Review article
Systematic review on the association between calcification in carotid plaques and clinical ischemic symptoms

https://doi.org/10.1016/j.jvs.2009.08.072Get rights and content
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Objective

The association between carotid plaque calcification and clinical ischemic events is unclear. The aim of this study was to systematically review published studies comparing degree of calcification between clinically symptomatic and asymptomatic plaques.

Methods

A systematic search for relevant studies was performed in the PubMed/MEDLINE and Embase databases. For studies reporting a rating scale or a continuous measure of calcification, study-specific and pooled standardized mean differences (SMDs) between symptomatic and asymptomatic plaques were calculated. For studies reporting a dichotomous measure, study-specific and pooled odds ratios (ORs) were calculated. If no significant heterogeneity was present (I2 ≤50%), a fixed-effects pooling model was used. If significant heterogeneity was present (I2 >50%), a random-effects pooling model was used, and sources of heterogeneity were explored by subgroup analyses.

Results

The 24 studies included in this systematic review used a wide range of methodologies to quantify degree of calcification and a wide range of definitions to define clinically symptomatic and asymptomatic carotid plaques. Pooled fixed-effects SMD of calcification volume or weight between symptomatic and asymptomatic plaques was −0.425 (95% confidence interval [CI], −0.608 to −0.241); I2 = 39.3%. Pooled random-effects SMD of calcification percentage was −0.997 (95% CI, −1.793 to −0.200); I2 = 93.8. Subgroup analyses did not reveal homogeneous subgroups. Pooled fixed-effects OR for the association between high degree of plaque calcification and symptoms was 0.696 (95% CI, 0.528 to 0.918); I2 = 21.1%.

Conclusion

The results of this systematic review suggest that clinically symptomatic plaques have a lower degree of calcification than asymptomatic plaques. Assessment of degree of carotid plaque calcification may be useful to predict which plaques will cause cerebrovascular ischemic events.

Cited by (0)

This study was supported by Dutch Heart Foundation grant 2006B061.

Competition of interest: none.

The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a competition of interest.