New Tool Predicts Stroke Outcome with 93% Accuracy, Guiding Better Carotid Surgery Decisions

 Will your doctor GUARANTEE no adverse events?

I would never do carotid stenting, way too many possible complications.

Stents were never the permanent solution, they do nothing to address the inflammation in your arteries that creates plaque. And why would you want to put inflexible stents in flexible arteries?  I still don't understand why you would medically need to stent a carotid artery at all if the Circle of Willis is complete. (Unless the whole point is revenue and profit generation) It would seem to make more sense to just close it up and prevent problems from there.  My right carotid artery was closed for 10 years and I cognitively functioned quite well with no episodes of fainting.

Here is why your doctor needs to GUARANTEE NO complications from stenting!

• stenting (22 posts to May 2011)

• carotid stenting (21 posts to May 2016)

• carotid artery stenting (7 posts to November 2021)

 

 

Restenosis is a gradual re-narrowing of the stented segment that occurs mostly between 3 to 12 months after stent placement. 

So by not solving the inflammation problem you get this! Stents don't solve the underlying problem, why the fuck is your doctor prescribing them? Money?

New Tool Predicts Stroke Outcome with 93% Accuracy, Guiding Better Carotid Surgery Decisions

Researchers have developed a predictive model with a 93% accuracy rate in determining whether urgent carotid-intervention patients will regain functional independence.

This advanced model uses a data-driven approach that combines 4 critical clinical metrics -- stroke severity, frailty risk score, timing of intervention, and the use of thrombolysis -- to create a real-time decision-making tool. By leveraging these variables, physicians can improve patient care by tailoring treatment plans, optimising intervention timing, and ensuring that the most appropriate patients receive these complex procedures. 

The findings are published in the Journal of the American College of Surgeons. 

“We are entering a new era of stroke care where data-driven insights guide every decision,” said senior author Hernan A. Bazan, MD, chsner Clinic Foundation, New Orleans, Louisiana. “By integrating a real-time frailty risk score into the electronic medical record, presenting stroke severity and other variables, we can proactively identify who will benefit from immediate surgery and who may need ‘pre-habilitating’ before surgery to achieve better outcomes.”

Stroke requires timely intervention, with carotid endarterectomy (CEA) and carotid artery stenting (CAS) increasingly used in select acute carotid-related stroke patients. The researchers aimed to build a model to predict neurologic functional independence (modified Rankin scale [mRS], ≤2) in this high-risk group.

The researchers analysed data from 302 patients who had a stroke and undergoing urgent CEA or CAS between 2015 and 2023 at a tertiary Comprehensive Stroke Center. Predictors included: (1) stroke severity; (2) time to intervention (≤48 hours); (3) thrombolysis use; and (4) frailty risk score. Multiple models were constructed and selected based on the area under the ROC curve (AUC). The primary endpoint was discharge neurological functional independence (mRS ≤2).

Most (78%) patients were discharged functionally independent (mRS ≤2). The combined 30-day rate of stroke, death, and myocardial infarction was 8.3%, and 6.5% for CEA alone and 12.5% for CAS. The model, incorporating thrombolysis, time to intervention, stroke severity (NIHSS), and frailty risk, correctly predicted 93% of functional independence outcomes (area under the curve, 0.808).

“Predicting a patient’s recovery potential with such reliability gives us an unprecedented level of confidence in our treatment decisions,” said Leo Seoane, MD, Ochsner Health. “This innovation ensures that every patient receives the care best suited to their situation, further advancing our commitment to excellence.”

Reference: https://journals.lww.com/journalacs/abstract/9900/precision_in_stroke_care__a_novel_model_for.1125.aspx

SOURCE: Ochsner Health

Mediation Analysis of Acute Carotid Stenting in Tandem Lesions

I would never do carotid stenting, way too many possible complications.

Stents were never the permanent solution, they do nothing to address the inflammation in your arteries that creates plaque. And why would you want to put inflexible stents in flexible arteries?  I still don't understand why you would medically need to stent a carotid artery at all if the Circle of Willis is complete. (Unless the whole point is revenue and profit generation) It would seem to make more sense to just close it up and prevent problems from there.  My right carotid artery was closed for 10 years and I cognitively functioned quite well with no episodes of fainting.

Here is why your doctor needs to guarantee NO complications from stenting!

• stenting (22 posts to May 2011)

• carotid stenting (21 posts to May 2016)

• carotid artery stenting (7 posts to November 2021)

 

 

Restenosis is a gradual re-narrowing of the stented segment that occurs mostly between 3 to 12 months after stent placement. 

So by not solving the inflammation problem you get this! Stents don't solve the underlying problem, why the fuck is your doctor prescribing them? Money?

Mediation Analysis of Acute Carotid Stenting in Tandem Lesions

Aaron Rodriguez Calienes, MD https://orcid.org/0000-0002-8413-6954, Milagros Galecio-Castillo, MD, Nils H. Petersen, MD, MSc https://orcid.org/0000-0001-9711-3340, Marc Ribo https://orcid.org/0000-0001-9242-043X, Mudassir Farooqui, MD, MPH https://orcid.org/0000-0003-3697-5697, Ameer E. Hassan, DO, Mouhammad A. Jumaa, MD https://orcid.org/0000-0002-7165-797X, … Show All … , and Santiago Ortega-Gutierrez, MD, MSc https://orcid.org/0000-0002-3408-1297Authors Info & Affiliations

August 13, 2024 issue

103 (3)

https://doi.org/10.1212/WNL.0000000000209617

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Abstract

Background and Objectives

Current evidence suggests that acute carotid artery stenting (CAS) for cervical lesions is associated with better functional outcomes in patients with acute stroke with tandem lesions (TLs) treated with endovascular therapy (EVT). However, the underlying causal pathophysiologic mechanism of this relationship compared with a non-CAS strategy remains unclear. We aimed to determine whether, and to what degree, reperfusion mediates the relationship between acute CAS and functional outcome in patients with TLs.

Methods

This subanalysis stems from a multicenter retrospective cohort study across 16 stroke centers from January 2015 to December 2020. Patients with anterior circulation TLs who underwent EVT were included. Successful reperfusion was defined as a modified Thrombolysis in Cerebral Infarction scale ≥2B by the local team at each participating center. Mediation analysis was conducted to examine the potential causal pathway in which the relationship between acute CAS and functional outcome (90-day modified Rankin Scale) is mediated by successful reperfusion.

Results

A total of 570 patients were included, with a median age (interquartile range) of 68 (59–76), among whom 180 (31.6%) were female. Among these patients, 354 (62.1%) underwent acute CAS and 244 (47.4%) had a favorable functional outcome. The remaining 216 (37.9%) patients were in the non-CAS group. The CAS group had significantly higher rates of successful reperfusion (91.2% vs 85.1%; p = 0.025) and favorable functional outcomes (52% vs 29%; p = 0.003) compared with the non-CAS group. Successful reperfusion was a strong predictor of functional outcome (adjusted common odds ratio [acOR] 4.88; 95% CI 2.91–8.17; p < 0.001). Successful reperfusion partially mediated the relationship between acute CAS and functional outcome, as acute CAS remained significantly associated with functional outcome after adjustment for successful reperfusion (acOR 1.89; 95% CI 1.27–2.83; p = 0.002). Successful reperfusion explained 25% (95% CI 3%–67%) of the relationship between acute CAS and functional outcome.

Discussion

In patients with TL undergoing EVT, successful reperfusion predicted favorable functional outcomes when CAS was performed compared with non-CAS. A considerable proportion (25%) of the treatment effect of acute CAS on functional outcome was found to be mediated by improvement of successful reperfusion rates.

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Relationship between in-stent restenosis following carotid artery stenting and platelet reactivity to clopidogrel

Stents were never the permanent solution, they do nothing to address the inflammation in your arteries that creates plaque. And why would you want to put inflexible stents in flexible arteries?  I still don't understand why you would medically need to stent a carotid artery at all if the Circle of Willis is complete. (Unless the whole point is revenue and profit generation) It would seem to make more sense to just close it up and prevent problems from there.  My right carotid artery was closed for 10 years and I cognitively functioned quite well with no episodes of fainting.

Here is why your doctor needs to guarantee NO complications from stenting!

• stenting (22 posts to May 2011)

• carotid stenting (21 posts to May 2016)

• carotid artery stenting (7 posts to November 2021)

 

 

Restenosis is a gradual re-narrowing of the stented segment that occurs mostly between 3 to 12 months after stent placement. 

So by not solving the inflammation problem you get this! Stents don't solve the underlying problem, why the fuck is your doctor prescribing them? Money?

 Relationship between in-stent restenosis following carotid artery stenting and platelet reactivity to clopidogrel

1. http://orcid.org/0000-0002-4474-1295Min-Yong Kwon1,
2. http://orcid.org/0000-0001-5508-7172Sang Hyo Lee2,
3. Yongjae Lee2,
4. Young Deok Kim2,
5. Si Un Lee2,
6. Jae Seung Bang2,
7. O-Ki Kwon2,3,
8. Chang Wan Oh2,3,
9. http://orcid.org/0000-0002-7774-0467Seung Pil Ban2,3

1. Correspondence to Dr Seung Pil Ban, Neurosurgery, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Korea (the Republic of); neurosurgeryban@gmail.com

Abstract

Objective To analyze the relationship between in-stent restenosis (ISR) following carotid artery stenting (CAS) and platelet clopidogrel reactivity confirmed by the P2Y12 reaction unit (PRU) and inhibition rate (IR).

Methods We retrospectively analyzed 171 patients who underwent CAS with extracranial carotid stenosis from January 2016 to December 2019. Dual antiplatelet therapy with 100 mg aspirin and 75 mg clopidogrel was started ≥5 days before CAS. Clopidogrel resistance was measured with the PRU and IR the day before CAS. The ISR degree was classified into R1, R2, and R3 (moderate to severe luminal stenosis of ≥50% or occlusion) by carotid CT angiography after 24–30 months. The degree of quantitative association between platelet reactivity and ISR R3 was determined by the receiver operating characteristic curve method. The optimal cut-off values of PRU and IR were derived using the maximum Youden index.

Results There were 33 R3 degrees of ISR (19.3%) and nine ipsilateral ischemic strokes (5.3%). The PRU and IR were different between R1+R2 degrees (176.4±50.1, 27.5±18.7%) and R3 degree (247.5±55.0, 10.3±13.4%) (P<0.001). The areas under the curves of PRU and IR were 0.841 and 0.781, and the optimal cut-off values were 220.0 and 14.5%, respectively. Multivariate logistic regression analysis showed that PRU ≥220 and IR ≤14.5% were significant predictive factors for ISR R3 (P<0.001 and P=0.017, respectively). ISR R3 was independently associated with ipsilateral ischemic stroke after CAS (P=0.012).

Conclusions High PRU (≥220) and low IR (≤14.5%) are related to ISR R3 following CAS, which may cause ipsilateral ischemic stroke.

Data availability statement

No data are available.

https://doi.org/10.1136/jnis-2024-021445

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Outcomes of Carotid Revascularization in the Treatment of Restenosis After Prior Carotid Endarterectomy

You doctor needs to give compelling exact reasons for that carotid endarterectomy. But I'm not medically trained so don't listen to me, your doctor is, what are her reasons?

This is why I would never consider a carotid endarterectomy as long as the Circle of Willis is complete.

Cognitive Dysfunction and Mortality After Carotid Endarterectomy

 

 Restenosis (“re” + “stenosis”) is when a part of the artery that was previously treated for blockage becomes narrow again.

This is the outcome if your doctor doesn't treat the reason for the arteries getting blocked, removing the symptom doesn't solve anything. 

The latest here:

Outcomes of Carotid Revascularization in the Treatment of Restenosis After Prior Carotid Endarterectomy

Nadin Elsayed

,

Ganesh Ramakrishnan

,

Isaac Naazie

,

Sharvil Sheth

,

Mahmoud B. Malas

Originally published20 Jul 2021https://doi.org/10.1161/STROKEAHA.120.033667Stroke. ;0:STROKEAHA.120.033667

Abstract

Background and Purpose:

Restenosis after carotid endarterectomy (CEA) is associated with an increased risk of ipsilateral stroke. The optimal procedural modality for this indication has yet to be determined. Here, we evaluate the in-hospital outcomes of transcarotid artery revascularization (TCAR), redo-CEA, and transfemoral carotid artery stenting (TFCAS) in a large contemporary cohort of patients who underwent treatment for restenosis after CEA.

Methods:

We performed a retrospective analysis of all patients in the vascular quality initiative database who underwent TCAR, redo-CEA, or TFCAS after ipsilateral CEA between September 2016 and April 2020. Patients with prior ipsilateral CAS were excluded from this analysis. In-hospital outcomes following TCAR versus CEA and TCAR versus TFCAS were evaluated using multivariate logistic regression analysis.

Results:

A total of 4425 patients were available for this analysis. There were 963 (21.8%) redo-CEA, 1786 (40.4%) TFCAS, and 1676 (37.9%) TCAR. TCAR was associated with lower odds of in-hospital stroke/death (odds ratio [OR], 0.41 [95% CI, 0.24–0.70], P=0.021), stroke (OR, 0.46 [95% CI, 0.23–0.93], P=0.03), myocardial infarction (MI; OR, 0.32 [95% CI, 0.14–0.73], P=0.007), stroke/transient ischemic attack (OR, 0.42 [95% CI, 0.24–0.74], P=0.002), and stroke/death/MI (OR, 0.41 [95% CI, 0.24–0.70], P=0.001) when compared with redo-CEA. There was no significant difference in the odds of death between the 2 groups (OR, 0.99 [95% CI, 0.28–3.5], P=0.995). TCAR was also associated with lower odds of stroke/transient ischemic attack (OR, 0.37 [95% CI, 0.18–0.74], P=0.005) when compared with TFCAS. There was no significant difference in the odds of stroke, death, MI, stroke/death, or stroke/death/MI between TCAR and TFCAS.

Conclusions:

TCAR was associated with significantly lower odds of in-hospital stroke, MI, stroke/transient ischemic attack, stroke/death, and stroke/death/MI when compared with redo-CEA and lower odds of in-hospital stroke/transient ischemic attack when compared with TFCAS. Additional long-term studies are warranted to establish the role of TCAR for the treatment of restenosis after CEA.

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Long-Term Risk Factors for Intracranial In-Stent Restenosis From a Multicenter Trial of Stenting for Symptomatic Intracranial Artery Stenosis Registry in China

 I'm sure there is something important here but beyond my pay grade of understanding.

Long-Term Risk Factors for Intracranial In-Stent Restenosis From a Multicenter Trial of Stenting for Symptomatic Intracranial Artery Stenosis Registry in China

Xu Guo^†, Ning Ma, Feng Gao, Da-Peng Mo, Gang Luo and Zhong-Rong Miao^*

• Department of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

Background: For patients with symptomatic intracranial artery stenosis (sICAS), endovascular treatment has been shown to be feasible and safe in recent studies. However, in-stent restenosis (ISR) risks the recurrence of ischemic stroke. We attempt to elucidate the risk factors for ISR.

Methods: We retrospectively analyzed 97 patients with sICAS from a prospective registry trial that included 20 centers from September 2013 to January 2015. Cases were classified into the ISR≥ 50% group or the ISR < 50% group. The baseline characteristics and long-term follow-up were compared between the two groups. Binary logistic regression analyses were identified as an association between ISR and endovascular technique factors.

Results: According to whether ISR was detected by CT angiography, 97 patients were divided into the ISR group (n = 24) and the non-ISR group (n = 73). The admission baseline features and lesion angiography characteristics were similar, while plasma hs-CRP (mg/L) was higher in the ISR≥ 50% group at admission (8.2 ± 11.4 vs. 2.8 ± 4.1, p = 0.032). Binary logistic regression analysis identified the longer stents (adjusted OR 0.816, 95% CI 0.699–0.953; p = 0.010), balloon-mounted stents (adjusted OR 5.748, 95% CI 1.533–21.546; p = 0.009), and local anesthesia (adjusted OR 6.000, 95% CI 1.693–21.262; p = 0.006) as predictors of ISR at the 1-year follow-up.

Conclusions: The longer stents, balloon-mounted stents implanted in the intracranial vertebral or basilar artery, and local anesthesia were significantly associated with in-stent restenosis. Further studies are required to identify accurate biomarkers or image markers associated with ISR in ICAS patients.

Clinical Trial Registration: www.ClinicalTrials.gov, identifier: NCT01968122.

Introduction

The prevalence of intracranial atherosclerotic stenosis (ICAS) in Chinese patients was up to 46.6% in symptomatic ischemic stroke patients (1). Symptomatic ICAS (sICAS) is associated with recurrent ischemic stroke (2). SAMMPRIS and VISSIT trials have shown that aggressive medical management has been more effective and safer than endovascular therapy in the past decade (3, 4). However, a recent Wingspan Stent System Post Market Surveillance Study (WEAVE) indicated that the perioperative complication rate is quite low for on-label patients (2.6%). Patients enrolled in this study, including patients with symptomatic and severe ICAS lesions, had suffered at least two ischemic strokes (5). It is obvious that patients with sICAS who failed the best medical treatment would benefit from endovascular therapy.

As we reported, the 30-days rate of primary endpoints, including stroke, transient ischemic attack, and death, was 4.3% in a multicenter prospective registry study of stenting for sICAS in China (6). The incidence of the composite endpoint in this study at 1 year was 8.1%, and restenosis ≥50% was found in 27.6% of patients at the 12-months follow-up. Although the majority of patients (78.9%) were asymptomatic (7), restenosis would be a risk factor for ischemic stroke, causing acute large vessel occlusion or transient ischemic attack (TIA) (2). Therefore, in the present study, according to the inflammatory index (hs-CRP), features of the lesion in angiography, and characteristics of the stent in the operation procedure, we aimed to identify risk factors for in-stent restenosis of endovascular treatment in intracranial atherosclerotic stenosis in a 12-months follow-up.

More at link.

 

Cilostazol Helps Prevent Carotid In-Stent Restenosis

I would think this whole problem could be eliminated by:

1. Determining if the Circle of Willis is complete.

2. If yes, then close the artery off to prevent ANY POSSIBILITY of clots breaking off and traveling to the brain.

3. This prevents stent placement complications per European Society of Cardiology

A - Minor complications

• Carotid artery spasm
• Sustained hypotension / bradycardia
• Carotid artery dissection
• Contrast encephalopathy (very rare)
• Minor embolic neurological events (TIAs)

B - Major complications

• Major embolic stroke
• Intracranial hemorrhage
• Hyperperfusion syndrome
• Carotid perforation (very rare)
• Acute stent thrombosis (very rare)
• Complications at the site of the vascular access

Don't listen to me, I'm not medically trained and I don't have a Dr. in front of my name.  But pepper your doctor with lots of questions, including GUARANTEEING NO PROBLEMS. Why would you want to place an inflexible stent in a flexible artery? Hell, my right carotid artery was 80% blocked at time of stroke which my doctors never found so luckily they didn't try to stent me. It eventually completely closed on its own with absolutely no cognitive problems encountered.

 

Cilostazol Helps Prevent Carotid In-Stent Restenosis

By Alex Morrisson

LOS ANGELES -- February 25, 2020 -- Patients undergoing carotid artery stenting to prevent recurrence of stroke who receive cilostazol tend to have a lower incidence of in-stent restenosis after 2 years, according to a study presented here at the 2020 International Stroke Conference (ISC).

In the Carotid Artery Stenting with Cilostazol Addition for Restenosis (CAS-CARE) study, Hiroshi Yamagami, MD, Osaka National Hospital, Osaka, Japan, and colleagues analysed 631 patients aged 45 to 80 years with symptomatic (≥50%) or asymptomatic (≥80%) carotid artery stenosis who were scheduled for carotid artery stenting within 30 days of enrolment. The patients were randomised 1:1 to receive cilostazol (50 mg or 100 mg twice daily) or any antiplatelet agents other than cilostazol, from 3 days before carotid artery stenosis and continued for 2 years.

The study found that in-stent restenosis occurred in 10.8% of patients receiving cilostazol and in 19.6% of patients who did not receive cilostazol -- a 36% reduction in the risk of in-stent restenosis that approached statistical significance (P = .056).

In secondary endpoints, occurrences of cardiovascular events or death from any cause and bleeding events were similar between the groups (5.8% vs 6.2% and 1.1% vs 0.3%, respectively).

Dr. Yamagami suggested that the study may have failed to reach significance because the trial recruited just 79% of its planned enrolment.

“This is the first trial to show potential effectiveness of medical management for the prevention of in-stent restenosis after carotid artery stenting,” he concluded.

ISC is sponsored by the American Heart Association and the American Stroke Association.

[Presentation title: Cilostazol Versus Other Antiplatelet Drugs for the In-Stent Restenosis After Carotid Artery Stenting: The Carotid Artery Stenting With Cilostazol Addition for Restenosis (CAS-CARE) Trial. Abstract LB21]

Stent, then angioplasty, could increase the risk of stroke, suggests CREST analysis

I'm putting this out there for two reasons.
1. Letting you know about risks your doctor should be telling you about.
2. highlighted text about why carotid arteries are cleaned.
http://www.theheart.org/article/1538115.do?utm_medium=email&utm_source=20130513_heartwire&utm_campaign=newsletter
Performing balloon angioplasty following the deployment of a carotid stent reduces the risk of restenosis but also appears to increase the risk of stroke, according to an analysis of the Carotid Revascularization Endarterectomy Versus Stenting Trial (CREST) [1].

The analysis, presented at the Society for Cardiovascular Angiography and Intervention (SCAI) 2013 Scientific Sessions, showed that poststent angioplasty reduced the risk of restenosis by 64% but was associated with a nearly fourfold increased risk of periprocedural stroke (hazard ratio 3.7; 95% CI 0.5-27.9).

Speaking with the media, lead investigator Dr Mahmoud Malas (Johns Hopkins University, Baltimore, MD) noted that the 30-day stroke risk following carotid stenting in CREST, at 4.1%, was the lowest reported in all the clinical trials to date, with a stroke rate approximately half that observed in the European trials. Still, there are aspects of the procedure, including technical aspects, which might help reduce the risk of stroke further.

Do you believe the p value or the clinical outcomes?

"A lot of interventionalists like to balloon after stenting, and I always thought that might increase the risk of showering emboli to the brain and increase the risk of stroke," said Malas. "We went back to the CREST data to see the effects [of balloon angioplasty after stenting] on the risk of stroke and restenosis. We found that there was a difference in the risk of stroke. It was not statistically significant, but there was a lot more stroke in the group that had the stent ballooned after it was deployed compared with the group that only had the balloon prior to stenting."

19 strokes vs one stroke in the two arms

The CREST study compared carotid artery stenting and carotid endartectomy for stroke prevention in patients with both asymptomatic and symptomatic extracranial carotid stenosis. The primary end point was a composite, including any clinical stroke, MI, or death during the periprocedural period, plus ipsilateral stroke on the vessel that was treated, with patients followed up to four years. No significant difference between the two treatment groups was seen on the primary end point, and Kaplan-Meier curves confirmed most events were periprocedural.

Led by Malas, the researchers retrospectively analyzed the data on patients who received a carotid stent in CREST and compared the risk of stroke and two-year restenosis rates in patients who received only balloon angioplasty before the procedure vs those who received poststent-deployment angioplasty. In total, 69 patients underwent predilation angioplasty, 344 underwent poststent-deployment angioplasty, and 687 received both pre- and poststent angioplasty.

There were 20 periprocedural strokes, including 19 among patients who underwent poststent deployment angioplasty and one patient who received balloon angioplasty before the stent (5.5% vs 1.5%, respectively; p=0.26). Two-year rates of restenosis were 10.3% in the group who received prestent balloon angioplasty and 3.7% in the group treated with balloon angioplasty following stenting, a difference that was statistically significant (p=0.02).

Stroke vs restenosis: The tradeoff

Despite the reduction in restenosis, Malas said the improvement is not a clinically meaningful measurement, because most cases are asymptomatic, and physicians do not necessarily need to intervene if it occurs. In contrast to the coronary arteries, where restenosis is a major issue because of blood flow to the heart muscle, the carotid artery is a "very different animal."

"When we're trying to fix the carotid artery, we're not really trying to improve blood flow to the brain," said Malas. "That's a very common misunderstanding. The idea is that when you have this atherosclerotic lesion, it can break off and cause a stroke. The whole idea with carotid endartectomy is to remove the plaque, and the amazing thing is that stents work because even though you're not removing the plaque, you're just pushing the plaque against the wall of the artery, you get this nice intimal hyperplasia."

Currently, there are no guidelines to direct physicians with regard to postdilation following stent deployment. There is a tendency among interventionalists to position the stent as perfectly as possible, and for this reason angioplasty is frequently employed after the procedure. However, this study questions whether that extra risk is needed, said Malas. Although the study was not powered to detected differences between the pre- and poststent angioplasty groups, and despite the lack of statistical significance, Malas said clinicians should be aware of the potential stroke risks if they elect to perform angioplasty after the stent is placed.

"It becomes a judgment call on the part of the interventionalist doing the procedure," said Malas. "Do you believe the p value or the clinical outcomes? To me, I don't want the patient to have a stroke. I'd rather have restenosis."