Complicated and delicate role of carotid intima-media thickness in cardiovascular risk assessment in patients with type 1 diabetes
CC BY 4.0
Complicated and delicate role of carotid intima-media thickness in cardiovascular risk assessment in patients with type 1 diabetes
CC BY 4.0
To the editor
In the April issue of Polish Archives of Internal Medicine, Naskręt et al1 published a study titled “How to improve cardiovascular risk assessment in type 1 diabetes: the role of vascular age and arterial stiffness.”1 The authors analyzed vascular age (VA) and arterial stiffness (AS) as potential markers for improving cardiovascular risk (CVR) assessment in individuals with type 1 diabetes mellitus (T1DM). Included were 109 patients with T1DM at a median (interquartile range [IQR]) age of 32.4 (25.5–38.6) years, with at least 5 years of disease duration. None had been diagnosed with cardiovascular disease or hypertension.1 VA was calculated using carotid intima‑media thickness (cIMT), an ultrasound surrogate marker for preclinical atherosclerosis. The authors stated that “Using VA in the modified steno type 1 risk engine (ST1RE) score, we reclassified 32.1% of the participants into a higher CVR category. The median (IQR) CVR for the modified ST1RE was 9.68% (4.61%–20.08%), as compared with 4.74% (3.24%–8.12%) using the standard score. The modified ST1RE score was positively associated with pulse wave velocity (odds ratio, 2.37; 95% CI, 1.46–3.84; P = 0.004) after adjustment for sex, body mass index, and at least 1 diabetic complication.”1 The study concluded that VA and AS could enhance risk assessment in T1DM individuals, especially in high‑risk populations.1 Some comments are needed to evaluate the results of this study in a more balanced way.
Left vs right carotid intima‑media thickness
The cIMT was measured solely at the right common carotid artery (CCA).1 The authors stated that the measurements were based on the Mannheim carotid intima‑media thickness and plaque consensus paper (henceforth referred to as the Mannheim consensus paper).2 However, the Mannheim consensus paper recommends averaging the right and left cIMT values, although the left cIMT values are almost always significantly higher.2 Performing measurements only at 1 side potentially will not capture the whole atherosclerotic burden, consequently providing an inaccurate cIMT.
Carotid intima‑media thickness measurement location
As stated above, Naskręt et al1 measured the cIMT solely at 1 location, that is, the far wall of the CCA. Given that atherosclerosis has an asymmetric presentation, a more extensive interrogation of the CA tree including several sections (eg, the far / near walls of the CCA, bifurcation, and the internal CA) may reflect the actual atherosclerotic vessel state more accurately than a single measurement made in a predetermined vessel section.3 As stated by Johnsen and Mathiesen, “Although IMT and plaques are highly intercorrelated, IMT’s role as a marker of atherosclerosis has been questioned, especially when measurements include the CCA only.”4
Cardiac synchronization
International guidelines recommend to measure cIMT at the end‑diastolic phase.2 Although Naskręt et al1 claimed they performed the measurements according to the Mannheim consensus paper,2 they later wrote that “In arteries, longitudinal projection images were captured at 16 frames per second for 5 seconds.” That statement is unclear and needs specification. Which images were subsequently selected? If the sole criterion was image quality, and given that the duration of the whole cardiac cycle is circa 0.8 seconds (by normocardia), it appears that Naskręt et al1 did not synchronize the measurement with the cardiac cycle. Previously reported mean differences in cIMT between the 2 cardiac phases were 0.041 mm.5 Consequently, in the present study,1 measurements appear to have been made in both cardiac phases, rendering the cIMT measures, both for a single patient and between the patients, incomparable.
Conclusions
cIMT measurement is a noninvasive, fast, and inexpensive procedure; however, as a surrogate marker, cIMT has noteworthy disadvantages. Measurements need to be performed by a highly trained sonographer who understands not only the complexity of the highly variable interindividual course of the CA but also the issue of an asymmetric presentation of atherosclerosis.3 The most delicate matter, however, remains that cIMT is expressed at a submillimeter level (eg, the normal range is <0.6–0.9 mm). Consequently, even the smallest inaccuracies (within the same submillimeter range) resulting from the applied measurement technique or a suboptimal measurement protocol (eg, single‑location measurement, no cardiac synchronization) may suffice to misclassify patients into different cIMT categories. Given these multiple methodological issues, the cIMT results and related conclusions of the study by Naskręt et al1 should be analyzed within the abovementioned limitations.
- Naskręt D, Kulecki M, Kamiński M, et al. How to improve cardiovascular risk assessment in type 1 diabetes: the role of vascular age and arterial stiffness. Pol Arch Intern Med. 2025; 135: 16956. | Crossref
- Touboul P‑J, Hennerici MG, Meairs S, et al. Mannheim carotid intima‑media thickness and plaque consensus (2004‑2006‑2011). An update on behalf of the advisory board of the 3rd, 4th and 5th watching the risk symposia, at the 13th, 15th and 20th European Stroke Conferences, Mannheim, Germany, 2004, Brussels, Belgium, 2006, and Hamburg, Germany, 2011. Cerebrovasc Dis. 2012; 34: 290‑296. | Crossref
- Tajik P, Meijer R, Duivenvoorden R, et al. Asymmetrical distribution of atherosclerosis in the carotid artery: identical patterns across age, race, and gender. Eur J Prev Cardiol. 2012; 19: 687‑697. | Crossref
- Johnsen SH, Mathiesen EB. Carotid plaque compared with intima‑media thickness as a predictor of coronary and cerebrovascular disease. Curr Cardiol Rep. 2009; 11: 21‑27.
- Polak JF, Johnson C, Harrington A, et al. Changes in carotid intima‑media thickness during the cardiac cycle: the multi‑ethnic study of atherosclerosis. J Am Heart Assoc. 2012; 1: e001420. | Crossref
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