Paper Presented to the Peripheral Vascular Surgery Society – 22nd Annual Winter MeetingThe Effect of Statin Use on Embolic Potential During Carotid Angioplasty and Stenting
Introduction
Although there is significant progress in endovascular technology, multiple trials have failed to show equivalency in outcomes between carotid artery stenting (CAS) and carotid endarterectomy (CEA).1, 2, 3 The most recent randomized controlled trial, the Carotid Revascularization Endarterectomy vs. Stenting Trial (CREST), showed a 30-day stroke rate of 4.1% after CAS compared to only 2.3% after CEA (P = 0.01).4 Therefore, although less invasive, CAS results in more cerebrovascular sequelae.1, 2, 3, 4 These neurologic complications occur due to distal embolization during and after the procedure. For carotid stenting to have greater applicability, the rates of transient ischemic attack (TIA), stroke, and death associated with CAS must be reduced to a level comparable with those of CEA. Identifying and minimizing factors that increase the risk of distal embolization during and following carotid stenting are crucial to reduce the overall probability of cerebrovascular events.
HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitors, or statins, are a group of medications used to treat hypercholesterolemia and other dyslipidemias.5 Statins directly improve low-density lipoprotein (LDL) and high-density lipoprotein (HDL) levels. This therapeutic effect occurs as a result of decreased de novo cholesterol synthesis and increased LDL uptake by hepatocytes.5, 6 The lipid-modifying properties of statins, however, do not fully explain their therapeutic effects.5, 6, 7, 8, 9 Statins improve endothelial function, decrease monocyte migration and macrophage activation, limit platelet aggregation and degranulation, blunt the negative effects of smooth muscle cells (SMC), and reduce atherosclerotic inflammation.5, 7, 8, 9 Collectively, these pleiotropic effects promote atheroma stability. Stable atheromata are less likely to cause the harmful sequelae of atherosclerotic vascular diseases.6, 9, 10, 11, 12 Specifically, an improved stroke and death rate following CEA and CAS in patients utilizing HMG-CoA reductase inhibitors has been observed.13, 14 Statins appear to be beneficial after other vascular procedures as well.15, 16, 17
In our study, we sought to determine the effects of statins on the embolic potential during CAS by characterizing captured debris. Moreover, we assessed the impact of HMG-CoA reductase inhibitors on major and minor peri-procedural complications.
Section snippets
Methods
A retrospective review of a prospectively maintained database was performed. Between 2003 and 2010, carotid filters from a total of 251 consecutive CAS procedures were collected and available for analysis. Of these 251 embolic protections devices (EPD), information on peri-procedural statin use was available for 62 consecutive carotid interventions performed after September 2007. These filters were collected and the captured debris was analyzed. The number of particles within each EPD was
Results
Of the 251 CAS procedures performed, the status of statin use was identified in 62 cases. Of this cohort of 62 carotid interventions, 41 (66%) patients were on statin therapy at the time of CAS. A variety of HMG-CoA reductase inhibitors were utilized in our population. Of the 41 patients on statin therapy, 15 (36.6%) were on Rosuvastatin, 14 (34.1%) were on Atorvastatin, 11 (26.8%) were on Simvastatin, and 1 (2.4%) was on Lovastatin (Table I). The mean age of our study population was 68.2 ± 9.8
Discussion
It is well established that atherosclerosis is a systemic illness affecting multiple vascular territories. Therefore, the manifestations of this disease are a reflection of the individual vessels involved. Nevertheless, this process is not mutually exclusive. Patients with carotid artery disease often have concomitant coronary artery disease. Improving CAS outcomes, therefore, is dependent on reducing both the cerebrovascular and cardiovascular adverse events.
Atherosclerotic plaque instability
Conclusion
This study demonstrates that statin use is associated with less embolic debris during CAS as exemplified by fewer captured particles seen within carotid filters after their retrieval. These results further support the effects of statin therapy on plaque stability and their contribution to improved CAS outcomes.
References (30)
- et al.
Lessons from carotid endarterectomy and stenting trials
Lancet
(2010) - et al.
Effect of statins on cholesterol crystallization and atherosclerotic plaque stabilization
Am J Cardiol
(2011) - et al.
3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors reduce the risk of perioperative stroke and mortality after carotid endarterectomy
J Vasc Surg
(2005) - et al.
Effects of statins on early and late results of carotid stenting
J Vasc Surg
(2011) - et al.
Reduction in cardiovascular events after vascular surgery with atorvastatin: a randomized trial
J Vasc Surg
(2004) - et al.
Statin therapy is associated with superior clinical outcomes after endovascular treatment of critical limb ischemia
J Vasc Surg
(2012) - et al.
Markers of instability in high-risk carotid plaques are reduced by statins
J Vasc Surg
(2008) - et al.
Carotid plaque regression following 6-month statin therapy assessed by 3T cardiovascular magnetic resonance: comparison with ultrasound intima media thickness
J Cardiovasc Magn Reson
(2011) - et al.
New ischaemic brain lesions on MRI after stenting or endarterectomy for symptomatic carotid stenosis: a substudy of the International Carotid Stenting Study (ICSS)
Lancet Neurol
(2010) Fire in the hole: carotid stenting versus endarterectomy
Circulation
(2011)