Breast Arterial Calcium: A Game Changer in Women's Cardiovascular Health?

In 2018, cardiovascular disease (CVD) was the leading cause of death among women, and current CVD prevention paradigms may not be sufficient in this group. In that context, it has recently been proposed that detection of calcification in breast arteries may help improve CVD risk screening and assessment in apparently healthy women. This review provides an overview of breast arterial anatomy; and the epidemiology, pathophysiology, and measurement of breast artery calcium (BAC); and discusses the features of the BAC-CVD link. The potential clinical applications that BAC may offer for CVD prevention in the context of current clinical practice guidelines and recommendations are also discussed. Finally, current gaps in evidence gaps are outlined, and future directions in the field are explored with a focus on the implementation of BAC mammography as a CVD risk-screening tool in routine clinical practice.

Improving the relationship between coronary artery calcium score and coronary plaque burden: addition of regional measures of coronary artery calcium distribution.

BACKGROUND: The Agatston coronary artery calcium (CAC) score predicts cardiovascular events through its association with overall burden of coronary atherosclerosis. It is unclear whether adding regional measures of CAC distribution to the Agatston score improves this association. METHODS: We studied 920 consecutive patients (mean age 57 ± 12, 53% female), referred for 64-slice Coronary CT angiography (CCTA) who had concomitant CAC scoring. Total atherosclerosis burden was quantified as the segment involvement score (SIS), which describes the number of coronary segments with plaque on CCTA. We studied the heterogeneity between CAC group (0, 1-100, 101-400, >400) and the number of vessels with CAC (0-4), and related this to SIS on CCTA. In patients with multi-vessel disease, we examined the relationship of concentrated vs. diffuse CAC (> or ≤75% total CAC in one vessel) with SIS. RESULTS: When CAC was intermediate (1-400), considerable heterogeneity was noted between CAC group and the number of vessels with CAC (CAC 1-100: 53% 1-vessel, 29% 2-vessel, 16% 3-vessel, 2% 4-vessel; CAC 101-400: 9% 1-vessel, 28% 2-vessel, 43% 3-vessel, 20% 4-vessel). Within each CAC group, increase in the number of vessels with CAC was significantly associated with increased SIS. In multi-vessel disease, a higher SIS was associated with diffuse versus concentrated CAC (CAC 1-100: 3.8 vs. 2.8, CAC 101-400: 5.5 vs. 4.3 [both p < 0.01]). These associations persisted after adjustment for age, gender, and the absolute Agatston CAC score (p < 0.01). CONCLUSION: Addition of measures of regional CAC distribution improves the association of the Agatston CAC score with total plaque burden.

All-cause mortality in asymptomatic persons with extensive Agatston scores above 1000.

BACKGROUND: Risk assessment in the extensive calcified plaque phenotype has been limited by small sample size. OBJECTIVE: We studied all-cause mortality rates among asymptomatic patients with markedly elevated Agatston scores > 1000. METHODS: We studied a clinical cohort of 44,052 asymptomatic patients referred for coronary calcium scans. Mean follow-up was 5.6 years (range, 1-13 years). All-cause mortality rates were calculated after stratifying by Agatston score (0, 1-1000, 1001-1500, 1500-2000, and >2000). A multivariable Cox regression model adjusting for self-reported traditional risk factors was created to assess the relative mortality hazard of Agatston scores 1001 to 1500, 1501 to 2000, and >2000. With the use of post-estimation modeling, we assessed for the presence of an upper threshold of risk with high Agatston scores. RESULTS: A total of 1593 patients (4% of total population) had Agatston score > 1000. There was a continuous graded decrease in estimated 10-year survival across increasing Agatston score, continuing when Agatston score > 1000 (Agatston score 1001-1500, 78%; Agatston score 1501-2000, 74%; Agatston score > 2000, 51%). After multivariable adjustment, Agatston scores 1001 to 1500, 1501 to 2000, and >2000 were associated with an 8.05-, 7.45-, and 13.26-fold greater mortality risk, respectively, than for Agatston score of 0. Compared with Agatston score 1001 to 1500, Agatston score 1501 to 2000 had a similar all-cause mortality risk, whereas Agatston score > 2000 had an increased relative risk (Agatston score 1501-2000: hazard ratio [HR], 1.01 [95% CI, 0.67-1.51]; Agatston score > 2000: HR, 1.79 [95% CI, 1.30-2.46]). Graphical assessment of the predicted survival model suggests no upper threshold for risk associated with calcified plaque in coronary arteries. CONCLUSION: Increasing calcified plaque in coronary arteries continues to predict a graded decrease in survival among patients with extensive Agatston score > 1000 with no apparent upper threshold.

Utility of coronary artery calcium scoring in the evaluation of patients with chest pain.

Although coronary artery calcium (CAC) scoring has an established role in risk-stratifying asymptomatic patients at intermediate risk of coronary heart disease (CHD), its utility in the evaluation of patients with chest pain is uncertain. We conducted a literature review of articles investigating the utility of: (1) CAC scoring in elective patients with indeterminate chest pain symptoms, (2) CAC as a "gatekeeper" in the triage of patients presenting to the emergency department (ED) with chest pain, and (3) the cost-effectiveness of the use of CAC scoring in the ED. We also evaluated the predictive accuracy of the absence of CAC in a pooled analysis of applicable studies. Only studies evaluating patients classified as low or intermediate risk were included. Low to intermediate risk was established by Framingham risk scores, Thrombolysis in Myocardial Infarction scores, Diamond-Forrester classification, or by the absence of typical angina symptoms, ischemic electrocardiogram, positive cardiac biomarkers, or a prior history of CHD. In our pooled analysis, the presence of any CAC resulted in a high sensitivity (range 70%-100%) for predicting the presence of obstructive coronary disease among symptomatic patients subsequently referred for coronary angiography. More importantly, a CAC score of 0 in low- and intermediate-risk ED populations with chest pain had a high negative predictive value (99.4%) for CHD events over an average follow-up of 21 months. CAC scoring also seems cost-effective in this population. Although further research is needed, carefully selected ED patients with a normal electrocardiogram, normal cardiac biomarkers, and CAC = 0 may be considered for early discharge without further testing.