Coronary artery calcium prevalence did not differ between cancer patients and non-cancer controls, but cancer patients had modestly higher CAC severity (Cohen’s d = 0.29).
Does a history of cancer increase the prevalence and severity of coronary artery calcium in adult patients compared to non-cancer controls?
Despite higher cardiovascular risk in cancer survivors, coronary artery calcium prevalence is not significantly increased compared to non-cancer controls, suggesting their elevated risk may be driven by non-calcified plaque, plaque vulnerability, or other mechanisms.
Absolute Event Rate: 0% vs 0%
Coronary artery disease (CAD) events contribute to morbidity in cancer survivors, yet it is unclear whether this reflects increased atherosclerotic burden. Coronary artery calcium (CAC) scoring is a sensitive, non-invasive marker of atherosclerotic burden. This review aims to establish differences in the prevalence and severity of CAC between cancer survivors and non-cancer controls. MEDLINE, EMBASE, and Cochrane databases were searched from inception to January 2025 for studies comparing CAC between adult cancer patients and matched non-cancer controls. The primary outcome was CAC presence (Agatston score > 0) and the secondary outcome was CAC score. We recorded differences in demographic and cardiovascular risk profiles between cancer patients and controls. Random-effects meta-analysis was used to estimate pooled risk differences and Cohen’s d. Twelve studies (2,182 cancer patients mean age 59.8 years, 49% female; 16,524 controls mean age 58.7 years, 54% female) were included. Cancer patients and controls had overall comparable cardiovascular risk profiles. Cancer patients were older, more often male, and had more dyslipidaemia but less hypertension and diabetes. CAC prevalence did not differ between groups (risk difference 0.05; 95% CI: − 0.03 to 0.12; p = 0.22). A secondary analysis found modestly higher CAC severity in cancer patients (Cohen’s d = 0.29; 95% CI: 0.01 to 0.57; p = 0.04), though between-study heterogeneity was high. Female sex was a potential contributor to this increase. There was no significant difference in CAC prevalence between cancer survivors and non-cancer controls. Further research could clarify whether the CAD mortality in this population reflects plaque vulnerability, thrombotic risk or other causes.
Wang et al. (Wed,) reported a other. Coronary artery calcium prevalence did not differ between cancer patients and non-cancer controls, but cancer patients had modestly higher CAC severity (Cohen’s d = 0.29).