Cardiovascular computed tomography imaging for coronary artery disease risk: plaque, flow and fat

Cardiac imaging is central to the diagnosis and risk stratification of coronary artery disease, beyond symptoms and clinical risk factors, by providing objective evidence of myocardial ischaemia and characterisation of coronary artery plaque. CT coronary angiography can detect coronary plaque with high resolution, estimate the degree of functional stenosis and characterise plaque features. However, coronary artery disease risk is also driven by biological processes, such as inflammation, that are not fully reflected by severity of stenosis, myocardial ischaemia or by coronary plaque features. New cardiac CT techniques can assess coronary artery inflammation by imaging perivascular fat, and this may represent an important step forward in identifying the ‘residual risk’ that is not detected by plaque or ischaemia imaging. Coronary artery disease risk assessment that incorporates clinical factors, plaque characteristics and perivascular inflammation offers a more comprehensive individualised approach to quantify and stratify coronary artery disease risk, with potential healthcare benefits for prevention, diagnosis and treatment recommendations. Furthermore, identifying new biomarkers of cardiovascular risk has the potential to refine early-life prevention strategies, before atherosclerosis becomes established.

Association Between Carotid Artery Perivascular Fat Density and Intraplaque Hemorrhage

Objectives: Perivascular adipose tissue plays a key role in atherosclerosis, but its effects on the composition of carotid atherosclerotic plaques are unknown. This study aimed to investigate the association between inflammatory carotid artery and intraplaque hemorrhage (IPH) in the carotid artery.Methods: This is a single-center retrospective study. Carotid inflammation was assessed by perivascular fat density (PFD) in 72 participants (mean age, 65.1 years; 56 men) who underwent both computed tomography angiography (CTA) and magnetic resonance imaging (MRI) within 2 weeks. The presence of IPH was assessed with MRI. Carotid stenosis, maximum plaque thickness, calcification, and ulceration were evaluated through CTA. The association between PFD and the occurrence of IPH was studied using generalized estimating equations analysis.Results: Of 156 plaques, 72 plaques (46.2%) had IPH. Plaques with IPH showed higher PFD than those without [−41.4 ± 3.9 vs. −55.8 ± 6.5 Hounsfield unit (HU); p < 0.001]. After age, calcification, degree of stenosis, maximum plaque thickness, and ulceration were adjusted for, PFD (OR, 1.96; 95% CI, 1.41–2.73; p < 0.001) was found to be strongly associated with the presence of IPH.Conclusions: A higher PFD is associated with the presence of IPH in the carotid artery. These findings may provide a novel marker to identify carotid IPH and risk stratification.

Coronary Inflammation Assessed by Perivascular Fat Attenuation Index in Patients with Psoriasis: A Propensity Score-Matched Study

<b><i>Objectives:</i></b> This study aimed to evaluate coronary inflammation by measuring the perivascular fat attenuation index (FAI) and quantify the atherosclerosis burden in patients with psoriasis and control individuals without psoriasis based on coronary computed tomography angiography (CCTA) images. <b><i>Methods:</i></b> A total of 98 consecutive patients with psoriasis (76 male [77.6%], aged 56.5 years, range 45.5–65.0) were recruited, and 196 patients (157 male [80.1%]; aged 54.6 ± 14.1 years) without established cardiovascular disease (CVD) who underwent CCTA within the same period were enrolled in the control group. Coronary plaque burden was quantified using the computed tomography-adapted Leaman score (CT-LeSc), and the FAI surrounding the proximal of three main epicardial vessels was measured to represent coronary inflammation. <b><i>Results:</i></b> Patients with psoriasis and the control subjects were well matched in CVD risk factors (all <i>p</i> &#x3e; 0.05). Psoriasis patients had a greater overall CT-LeSc (5.86 vs. 4.69, <i>p</i> = 0.030) and lower perivascular FAI (−80.19 ± 7.48 vs. −78.14 ± 7.81 HU, <i>p</i> &#x3c; 0.001). A similar result was found upon comparing psoriasis patients without biological or statin therapy with non-psoriasis individuals without statin treatments. Furthermore, the psoriasis group had a higher prevalence of non-calcified plaques (30.3% in the psoriasis group vs. 20.1% in the control subjects, <i>p</i> = 0.001). No difference in perivascular FAI on either calcified and mixed plaques or non-calcified plaques between the two groups was found. <b><i>Conclusion:</i></b> Patients with psoriasis have a higher atherosclerotic burden as quantified by CT-LeSc and less coronary inflammation as detected by perivascular FAI around the most proximal of the three major epicardial vessels. The usefulness of perivascular FAI for evaluating coronary inflammation in patients with chronic low-grade inflammatory disease such as psoriasis should be verified.

Standardised measurement of coronary inflammation using cardiovascular CT: integration in clinical care as a prognostic medical device

Aims Coronary CT angiography (CCTA) is a first-line modality in the investigation of suspected coronary artery disease (CAD). Mapping of perivascular Fat Attenuation Index (FAI) on routine CCTA enables the non-invasive detection of coronary artery inflammation by quantifying spatial changes in perivascular fat composition. We now report the performance of a new medical device, CaRi-Heart®, which integrates standardised FAI mapping together with clinical risk factors and plaque metrics to provide individualised cardiovascular risk prediction. Methods and Results The study included 3912 consecutive patients undergoing CCTA as part of clinical care in the United States (n = 2040) and Europe (n = 1872). These cohorts were used to generate age-specific nomograms and percentile curves as reference maps for the standardised interpretation of FAI. The first output of CaRi-Heart® is the FAI-Score of each coronary artery, which provides a measure of coronary inflammation adjusted for technical, biological and anatomical characteristics. FAI-Score is then incorporated into a risk prediction algorithm together with clinical risk factors and CCTA-derived coronary plaque metrics to generate the CaRi-Heart® Risk that predicts the likelihood of a fatal cardiac event at 8 years. CaRi-Heart® Risk was trained in the US population and its performance was validated externally in the European population. It improved risk discrimination over a clinical risk factor-based model (Δ[C-statistic] of 0.085, P = 0.01 in the US Cohort and 0.149, P &lt; 0.001 in the European cohort) and had a consistent net clinical benefit on decision curve analysis above a baseline traditional risk factor-based model across the spectrum of cardiac risk. Conclusion CaRi-Heart® reliably improves cardiovascular risk prediction by incorporating traditional cardiovascular risk factors along with comprehensive CCTA coronary plaque and perivascular adipose tissue phenotyping. This integration advances the prognostic utility of CCTA for individual patients and paves the way for its use as a screening tool among patients referred for CCTA. Translational Perspective Mapping of perivascular Fat Attenuation Index (FAI) on coronary computed tomography angiography (CCTA) enables the non-invasive detection of coronary artery inflammation by quantifying spatial changes in perivascular fat composition. We now report the performance of a new medical device, CaRi-Heart®, which integrates standardised FAI mapping together with clinical risk factors and plaque metrics to provide age-standardised reference maps and individualised cardiovascular risk prediction. This integration advances the prognostic value of CCTA and paves the way for its use as a screening tool among patients referred for CCTA.

What is the impact of preserving the endothelium on saphenous vein graft performance? Comments on the ‘NO’ touch harvesting technique

Saphenous veins used for coronary artery bypass surgery are subjected to considerable vascular trauma when harvested by conventional methods. This vascular damage is responsible, at least in part, for the inferior patency of the saphenous vein when compared with the internal thoracic artery. The performance of saphenous vein grafts is improved when this conduit is harvested atraumatically using the no-touch technique. There is growing evidence that the success of the no-touch technique is due to the preservation of a number of vascular structures including the endothelium, vasa vasorum and perivascular fat. There is conflicting evidence regarding the degree of endothelial damage to the endothelium of conventional versus no-touch saphenous vein grafts. In general, it has been shown that this single layer of cells lining the lumen exhibits considerable damage associated with a combination of vascular trauma and high pressure intraluminal distension. Increased platelet aggregation and thrombus formation at the exposed subendothelial membrane is due to a local reduction of endothelium-derived factors including nitric oxide. In addition, damage to the vasa vasorum of conventionally-harvested veins will reduce transmural blood flow, a condition shown to promote neointimal hyperplasia and atheroma formation. By stripping off the perivascular fat during conventional harvesting, mechanical support of the graft is reduced and the source of adipocyte-derived factors potentially beneficial for graft patency removed. While most agree that endothelial damage to the saphenous vein affects graft patency, the contribution of other tissue-derived factors affected by vascular damage at harvesting need to be considered.