Thoracic Aortic Calcification Research Articles

Vascular calcification and fibroblast growth factor in resistant hypertension

Background . Pathological vascular calcification in hypertension (HTN) is studied worldwide. The relationship between endothelial dysfunction (ED) and vascular wall calcification in HTN has been demonstrated, and an increase in the level of fibroblast growth factor (FGF23) is considered one of the contributing factors. The aim of the study was to assess the incidence and severity of thoracic aortic calcification, and its relationship with fibroblast growth factor and ED in patients with resistant HTN. Design and methods . Ninety-two patients with resistant HTN were included. All of them underwent: 24-hour blood pressure monitoring (ABPM), the assessment ofendothelial function, the thoracic aortic calcium (TAC) index using multispiral computed tomography, and the level of FGF23. Results . According to the results of ABPM, patients were divided into group 1 with controlled HTN (n = 44) and group 2 with uncontrolled (n = 48) resistant HTN. In the 2nd group, there was an increase in TAC and ED, in both groups, changes in the blood flow velocity were recorded. There were no significant differences in FGF23 levels between the groups. We found a positive relationship between TAC and pulse pressure according to the results of ABPM (r = 0,49, p = 0,007), HTN duration (r = 0,68, p = 0,04) and a negative relationship with the duration of regular antihypertensive therapy (r = –0,33, p = 0,02). In addition, participants with higher FGF23 levels were older (r = 0,663, p = 0,006) and had a longer history of HTN (r = 0,57, p = 0,03). Conclusions . In patients with resistant HTN, ED and calcification of the thoracic aorta are more pronounced when the target blood pressure level is not achieved. The level of FGF23 is associated with an increase in the resistance indices assessed by dopplerography of the brachial artery and the severity of calcification of the thoracic aorta.

Favorable Cardiovascular Health Is Associated With Lower Prevalence, Incidence, Extent, and Progression of Extracoronary Calcification: MESA.

Ideal cardiovascular health (CVH) is associated with a lower incidence of cardiovascular disease. Extracoronary calcification (ECC)-measured at the aortic valve, mitral annulus, ascending thoracic aorta, and descending thoracic aorta-is an indicator of systemic atherosclerosis. This study examined whether favorable CVH was associated with a lower risk of ECC. We analyzed data from MESA (Multi-Ethnic Study of Atherosclerosis) participants aged 45 to 84 years without cardiovascular disease at baseline. ECC was measured by noncontrast cardiac computed tomography scan at baseline and after an average of 2.4 years. Prevalent ECC was defined as an Agatston score >0 at the baseline scan. Incident ECC was defined as Agatston score >0 at the follow-up scan among participants with Agatston score of 0 at the baseline scan. Each CVH metric (smoking, physical activity, body mass index, diet, blood pressure, total cholesterol, and blood glucose) was scored 0 to 2 points, with 2 indicating ideal; 1, intermediate; and 0, poor. The aggregated CVH score was 0 to 14 points (0-8, inadequate; 9-10, average; 11-14, optimal). We used Poisson and linear mixed-effects regression models to examine the association between CVH and ECC adjusted for sociodemographic factors. Of 6504 participants, 53% were women with a mean age (SD) of 62 (10) years. Optimal and average CVH scores were associated with lower ECC prevalence, incidence, and extent. For example, optimal CVH scores were associated with 57%, 56%, 70%, and 54% lower risk of incident aortic valve calcification, mitral annulus calcification, ascending thoracic aorta calcification, and descending thoracic aorta calcification, respectively. In addition, optimal and average CVH scores were associated with lower ECC progression at 2 years, although these associations were only significant for mitral annulus calcification and descending thoracic aorta calcification. In this multiethnic cohort, favorable CVH was associated with a lower risk of extracoronary atherosclerosis. These findings emphasize the importance of primordial prevention as an intervention to reduce the burden of cardiovascular disease.

Thoracic Aortic 18F-Sodium Fluoride Activity and Ischemic Stroke in Patients With Established Cardiovascular Disease

BackgroundAortic atherosclerosis represents an important contributor to ischemic stroke risk. Identifying patients with high-risk aortic atheroma could improve preventative treatment strategies for future ischemic stroke. ObjectivesThe purpose of this study was to investigate whether thoracic 18F-sodium fluoride positron emission tomography (PET) could improve the identification of patients at the highest risk of ischemic stroke. MethodsIn a post hoc observational cohort study, we quantified thoracic aortic and coronary 18F-sodium fluoride activity in 461 patients with stable cardiovascular disease undergoing PET combined with computed tomography (CT). Progression of atherosclerosis was assessed by change in aortic and coronary CT calcium volume. Clinical outcomes were determined by the occurrence of ischemic stroke and myocardial infarction. We compared the prognostic utility of 18F-sodium fluoride activity for predicting stroke to clinical risk scores and CT calcium quantification using survival analysis and multivariable Cox regression. ResultsAfter 12.7 ± 2.7 months, progression of thoracic aortic calcium volume correlated with baseline thoracic aortic 18F-sodium fluoride activity (n = 140; r = 0.31; P = 0.00016). In 461 patients, 23 (5%) patients experienced an ischemic stroke and 32 (7%) a myocardial infarction after 6.1 ± 2.3 years of follow-up. High thoracic aortic 18F-sodium fluoride activity was strongly associated with ischemic stroke (HR: 10.3 [95% CI: 3.1-34.8]; P = 0.00017), but not myocardial infarction (P = 0.40). Conversely, high coronary 18F-sodium fluoride activity was associated with myocardial infarction (HR: 4.8 [95% CI: 1.9-12.2]; P = 0.00095) but not ischemic stroke (P = 0.39). In a multivariable Cox regression model including imaging and clinical risk factors, thoracic aortic 18F-sodium fluoride activity was the only variable associated with ischemic stroke (HR: 8.19 [95% CI: 2.33-28.7], P = 0.0010). ConclusionsIn patients with established cardiovascular disease, thoracic aortic 18F-sodium fluoride activity is associated with the progression of atherosclerosis and future ischemic stroke. Arterial 18F-sodium fluoride activity identifies localized areas of atherosclerotic disease activity that are directly linked to disease progression and downstream regional clinical atherothrombotic events. (DIAMOND–Dual Antiplatelet Therapy to Reduce Myocardial Injury [DIAMOND], NCT02110303; Study Investigating the Effect of Drugs Used to Treat Osteoporosis on the Progression of Calcific Aortic Stenosis [SALTIRE II], NCT02132026; Novel Imaging Approaches To Identify Unstable Coronary Plaques, NCT01749254; and Role of Active Valvular Calcification and Inflammation in Patients With Aortic Stenosis, NCT01358513)

Relationship between Cardiovascular Calcium and Atrial Fibrillation.

Coronary artery calcium score (CACS) is associated with increased risk of atrial fibrillation (AF). However, the relationship between the burden of CACS and extra-coronary calcium and the AF is unclear. This cross-sectional study retrospectively analyzed the data of 143,529 participants (74.9% men; mean age, 41.7 ± 8.6 years) who underwent health examination including non-contrast cardiac CT and electrocardiography, from 2010 to 2018 to evaluate the association between cardiac calcium and AF. AF was diagnosed in 679 participants. The prevalence of AF was significantly increased as the CACS increased (p < 0.01). Multivariable analysis adjusted for age, sex, body mass index, hypertension, diabetes, hyperlipidemia, smoking, alcohol, and history of coronary artery disease showed a significant association between a high CACS ≥1000 and AF (OR 2.26, 95% CI 1.07–4.77, p = 0.032). In a subgroup analysis of participants with a CACS ≥100, aortic valve and thoracic aorta calcium were significantly associated with AF (OR 3.49, 95% CI 1.57–7.77, p = 0.002 and OR 2.19, 95% CI 1.14–4.21, p = 0.01, respectively). High CACS was associated with AF, and extra-coronary atherosclerosis was associated with AF in participants with a moderate to very high CACS.

Radiologist opinions regarding reporting incidental coronary and cardiac calcification on thoracic CT.

Objectives:Coronary and cardiac calcification are frequent incidental findings on non-gated thoracic computed tomography (CT). However, radiologist opinions and practices regarding the reporting of incidental calcification are poorly understood.Methods:UK radiologists were invited to complete this online survey, organised by the British Society of Cardiovascular Imaging (BSCI). Questions included anonymous information on subspecialty, level of training and reporting practices for incidental coronary artery, aortic valve, mitral and thoracic aorta calcification.Results:The survey was completed by 200 respondents: 10% trainees and 90% consultants. Calcification was not reported by 11% for the coronary arteries, 22% for the aortic valve, 35% for the mitral valve and 37% for the thoracic aorta. Those who did not subspecialise in cardiac imaging were less likely to report coronary artery calcification (p = 0.005), aortic valve calcification (p = 0.001) or mitral valve calcification (p = 0.008), but there was no difference in the reporting of thoracic aorta calcification. Those who did not subspecialise in cardiac imaging were also less likely to provide management recommendations for coronary artery calcification (p < 0.001) or recommend echocardiography for aortic valve calcification (p < 0.001), but there was no difference for mitral valve or thoracic aorta recommendations.Conclusion:Incidental coronary artery, valvular and aorta calcification are frequently not reported on thoracic CT and there are differences in reporting practices based on subspeciality.Advances in knowledge:On routine thoracic CT, 11% of radiologists do not report coronary artery calcification. Radiologist reporting practices vary depending on subspeciality but not level of training.

Epicardial and periaortic fat characteristics in ischemic stroke: Relationship with stroke etiology and calcification burden

PurposeWe explored epicardial (EAT) and periaortic (PAT) adipose tissue characteristics in patients with acute ischemic stroke (AIS), and the relationship with stroke etiology, calcification burden, and inflammation. MethodWe included a retrospective cohort of consecutive patients admitted with AIS between 2015 and 2020 who underwent a chest computed tomography. We calculated volumes and attenuation of EAT and PAT, and coronary artery (CAC), and thoracic aortic (TAC) calcification. Admission’s neutrophil/lymphocyte ratio (NLR) was recorded. Stroke severity was assessed using the National Institute of Health Stroke Scale (NIHSS), and patients were discriminated between cardioembolic (CE), non-CE, and embolic strokes of uncertain source (ESUS). ResultsA total of 182 patients were included. EAT (non-CE 127.4 ± 47.1 cm3; CE 133.3 ± 56.7 cm3; ESUS 121.6 ± 63.5 cm3, p > 0.05) and PAT (non-CE 37.4 ± 18.6 cm3; CE 40.4 ± 17.2 cm3; ESUS 34.5 ± 14.1 cm3, p > 0.05) volumes were similar between stroke etiologies. Patients with CE stroke had higher PAT attenuation (PAT = non-CE −84.4 ± 7.0 HU; CE −78.1 ± 9.9 HU; ESUS −82.3 ± 9.3 HU, p < 0.001). Using multiple linear regression, albeit weak, we found a significant relationship between NLR and PAT attenuation [Beta 0.24; (95% CI 0.04–0.51), p < 0.05). Despite similar volume, PAT attenuation was higher (p < 0.01) among demised patients. ConclusionIn this study, we identified higher periaortic fat attenuation, despite similar fat volume, in patients with CE stroke.

Dexamethasone is Associated With a Lower Risk of the Progression of Thoracic Aortic Calcification in Breast Cancer Survivors.

Background and Purpose: Breast cancer survivors have an increased cardiovascular risk, and vascular calcification is the pathological basis of cardiovascular disease. Some factors that affect the progression of thoracic aortic calcification (TAC) in survivors are unclear, and this study aims to explore the relationship between dexamethasone or radiotherapy and the progression of TAC in survivors. Materials and Methods: This study included 189 female patients with breast cancer, and they were divided into the progression and non-progression TAC groups. Radiation or dexamethasone doses, and related laboratory parameters were collected. Results: The cumulative dose of dexamethasone was higher [40 (10–180) mg versus 180 (80–270) mg, p < 0.001], and the cycle was longer [4 (1–6) cycles versus 6 (4–8) cycles, p < 0.001] in the non-progression TAC group. The cumulative dose (r = −0.303, p < 0.001) and cycle (r = −0.357, p < 0.001) of dexamethasone were negatively correlated with the level of increased TAC Agatston scores in survivors. Logistic regression analysis showed that dexamethasone was a protective factor for the progression of TAC (p = 0.029, odds ratio = 0.263, 95% confidence interval = 0.08–0.872). However, there wasn’t significant relationship between radiotherapy, radiation dose, follow-up time and the progression of TAC (all p > 0.05). In addition, aorta volume was positively correlated with the level of increased TAC Agatston scores in intensity modulated radiation therapy (r = 0.460, p < 0.001). Conclusion: Dexamethasone is associated with a lower risk of the progression of TAC in breast cancer survivors, and there’s no correlation between radiotherapy and progression of TAC, but the aorta volume may be a predictor of the severity of progression of TAC.

Association of coronary artery calcification and thoracic aortic calcification with incident peripheral arterial disease in the Multi-Ethnic Study of Atherosclerosis (MESA).

AimsThe association of subclinical atherosclerotic disease in the coronary arteries and thoracic aorta with incident peripheral arterial disease (PAD) is unknown. We investigated the association between coronary artery calcium score (CACs) and thoracic aortic calcium score (TACs) with incident clinical and subclinical PAD.Methods and resultsThe Multi-Ethnic Study of Atherosclerosis (MESA) recruited 6814 men and women aged 45–84 from four ethnic groups who were free of clinical cardiovascular disease at enrolment. Coronary artery calcium score and thoracic aortic calcium score were measured from computed tomography scans. Participants with a baseline ankle-brachial index (ABI) ≤0.90 or >1.4 were excluded. Abnormal ABI was defined as ABI ≤0.9 or >1.4 at follow-up exam. Multivariable logistic regression and Cox proportional hazards models were used to test the associations between baseline CACs and TACs with incident abnormal ABI and clinical PAD, respectively. A total of 6409 participants (female: 52.8%) with a mean age of 61 years were analysed. Over a median follow-up of 16.7 years, 91 participants developed clinical PAD. In multivariable analysis, each unit increase in log (CACS + 1) and log (TACs + 1) were associated with 23% and 13% (P < 0.01for both) higher risk of incident clinical PAD, respectively. In 5725 (female: 52.6%) participants with an available follow-up ABI over median 9.2 years, each 1-unit increase in log (CACs + 1) and log (TACs + 1) were independently associated with 1.15-fold and 1.07-fold (P < 0.01for both) higher odds of incident abnormal ABI, respectively.ConclusionHigher baseline CACs and TACs predict abnormal ABI and clinical PAD independent of traditional cardiovascular risk factors and baseline ABI.

Long-Term Prognostic Implications and Role of Further Testing in Adults Aged ≤55 Years With a Coronary Calcium Score of Zero (from the Multi-Ethnic Study of Atherosclerosis)

The long-term prognostic significance of a coronary artery calcium (CAC) score of 0 is poorly defined in younger adults. We evaluated this among participants aged 45 to 55years from the Multi-Ethnic Study of Atherosclerosis, and assessed whether additional biomarkers can identify subgroups at increased absolute risk. We included 1,407 participants (61% women) without diabetes or severe hypercholesterolemia, with estimated 10-year risk <20% and CAC=0. We evaluated all and hard cardiovascular disease (CVD) events, overall and among subjects with each of the following: high-sensitivity C-reactive protein levels ≥2mg/L, homocysteine ≥10µmol/L, high-sensitivity cardiac troponin T ≥95th percentile, lipoprotein (a) >50mg/dl, triglycerides ≥175mg/dl, apolipoprotein B ≥130mg/dl, albuminuria, thoracic aortic calcium, aortic valve calcium (AVC), mitral annular calcium, ankle-brachial index <0.9, any carotid plaque, and maximum internal carotid artery intima-media thickness (ICA-IMT) ≥1.5mm. Median follow-up was 16years, and overall CVD event rates were low (4% at 15years). For most exposures evaluated, rates of all CVD events were <6 per 1,000 person-years, except for ICA-IMT ≥1.5mm (6.43) and AVC (13.8). The number needed to screen to detect ICA-IMT ≥1.5mm was 8, and 84 for AVC. Among participants with borderline/intermediate risk or premature family history, hard CVD event rates were <7 per 1,000 for most exposures, except for ICA-IMT ≥1.5mm (8.25), albuminuria (8.30), and AVC (13.47). Nonsmokers and those with ICA-IMT <1.5mm had very low rates. In conclusion, our results demonstrate a favorable long-term prognosis of CAC=0 among adults aged ≤55 years, particularly among nonsmokers. ICA-IMT testing could be considered for further risk assessment in adults ≤55years with CAC=0 and uncertain management.

Associations of endogenous sex hormone levels with the prevalence and progression of valvular and thoracic aortic calcification in the Multi-Ethnic Study of Atherosclerosis (MESA)

Background and aimsSex hormones (SH) may contribute to sex differences in cardiovascular disease (CVD). High free testosterone (T) and low sex hormone binding globulin (SHBG) have been associated with progression of coronary artery calcification in women. We now examined the association of SH with extra-coronary calcification (ECC) prevalence and progression among MESA participants. MethodsWe studied 2,737 postmenopausal women and 3,130 men free of clinical CVD with baseline SH levels. ECC measurements [ascending and descending thoracic aortic calcification (ATAC, DTAC), mitral annular calcification (MAC), aortic valve calcification (AVC)] were obtained by computed tomography at baseline and after 2.4 ± 0.9 years. We used multivariable Poisson regression to evaluate associations with ECC prevalence and incidence (Agatston scores >0) and linear mixed effects models for ECC progression, per 1-SD increment in log(SH) in women and men separately. ResultsThe mean age was 65 ± 9 and 62 ± 10 years for women and men, respectively. In women, greater free T and lower SHBG were associated with MAC incidence in a demographic-adjusted model only. In men, lower free T was associated with MAC prevalence, DTAC incidence and progression, while greater SHBG was associated with MAC prevalence and DTAC progression after further adjusting for CVD risk factors. ConclusionsIn this diverse cohort free of CVD, we found some associations of SH with ECC measures. In particular, free T was inversely associated with prevalent MAC and DTAC progression in men independent of CVD risk factors. SH may influence vascular calcification, but further work is needed to understand clinical implications of these findings.

Associations of adipokine levels with the prevalence and extent of valvular and thoracic aortic calcification: The Multi-Ethnic Study of Atherosclerosis (MESA)

Background and aimsExtra-coronary calcification (ECC) is a marker of atherosclerosis and independently associated with cardiovascular disease (CVD). Adipokines may mediate the effect of obesity on atherosclerosis. However, the relationship of adipokines with ECC is not well-established. We examined the associations of leptin, resistin and adiponectin with ECC in a diverse community-based cohort. MethodsWe performed a cross-sectional analysis of 1897 adults without clinical CVD in the MESA cohort. Serum adipokine levels and non-contrast cardiac CT scans were obtained at Exam 2 or 3 (randomly assigned). ECC was quantified by Agatston score and included calcification of the mitral annulus (MAC), aortic valve (AVC), ascending thoracic aorta (ATAC) and descending thoracic aorta (DTAC). We used multivariable regression to evaluate the associations between leptin, resistin and adiponectin [per 1 SD ln(adipokine] with ECC prevalence (score >0) and extent [ln(score+1)]. ResultsThe mean age of participants was 65 ± 10 years; 49% women. After adjusting for demographic factors, adiponectin was inversely associated with AVC prevalence and extent; leptin positively associated with MAC prevalence and extent; and resistin positively associated with ATAC prevalence and extent and DTAC extent. After adjustment for BMI and other CVD risk factors, adiponectin remained inversely associated with AVC prevalence, and resistin remained associated with greater ATAC prevalence and extent. Leptin was not associated with measures of ECC after full adjustment. No adipokine was associated with MAC after full adjustment. ConclusionsWe identified significant associations between select adipokines and specific markers of ECC. Adipokines may play a role in the development of systemic atherosclerosis.

Thoracic Aorta Calcium Detection and Quantification Using Convolutional Neural Networks in a Large Cohort of Intermediate-Risk Patients.

Arterial calcification is an independent predictor of cardiovascular disease (CVD) events whereas thoracic aorta calcium (TAC) detection might anticipate extracoronary outcomes. In this work, we trained six convolutional neural networks (CNNs) to detect aortic calcifications and to automate the TAC score assessment in intermediate CVD risk patients. Cardiac computed tomography images from 1415 patients were analyzed together with their aortic geometry previously assessed. Orthogonal patches centered in each aortic candidate lesion were reconstructed and a dataset with 19,790 images (61% positives) was built. Three single-input 2D CNNs were trained using axial, coronal and sagittal patches together with two multi-input 2.5D CNNs combining the orthogonal patches and identifying their best regional combination (BRC) in terms of lesion location. Aortic calcifications were concentrated in the descending (66%) and aortic arch (26%) portions. The BRC of axial patches to detect ascending or aortic arch lesions and sagittal images for the descending portion had the best performance: 0.954 F1-Score, 98.4% sensitivity, 87% of the subjects correctly classified in their TAC category and an average false positive TAC score per patient of 30. A CNN that combined axial and sagittal patches depending on the candidate aortic location ensured an accurate TAC score prediction.

The role of cardiovascular calcifications in COVID-19

Abstract Background Coronary, thoracic aorta and aortic valve calcium can be measured from a non-gated chest computer tomography (CT) and are validated predictors of cardiovascular events and all-cause mortality. However, their prognostic role in acute systemic inflammatory diseases, such as COVID-19, has not been investigated. Purpose The principal aim was to evaluate the association of coronary artery calcium (CAC) and total thoracic calcium on in-hospital mortality in COVID-19 patients. Then, to evaluate the prognostic impact of clinical and subclinical coronary artery disease (CAD), as assessed by CAC. Methods 1093 consecutive patients from 16 Italian hospitals with a positive swab for COVID-19 and an admission chest CT for pneumonia severity assessment were included in the SCORE COVID-19 registry (calcium score for COVID-19 Risk Evaluation). At CT, coronary, aortic valve and thoracic aorta calcium were qualitatively and quantitatively evaluated separately and combined together (total thoracic calcium) by a central Core-lab blinded to patients' outcomes. A specific sub analysis on CAC was performed stratifying the patients in three groups: (a) “clinical CAD” (prior revascularization history), (b) “subclinical CAD” (CAC &amp;gt;0), (c) “No CAD” (CAC=0). In-hospital mortality was the primary endpoint, while a composite of myocardial infarction and cerebrovascular accident (MI/CVA) was the secondary one. Results Non-survivors compared to survivors had higher coronary artery [(487.7±565.3 vs 207.7±406.8, p&amp;lt;0.001)], aortic valve [(322.4±390.9 vs 98.2±250.7 mm2, p&amp;lt;0.001)] and thoracic aorta [(3786.7±4225.5 vs 1487.6±2973.1 mm2, p&amp;lt;0.001)] calcium values. Coronary artery calcium (HR 1.308; 95% CI, 1.046 - 1.637, p=0.019) and total thoracic calcium (HR 1.975; 95% CI, 1.200 - 3.251, p=0.007) resulted to be independent predictors of in-hospital mortality. In the sub - analysis increasing rates of in-hospital mortality (11.3% vs. 27.3% vs. 39.8%, p&amp;lt;0.001) and MI/CVA events (2.3% vs. 3.8% vs. 11.9%, p&amp;lt;0.001) were observed from the No CAD to the clinical CAD groups. Among patients with subclinical CAD, increasing CAC burden was associated with higher rates of in-hospital mortality (20.5% vs. 27.9% vs. 38.7% for patients with CAC score thresholds ≤100, 101–400 and &amp;gt;400, respectively, p&amp;lt;0.001) Conclusion Coronary, aortic valve and thoracic aortic calcium assessment on admission non-gated CT permits to stratify the COVID-19 patients in-hospital mortality risk. Cardiovascular calcifications may represent a bystander of an impaired vascular reserve, both microvascular and endothelial, but also a sign of vascular senescence. Therefore, it can be considered an index of biological frailty, likely more accurate than age and other risk factors. Funding Acknowledgement Type of funding sources: None. Figure 1Figure 2

Associations and outcomes of cardiovascular calcifications by computed tomography in atrial fibrillation patients

Abstract Background Coronary (CAC), mitral annular (MAC), aortic valve (AVC) and thoracic aortic (TAC) calcifications are known imaging biomarkers for cardiovascular risk in the general population. Despite this, their prognostic value are not well established in atrial fibrillation (AF) patients who have elevated risk for cardiovascular events. Purpose We assessed the associated factors and outcomes of cardiovascular calcifications detected by computed tomography (CT) in AF patients undergoing pulmonary vein isolation (PVI). Methods Consecutive AF patients enrolled in a prospective PVI registry during 2014–2018 with CT performed within 1-year of their procedure were reviewed for the presence of cardiovascular calcifications on CT. Risk factors and outcomes for each type of cardiovascular calcifications were analyzed in univariable and multivariable regression models. Results Amongst 3604 AF patients, there were 2238 (62.1%), 308 (8.6%), 572 (15.9%) and 1048 (29.1%) patients with CAC, MAC, AVC and TAC respectively. Factors independently associated with these cardiovascular calcifications are listed in Table 1. During mean follow-up of 2.8±1.6 years, there were 97 (2.7%) all-cause deaths, and 158 (4.4%) major adverse cardiovascular events (MACE). Forest plots of unadjusted and adjusted hazards ratios of cardiovascular calcifications at predicting these outcomes are shown in Figure 1. Conclusion Cardiovascular calcifications especially CAC are prevalent in AF patients, and share common risk factors with cardiovascular events, except for female being protective for CAC and AVC but having higher risk of MAC and TAC. Although all cardiovascular calcifications were associated with death and MACE in unadjusted analyses, only CAC remained so for both outcomes in adjusted analyses. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): National Heart Foundation of New Zealand Table 1Figure 1

18F-Sodium fluoride positron emission tomography, aortic disease activity and ischaemic stroke risk

Abstract Background Arterial 18F-sodium fluoride (18F-NaF) activity on positron emission tomography (PET) is a marker of active microcalcification and atherosclerosis. Coronary 18F-NaF activity (CMA) predicts coronary artery disease progression and subsequent myocardial infarction. Objective To investigate whether aortic 18F-NaF activity (AMA) predicts thoracic aortic atherosclerotic disease progression and subsequent ischaemic stroke or myocardial infarction in patients with established cardiovascular disease. Methods In a post-hoc observational cohort study, we evaluated AMA and CMA in patients with stable coronary artery disease (n=239) or aortic stenosis (n=158) who had underwent thoracic 18F-NaF PET and computed tomography (CT). We assessed the associations between AMA or CMA and progression of calcified atherosclerotic plaque in both thoracic aortic and coronary territories on follow up CT, as well as subsequent ischaemic stroke or myocardial infarction. Results In 141 and 231 patients with repeat aortic and coronary CT imaging respectively at 12.7±2.7 months, AMA correlated with log progression of thoracic aortic calcium scores (r=0.21, p=0.011), volume (r=0.29, p&amp;lt;0.01) and mass (r=0.29, P&amp;lt;0.01) as well as log coronary calcium score progression (r=0.21, p=0.03). CMA correlated with log coronary (r=0.42, p&amp;lt;0.01), but not log aortic (p&amp;gt;0.80) calcium score progression. In 397 patients, 16 had an ischaemic stroke and 25 had a myocardial infarction after 4.7±1.6 years. After adjusting for clinical risk factors, CMA and calcium scoring, AMA was associated with stroke (hazard ratio, 1.71 [95% confidence interval 1.00–2.90], p=0.048]). AMA was superior to clinical risk and calcium scores in identifying patients with stroke (c-statistic 0.76 versus 0.58 versus 0.63 respectively, p&amp;lt;0.05). Survival analysis demonstrated that AMA was associated with ischaemic stroke (p&amp;lt;0.001) but not myocardial infarction (p=0.45), whereas CMA was associated with myocardial infarction (p&amp;lt;0.001) but not stroke (p=0.39). Conclusions In patients with established cardiovascular disease, AMA is associated with progression of aortic atherosclerosis and future ischaemic stroke. Arterial 18F-NaF identifies localised areas of atherosclerotic disease activity that relate to regional atherothrombotic events. Funding Acknowledgement Type of funding sources: Other. Main funding source(s): British Heart Foundation AMA, disease progression and outcomesVariables associated with stroke

Implication of thoracic aortic calcification over coronary calcium score regarding the 2018 ACC/AHA Multisociety cholesterol guideline: results from the CAC Consortium

ObjectiveTAC is associated with an increased atherosclerotic cardiovascular disease (ASCVD) risk, but it is unclear how to interpret thoracic aortic calcification (TAC) findings in conjunction with ASCVD risk and coronary artery calcium (CAC) score according to 2018 ACC/AHA Multisociety cholesterol guidelines. We evaluate the incremental value of thoracic aortic calcification TAC over CAC for predicting and reclassifying ASCVD mortality risk. MethodThe study included 30,630 asymptomatic individuals (mean age: 55 ± 8 years, male: 64%) from the CAC Consortium. TAC was categorized as TAC 0, 1-300, and >300. Patients were categorized as low (<5%), borderline (5–7.5%), intermediate (7.5–20%), or high (≥20%) 10-year ASCVD risk according to the Pooled Cohorts Equation. In the intermediate risk group, the utility of TAC beyond CAC for statin eligibility was assessed according to the guideline. CAC was categorized as CAC=0 (no statin), CAC 1-100 (favors statin), or CAC>100 (initiate stain). ResultsDuring the median 11.2 years (IQR 9.2–12.4) follow-up, 345 (1.1%) CVD deaths occurred. TAC>300 was associated with increased CVD mortality after adjusting for ASCVD risk and CAC (HR:4.72, 95% CI: 3.39–6.57, p<0.001). In borderline and intermediate risk groups, TAC improved discrimination when added to a model included ASCVD risk and CAC (C-statistic: 0.77 vs. 0.68 in borderline group; 0.67 vs. 0.63 in intermediate group, both p < 0.05). The addition of TAC over CAC improved risk reclassification in borderline, intermediate and high-risk groups (categorical net reclassification index: 0.40, 0.29, and 0.49, respectively, all p < 0.001). Of intermediate risk participants for whom consideration of CAC was recommended based on the guideline, TAC >300 was associated with an increased CVD mortality risk across each statin eligibility group (all p < 0.001, compared to TAC 0). ConclusionTAC was independently associated with CVD death. Among individuals with borderline or intermediate ASCVD risk, a TAC threshold of 300 may provide added prognostic and reclassification value beyond the current guideline-based approach.

Implication Of Thoracic Aortic Calcification Over Coronary Calcium Score Regarding The 2018 Acc/aha Cholesterol Guideline: Results From The Cac Consortium

Introduction: Thoracic aortic calcification (TAC) is associated with an increased atherosclerotic cardiovascular disease (ASCVD) risk, but it is unclear how to interpret TAC findings in conjunction with ASCVD risk and coronary artery calcium (CAC) score. We evaluated the implication of TAC over CAC for reclassifying statin eligibility groups according to 2018 ACC/AHA cholesterol management guidelines.

Associations And Outcomes Of Cardiovascular Calcifications By Computed Tomography In Atrial Fibrillation Patients

Introduction: Coronary (CAC), mitral annular (MAC), aortic valve (AVC) and thoracic aortic (TAC) calcifications are known imaging biomarkers for cardiovascular risk in the general population. Despite this, their prognostic value are not well established in atrial fibrillation (AF) patients who have elevated risk for cardiovascular events. We assessed the associated factors and outcomes of cardiovascular calcifications detected by computed tomography (CT) in AF patients undergoing pulmonary vein isolation (PVI).

Thoracic Aortic Calcification and Pre-Clinical Hypertension by New 2017 ACC/AHA Hypertension Guidelines.

The recently revised 2017 American College of Cardiology/American Heart Association (ACC/AHA) hypertension (HTN) guidelines employ a lower blood pressure threshold to define HTN, aiming for earlier prevention of HTN-related cardiovascular diseases (CVD). Thoracic aortic calcification (TAC), a new surrogate marker of aging and aortic medial layer degeneration, and different stages of HTN, according to the 2017 ACC/AHA HTN guidelines, remain unknown. We classified 3022 consecutive asymptomatic individuals enrolled into four HTN categories using the revised 2017 ACC/AHA guidelines: normal blood pressure (NBP), elevated blood pressure (EBP), and stage 1 (S1) and stage 2 (S2) HTN. The coronary artery calcification score and TAC metrics (total Agaston TAC score, total plaque volume (mm3), and mean density (Hounsfield units, HU)) were measured using multi-detector computed tomography. Compared to NBP, a graded and significant increase in the TAC metrics was observed starting from EBP and S1 and S2 HTN, using the new 2017 ACC/AHA guidelines (NBP as reference; all trends: p < 0.001). These differences remained consistent after being fully adjusted. Older age (>50 years), S1 and S2 HTN, prevalent diabetes, and chronic kidney disease (<60 mL/min/1.73 m2) are all independently contributing factors to higher TAC risk using multivariate stepwise logistic regressions (all p ≤ 0.001). The optimal cutoff values of systolic blood pressure, diastolic blood pressure, and pulse pressure were 121, 74, and 45 mmHg, respectively, for the presence of TAC after excluding subjects with known CVD and ongoing HTN medication treatment. Our data showed that the presence of TAC starts at a stage of elevated blood pressure not categorized as HTN from the updated 2017 ACC/AHA hypertension guidelines.

Carotid intima-media thickness (IMT) in patients with severe familial and non-familial hypercholesterolemia: The effect of measurement site on the IMT correlation with traditional cardiovascular risk factors and calcium scores.

The carotid intima-media thickness (IMT) measurement may be carried out proximally (pIMT) or distally (dIMT) in relation to the bulb of the common carotid artery which has significant implications on the results and correlation with risk factors. The aim of the study was to compare the pIMT and dIMT in patients with familial hypercholesterolemia confirmed by genetic testing (FH group) and patients with severe non-familial hypercholesterolemia, with negative results of genetic testing (NFH group) and to determine the correlation of results with traditional atherosclerotic risk factors and calcium scores. A total of 86 FH and 50 NFH patients underwent pIMT and dIMT measurements of both carotid arteries as well as computed tomography (CT) with coronary and thoracic aorta calcium scoring. The meanpIMT of both right and left common carotid artery were significantly higher in patients with FH compared to the NFH group (meanpRIMT 0.721 ± 0.152 vs. 0.644 ± 0.156, p < 0.01, meanpLIMT 0.758 ± 0.173 vs. 0.670 ± 0.110, p < 0.01). Patient age, pre-treatment lowdensity lipoprotein (LDL) cholesterol levels (LDLmax) at baseline and systolic blood pressure were independent predictors of pIMT increases in both carotid arteries. Smoking history, age and LDLmax were independent predictors of dIMT increase. There was a significant correlation between the calcium scores of the ascending aorta, coronary artery and aortic valve and all IMT parameters. The IMT measured proximally better between patients with familial and non-familial hypercholesterolemia. The association between IMT and traditional cardiovascular risk factors varies between measurement sites. IMT values correlate CT calcium scores in all patients with hypercholesterolaemia regardless of genetic etiology.