| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Oxford Heart Center, John Radcliffe Hospital, Headleyway, Headington, Oxford, OX3 9DU United Kingdom
(Email: suviteshluthra{at}yahoo.com).
We thank Dr Nakamura for his interesting observations and comments [1] regarding our article [2].
A number of articles have appeared recently (most of them case reports and a few from trial data) on drug-eluting stent (DES) induced aneurysms. We have been able to compile at least 30 such reports so far, and it remains a subject of ongoing clinical investigation as more are published in the literature. The spectrum of vessel wall changes has involved both sirolimus-eluting and paclitaxel-eluting stents.
As has been correctly pointed out, DES induced aneurysms are a new, rare, and unique problem, without a consensus on treatment options. Conservative management remains an option for asymptomatic aneurysms. Stenting of the aneurysms with "covered" bare metal stents has also been explored with good results [3]. However, the use of DES in this setting could potentially compound the problem further as the stent itself is believed to be inciting the inflammation. We believe that DES induced coronary aneurysms are a separate entity from aneurysms secondary to atherosclerosis and should be viewed as such.
The concerns for atheroembolism in the reported case had to be balanced against concerns for collateral flow and septal flow. This patient had 2 stents (18 x 2.5 mm) in situ covering a length of approximately 4 cms of the left anterior descending coronary artery. There were two significant septal arteries arising from the area. Excluding the aneurysms with ligation would have potentially blocked all flow in these septals. Furthermore, it has been clearly documented that ligation of stenosed coronaries or for that matter, even partially blocked previous grafts in ischemic territories, can cause distal hypoperfusion despite the new grafts [4].
Late rupture was clearly an overriding concern, and patch reinforcement seemed to be the most appropriate without "disturbing" the native coronary. By virtue of chemical fixation, Bioglue (CryoLife Inc, Kennesaw, GA) hardens and stabilizes the inflamed tissues. It can provide a stable reinforced environment over the thinned out parts of the aneurysm by extensive protein cross linkages and polymerization between the external surface of the aneurysm and the pericardial patch, and potentially decrease the risk of embolization by chemical fixation. The technique of pericardial patch reinforcement is novel and we have not found any previous references to bolster any claims or to recommend it as a routine strategy.
The concept of an "obstructive" versus "dilated" pattern of arterial remodeling needs to be appreciated in the context of treatment strategies for native coronary lesions and those that are stent induced. Both patterns can coexist in different segments of the same vessel. Although the patterns of remodeling are different, the microscopic pathophysiology is the same in laying down of new thrombus intraluminally and extraluminally between the stent struts and vessel wall in loose areas of stent malposition, plaque remodeling, characterized by further deposition and dissolution, fibroblastic migration, and proliferation, apoptosis, and changes in the media and external elastic membrane with potential expansion or regression of the thickness and boundaries of the vessel wall. The patterns differ only because of the difference in the intensity of the changes in segments of the vessel wall. Treatment strategies (namely the antiplatelet agents: statins, antioxidants, anti-inflammatories and the "beneficial" antimitotics eluting from the stents) that are effective for "obstructive" patterns must therefore be as effective for the "dilated" patterns. Once the excruciating mechanical manifestations, such as potential rupture and distal ischemia have been dealt with surgically, an exercise like removing a complex proximal plaque in the coronary for an obstructive lesion, or ligation of the native coronary or aneurysmectomy for a dilated lesion, would be unnecessary except for extraordinary circumstances, such as a very large aneurysm filled with thrombus; pressure effects on surrounding structures; fistulation into a vein or coronary sinus; an open aneurysm that has ruptured into the pericardium; or shunts into an atrium, aorta, or pulmonary artery; erosion into the fibrous skeleton of the heart with annular destruction; valve incompetence or conduction blocks and mycotic aneurysms. Such an exercise can be fraught with dangers of intraoperative coronary embolization, ischemia, septal infarction, and surgical suturing in an intensely inflamed and friable area with potential for cut through and late cardiac rupture.
The natural history of DES-induced aneurysms is unknown. Major adverse cardiac events in relation to DES have been largely ascribed to in-stent thrombosis rather than coronary embolism, and most have been related to clopidogrel withdrawal. Continuation of clopidogrel postoperatively might be beneficial, but the duration of therapy remains debatable [5]. We are not sure if removing the stents from the site of this smoldering inflammation in the artery would have helped reduce or even possibly reversed it. The problem has been sufficiently rare in our practice for us to formulate a routine strategy.
 |
References |
|---|
 Top References |
|---|
Related Article
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
