Carotid atherosclerotic plaque instability and cognition determined by ultrasound-measured plaque strain in asymptomatic patients with significant stenosis

Abstract

OBJECTIVE This article describes the use of ultrasound measurements of physical strain within carotid atherosclerotic plaques as a measure of instability and the potential for vascular cognitive decline, microemboli, and white matter changes. METHODS Asymptomatic patients with significant (> 60%) carotid artery stenosis were studied for dynamic measures of plaque instability, presence of microemboli, white matter changes, and vascular cognitive decline in comparison with normative controls and premorbid state. RESULTS Although classically asymptomatic, these patients showed vascular cognitive decline. The degree of strain instability measured within the atherosclerotic plaque directly predicted vascular cognitive decline in these patients thought previously to be asymptomatic according to classic criteria. Furthermore, 26% of patients showed microemboli, and patients had twice as much white matter hyperintensity as controls. CONCLUSIONS These data show that physical measures of plaque instability are possible through interpretation of ultrasound strain data during pulsation, which may be more clinically relevant than solely measuring degree of stenosis. The data also highlight the importance of understanding that the definition of symptoms should not be limited to motor, speech, and vision function but underscore the role of vascular cognitive decline in the pathophysiology of carotid atherosclerotic disease. Clinical trial registration no.: NCT02476396 (clinicaltrials.gov).

Keywords: CA = carotid artery; CAS = CA stenosis; HITS = high-intensity transient signal; MCA = middle cerebral artery; TCD = transcranial Doppler; TIA = transient ischemic attack; WMH = white matter hyperintensity; carotid atherosclerosis; plaque instability; stroke; ultrasound; ultrasound strain; vascular cognitive decline; vascular disorders.

Figure 1

B-mode image and segmented plaque with adventitia, showing strain line with pulsation.

Figure 2

Strain images superimposed on ultrasound B-mode images for an asymptomatic patient with higher values of the accumulated strain. A plot of the accumulated strain over two cardiac cycles is shown on the right.

Figure 3

Strain images superimposed on ultrasound B-mode images for an asymptomatic patient with lower values of the accumulated strain. A plot of the accumulated strain over two cardiac cycles is shown on the right.

Figure 4

Decline in Trails B Executive Function correlated with increase in maximal plaque p= 0.002

Figure 5

White Matter Hyperintensities in an asymptomatic patient (left side) and WMH lesion volume in asymptomatic plaque subjects (n=13) (right side). Mean WMH TLV in the N=64 control group = 25.30639 ml (mean age: 69.06 ± 4.52 years). Mean WMH TLV in the N=13 ASX plaque subjects = 54.64323 ml (mean age: 69.62 ± 6.79 years). Independent two-tailed t-test for WMH TLV:p value = 0.006 --- ASX plaque group has statistically greater WMH TLV than the ADRC control group.

Figure 6

Figure 6 demonstrates the Doppler signal from the RT MCA with the HIT identified by the yellow arrow. This HIT was also accompanied by an audible chirp, a change in complex, and was less than 300 ms in duration.