Vikas Pandey, MD

Toutouzas K, Benetos G, Drakopoulou M, Deligianni C, Spengos K, Stefanadis C, et al. Incremental Predictive Value of Carotid Inflammation in Acute Ischemic Stroke. Stroke. 2014

Carotid artery disease is a major risk factor for ischemic strokes and one that is important to discover during a patient’s stroke workup due to the striking benefit of treating symptomatic carotid disease. Current imaging modalities however, are limited to either measurement of blood velocities to determine hemodynamic significance (ultrasound) or anatomical structure based imaging (MRA or CTA). The group out of Greece felt that a different dimension would be added to qualifying a carotid plaque if it were possible to measure some indicator of carotid inflammation. They decided to use microwave radiometry (MWR) to non-invasively assess the internal temperature of carotid artery plaques (as an indicator of plaque inflammation) and wondered if there was a difference in those temperature measurements in patients who had ischemic strokes due to extracranial carotid disease and bilateral carotid plaques. 

The group collected patients with anterior circulation strokes in whom the isolated cause of their stroke was determined to be carotid disease with bilateral carotid plaques present on ultrasound. Patients with atrial fibrillation were excluded. These patients underwent MWR of bilateral carotid arteries within the first 24 hours of their admission. Patients would undergo a second brain imaging study (usually MRI) to rule out lacunar infarctions and TIAs, and also excluded patients found to have alternative causes of stroke. A total of 50 patients were analyzed in the study. MWR measurements were performed on culprit (side of the stroke) and nonculprit carotid arteries at target segments of the carotid artery (segment of each carotid artery with the highest plaque thickness). The temperature difference was defined as the temperature of the target segment minus the minimal temperature of each carotid.

The culprit arteries had thicker plaque segments compared to nonculprit sides (3.76 vs 2.53 mm, p <0.001), and this difference was also present after adjustment for sex, age, vascular risk factors and temperature difference values. Culprit carotid arteries had a higher temperature difference values compared to asymptomatic carotid arteries (0.93 vs 0.58 degress C, p<0.001). This would signify more plaque inflammation in culprit carotid arteries. The study provides key information regarding qualities of the culprit carotid artery in reference to plaque inflammation, a dimension currently unable to be measured reliably. This measurement may also have promise in determining the vulnerability of rupture of asymptomatic plaques. The group offers a great noninvasive technique that is a feasible additive to the information stroke neurologists obtain during a stroke workup, and a tool for use in stroke prevention.