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CEA with SCSO increases death risk and decreases ipsilateral, stroke risk

Key findings

  • Results of the study showed few differences across groups in regards to cardiovascular risk factors, yet multivariable logistic regression modeling determined severe contralateral stenosis or occlusion (SCSO) to be independently predicting of 30-day stroke, except for ipsilateral
  • Survival after CEA was worse in patients with SCSO than those without it. 91.5% of those with SCSO had survived at one-year after CEA versus 95.2% of those without SCSO
  • Being male and taking lipid therapy were considered protective of late mortality after CEA, yet, at 30 days after CEA, being male was an independent predictor of any stroke, ipsilateral stroke, and any stroke that led to death
  • Repeat CEA and history of diabetes were predictors of 30-day any stroke, including ipsilateral, and current smoking status was the only predictor of 30-day death after CEA

A team from Mass General’s Fireman Vascular Center set out to formally evaluate patients with severe (>70%) contralateral carotid stenosis or occlusion (SCSO) after carotid endarterectomy (CEA) and their outcomes, which are known to be varied. Among their findings published in the Journal of Vascular Surgery was that SCSO is not an independent risk factor of ipsilateral stroke after CEA, although it is for other forms of stroke, early myocardial infarction and, even, death.

From January 1989 through December 2005, outcomes of 2209 patients after CEA who had a patent artery or mild (<50%) and moderate (50-70%) contralateral carotid artery stenosis were compared to 736 of those with SCSO (70-99%).

Retrospectively, researchers evaluated perioperative outcomes data of 1,843 CEA patients. 60% were male. After first stratifying patients into groups based on the presence of SCSO, the team, using univariate and multivariate methods, analyzed outcomes post-CEA. Primary end points were 30-day and long-term ipsilateral stroke, as well as death and ipsilateral stroke that led to death. The secondary end point was any stroke leading to death.

Four to six weeks post-procedure, carotid noninvasive studies were performed. Also, the treating surgeon examined patients neurologically at 1-month, 6-month, and 1-year points.

Few differences were seen across groups in regards to cardiovascular risk factors. However, differences arose in other factors. 38.4% of patients with SCSO had primary closure compared to 26.9% of those without SCSO. 30.5% of those with SCSO versus 16.7% of those without it had a positive intraoperative EEG change, and 40.3% versus 28.1% had an intraoperative shunt placement.

While ipsilateral stroke rates for the two groups were relatively similar (1.5% vs 1.2%), they differed significantly on other measures including:

  • 2.8% of SCSO had higher rates of any stroke versus 1.5% of those without SCSO
  • 2.2% died compared to 1.1%
  • 4.3% had any stroke that led to death compared to 2.4%
  • 3.5% had perioperative myocardial infarction versus 1.7%
  • 4.9% had a surgical re-exploration versus 1.0%
  • 7.3% were re-admitted to a hospital compared to 3.4%

Multivariable logistic regression modeling determined SCSO to be independently predicting of 30-day stroke, except for ipsilateral.

Survival after CEA was worse in patients with SCSO than those without it, with more prominent differences over time. 91.5% of those with SCSO were alive at one-year post-CEA compared to 95.2% of patients without it. 63.9% of patients with SCSO were alive after five years following CEA compared to 34.1% of those without it, and 71.5% of those with SCSO were alive after five years following CEA compared to 43.5% of those without it at 10 years out.

Long-term survival rates in the SCSO group were only mitigated against if patients were male or on lipid therapy. Also, SCSO patients fared worse, long-term, if they had any symptoms before CEA, such as smoking, or had any symptoms associated with coronary artery disease, chronic obstructive pulmonary disease and diabetes mellitus, or prior neck irradiation.

A complex trend also emerged—across groups, male patients taking lipid therapy were considered protective of late mortality after CEA. Yet, shorter-term, at 30 days after CEA, being male was an independent predictor of any stroke, ipsilateral stroke and any stroke that led to death.

Another interesting finding was that having a repeat CEA and history of diabetes were predictors of 30-day any stroke, including ipsilateral, and that current smoking status was the only predictor of 30-day death after CEA.

In summary, even though the review showed significantly higher rates of intraoperative EEG changes and shunt placement in patients with SCSO than those without it, even more aggressive life-extending measures need to be taken after CEA to keep SCSO patients alive longer.

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