Progression of arterial calcifications: what, where, and in whom?

Objectives There is a lack of information on the development of arteriosclerosis over time. This study aims to assess long-term sex-specific changes in arterial calcifications in five arteries, and the influence of cardiovascular risk factors hereon. Methods From a population-based cohort, 807 participants (mean baseline age, 65.8; SD, 4.2) underwent a non-contrast computed tomography (CT) examination between 2003 and 2006, and after a median follow-up of 14 years. We assessed incidences and changes in volumes of coronary artery calcification (CAC), aortic arch calcification (AAC), extracranial (ECAC) and intracranial carotid artery calcification (ICAC), and vertebrobasilar artery calcification (VBAC). We investigated the simultaneous presence of severe progression (upper quartile of percentual change volumes). Associations of cardiovascular risk factors with changes in calcification volumes were assessed using multivariate linear regression models. Results The difference in AAC was most substantial; the median volume (mm3) increased from of 129 to 916 in men and from 93 to 839 in women. For VBAC, no change in volumes was observed though more than a quarter of participants without baseline VBAC developed VBAC during follow-up. Severe progression was most often observed in only one artery at the same time. Hypertension was most consistently associated with increase in calcifications. Associations of diabetes, hypercholesterolemia, and smoking with changes in calcifications varied across arteries and sex. Conclusions We found a considerable incidence and increase in volumes of calcifications in different arteries, over a 14-year time interval. Cardiovascular risk factors were associated with increase of calcifications with sex-specific differential effects across arteries. Clinical relevance statement There is a considerable incidence and increase in volumes of calcifications in different arteries, over a 14-year time interval. Cardiovascular risk factors are associated with increase of calcifications with sex-specific differential effects across arteries; thus, assessing changes in only one artery may thus not provide a good reflection of the systemic development of arteriosclerosis. Key Points • Assessing change in arterial calcification in only one artery does not reflect the systemic development of arterial calcification. • Cardiovascular risk factors are associated with progression of arterial calcifications. • Progression of arterial calcification is sex and artery-specific. Graphical Abstract Supplementary Information The online version contains supplementary material available at 10.1007/s00330-023-10566-7.


Scan protocol
At baseline, non-contrast CT images were obtained using 16-slice or 64-slice (z-flying focal spot (z-FFS)) MDCT scanners (SOMATOM Sensation 16 or 64; Siemens).Two scans were performed: a cardiac and a carotid scan.The cardiac scan covered the apex of the heart to the tracheal bifurcation.The carotid scan ranged from the aortic root to the Circle of Willis (1cm above the sella turcica).With the 16-slice scanner, cardiac images were obtained within a single breath-hold, with the following parameters: 12 mm × 1.5 mm collimation, 120 kVp, effective 30 mAs, prospective ECG triggering at 50% of the cardiac cycle.The scan parameters of the carotid scan were: 16 × 0.75 mm collimation, 120 kVp, 100 effective mAs, 0.5 s rotation time and normalized pitch of 1.For the 64-slice scanner, parameters were similar, except for collimation and effective mAs.The collimation was 32 × 0.6 mm and the mAs value was real time adapted to body weight (CARE Dose 4D, Siemens).
During the follow-up examination, non-contrast CT images were obtained using a 128-slice (z-FFS) dual source CT (DSCT) scanner (SOMATOM Drive, Siemens).Similar to the baseline examination, a cardiac and carotid scan were performed.Within a single breath-hold cardiac images were acquired with 64 mm × 0.6 mm collimation, 120 kVp, and effective 80 mAs (CARE Dose4D).The scan parameters of the carotid scan were: 64 × 0.6 mm collimation, 120 kVp, 50 effective mAs (CARE Dose4D), 0.5 s rotation time and normalized pitch of 0.8.
At baseline and follow-up, the matrix size was 512-by-512, and acquired images were reconstructed with an optimized field-of-view of 180 and 120 for the cardiac and carotid scans, respectively, slice thickness of 3.0 and 1.0 mm, and an increment of 1,5 and 0.5 mm using a medium non-iterative convolution kernel (B35f).On both baseline and follow-up scans, calcifications were assessed in the coronary arteries, aortic arch, extracranial, and intracranial carotid arteries, and the vertebrobasilar arteries.Coronary artery calcification (CAC), aortic arch calcification (AAC), and extracranial carotid artery calcification (ECAC) were quantified (in mm 3 ) using dedicated software (Syngo Calcium Scoring; Siemens).Intracranial carotid artery calcification (ICAC) and vertebrobasilar artery calcification (VBAC) were quantified using a semiautomatic scoring method that allows to manually segment calcification in each consecutive CT-slice after which the calcification volume is computed using the pixel size and the increment

Figures-
Figures -Fig I. Flowchart of the study population

Fig
Fig I. Flowchart of the study population

Fig. II .
Fig. II.Combinations of relative severe progression of calcification in different arteries

Fig. III .
Fig. III.Association between cardiovascular risk factors and cube root transformed absolute change in arterial calcification volumes

Fig. IV .
Fig. IV.Association between cardiovascular risk factors and cube root transformed relative change in arterial calcification volumes