a rare event.
Possible Mechanism
Although the underlying processes responsible for the development of neoatherosclerosis after stent implantation are likely multifactorial, we hypothesize that it may involve the inability to maintain a fully functional endothelialized luminal surface within the stented segment. The endothelium normally provides an efficient barrier against the excessive uptake of circulating lipid, and that may no longer be true in the in-stent regions of DES and BMS.
In the present study, BMS exhibited greater trends for neoatherosclerotic changes occurring in the more proximal than distal lesions relative to DES, thus indicating divergent mechanisms by which neoatherosclerosis attributed to DES may be more related to incompetent and incomplete endothelialization as opposed to shear stress for BMS. These findings in the BMS may be more akin to the development of atherosclerosis in native coronary arteries, and is most prominent in the proximal regions of the coronary arteries.
Recently, chronic endoplasmic reticular stress in endothelial cells at athero-susceptible sites with arterial flow disturbances has been linked to inflammation. Shear-induced changes in endothelial phenotype (collectively known as mechanotransduction) may promote the expression of transmembrane proteins, like integrins and platelet endothelial cell adhesion molecule-1, which further allow inflammatory cell attachment and migration to subendothelial spaces. Changes in endothelial cell permeability could presumably allow greater amounts of lipoproteins to enter the subendothelial space, with an affinity for matrix proteins, in particular proteoglycans that promote their retention.
The relatively faster development of neoatherosclerosis in DES than in BMS is probably related to drug effects, which are also responsible for incomplete endothelialization. Previous animal studies of DES suggest that the regenerating endothelial lining could be incompetent, and therefore may result in endothelial cells activation, which leads to monocyte adherence with subsequent subendothelial migration. Incomplete (delayed) endothelial regrowth and recovery observed with DES that may contribute to atherogenesis is characterized by poor cell-to-cell contacts identified by decreased expression of platelet endothelial cell adhesion molecule-1 and antithrombotic mediators such as thrombomodulin.
Experimental evidence suggests that neoatherosclerosis within stents can be associated with delayed arterial healing compounded by lethal injury to smooth muscle cells and endothelial cells. In humans, the pathology studies have reported neoatherosclerotic change occurring in vein graft and in native coronary arteries with foam cell infiltration after BMS implant. Previous clinical studies have also suggested endothelial dysfunction after DES implantation by showing impaired vasomotor function in the adjacent segment of stents, although the precise mechanism for the endothelial dysfunction in the stented segment in humans remains unknown.
In Simple Words, the Atherosclerosis occurs both BMS and DES, but with different mechanism. DES contain the anti-proliferative drugs, it will cause the endothelial dysfunction, because cell proliferation and growth is important in vessel repair of the mechanical injury cause by the stent itself. Blood flow in stent artery is causing mechanical shearing stress to the vessel thus needs to be repair by our body mechanism. But the anti-proliferative drugs inhibits the process causing prolong inflammation thus further promotes the lipid deposition in vessel walls. As the result, vessel wall become narrow.
Clinical Relevance
Eventhough the pathological studies showed that DES maybe more harmful than BMS, or less beneficial. But based on large scale follow up DES and BMS patient, there is no difference in mortality risk.
This result of study can't be apply yet, but can be considered for us, to evaluate more about Stent procedure choosing the best one for the sack of someone's life.
Coronary Heart Disease is still leading cause of death in developed nations, and also causing lot of morbidity and long term complications such as heart failure, impaired daily activity, etc. Because of that, cardiovascular disease is one of the major concern of the modern medicine. Many technology and knowledge have been developed recently about cardiovascular.
Since its invention coronary stent has been widely used in treatment of myocard ischemia, and extended to be used in other vascular problems such as peripheral artery ischemia, and carotid stenting. One of the innovation of the stent technology is the drug-eluting stent (DES). DES is a stent that contain the drug that can block cell proliferation. This prevents fibrosis that, together with clots (thrombus), could otherwise block the stented artery, a process called restenosis.
Drug-eluting stents in current clinical use were approved by the FDA after clinical trials showed they were statistically superior to bare-metal stents (BMS) for the treatment of native coronary artery narrowings, having lower rates of major adverse cardiac events (MACE) (usually defined as a composite clinical endpoint of death myocardial infarction repeat intervention because of restenosis).
Recent Evidence
On March 4 2011, scientist published their study in Journal of American College of Cardiology. The present study suggests that neoatherosclerosis or the new thickening of vessel walls occurs in both Bare Metal Stent and DES, however, for DES implants, it is observed more frequently and at an earlier time point (median 420 days) as compared with BMS (median 2,160 days). This is an interesting data since previous evidence showed that DES is superior than Bare Metal Stent.
For stent-related deaths, in-stent neoatherosclerosis incidence was similar for BMS and DES (18% vs. 20%). However, for nonstent-related death, the incidence of neoatherosclerosis was more frequent for DES than BMS (42% vs. 20%). Moreover, neoatherosclerosis in DES shows unstable characteristics by 2 years after implant, whereas similar features in BMS occur at relatively later times (average implant duration 6 years). These observations raise the question whether neoatherosclerosis seen within DES as well as BMS at follow-up may in part be responsible for some late thrombotic events. The implications of current findings may be of practical importance as the usage of DES implants continues to increase worldwide. The occurrence of uncovered struts complicated by a dysfunctional endothelium remains the primary cause of stent thrombosis in DES; nevertheless, the present study adds another risk factor, namely, in-stent plaque rupture, although a rare event.
Possible Mechanism
Although the underlying processes responsible for the development of neoatherosclerosis after stent implantation are likely multifactorial, we hypothesize that it may involve the inability to maintain a fully functional endothelialized luminal surface within the stented segment. The endothelium normally provides an efficient barrier against the excessive uptake of circulating lipid, and that may no longer be true in the in-stent regions of DES and BMS.
In the present study, BMS exhibited greater trends for neoatherosclerotic changes occurring in the more proximal than distal lesions relative to DES, thus indicating divergent mechanisms by which neoatherosclerosis attributed to DES may be more related to incompetent and incomplete endothelialization as opposed to shear stress for BMS. These findings in the BMS may be more akin to the development of atherosclerosis in native coronary arteries, and is most prominent in the proximal regions of the coronary arteries.
Recently, chronic endoplasmic reticular stress in endothelial cells at athero-susceptible sites with arterial flow disturbances has been linked to inflammation. Shear-induced changes in endothelial phenotype (collectively known as mechanotransduction) may promote the expression of transmembrane proteins, like integrins and platelet endothelial cell adhesion molecule-1, which further allow inflammatory cell attachment and migration to subendothelial spaces. Changes in endothelial cell permeability could presumably allow greater amounts of lipoproteins to enter the subendothelial space, with an affinity for matrix proteins, in particular proteoglycans that promote their retention.
The relatively faster development of neoatherosclerosis in DES than in BMS is probably related to drug effects, which are also responsible for incomplete endothelialization. Previous animal studies of DES suggest that the regenerating endothelial lining could be incompetent, and therefore may result in endothelial cells activation, which leads to monocyte adherence with subsequent subendothelial migration. Incomplete (delayed) endothelial regrowth and recovery observed with DES that may contribute to atherogenesis is characterized by poor cell-to-cell contacts identified by decreased expression of platelet endothelial cell adhesion molecule-1 and antithrombotic mediators such as thrombomodulin.
Experimental evidence suggests that neoatherosclerosis within stents can be associated with delayed arterial healing compounded by lethal injury to smooth muscle cells and endothelial cells. In humans, the pathology studies have reported neoatherosclerotic change occurring in vein graft and in native coronary arteries with foam cell infiltration after BMS implant. Previous clinical studies have also suggested endothelial dysfunction after DES implantation by showing impaired vasomotor function in the adjacent segment of stents, although the precise mechanism for the endothelial dysfunction in the stented segment in humans remains unknown.
In Simple Words, the Atherosclerosis occurs both BMS and DES, but with different mechanism. DES contain the anti-proliferative drugs, it will cause the endothelial dysfunction, because cell proliferation and growth is important in vessel repair of the mechanical injury cause by the stent itself. Blood flow in stent artery is causing mechanical shearing stress to the vessel thus needs to be repair by our body mechanism. But the anti-proliferative drugs inhibits the process causing prolong inflammation thus further promotes the lipid deposition in vessel walls. As the result, vessel wall become narrow.
Clinical Relevance
Eventhough the pathological studies showed that DES maybe more harmful than BMS, or less beneficial. But based on large scale follow up DES and BMS patient, there is no difference in mortality risk.
This result of study can't be apply yet, but can be considered for us, to evaluate more about Stent procedure choosing the best one for the sack of someone's life.
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