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PubMed2004

Alveolar echinococcosis of the liver: correlative color Doppler US, CT, and MRI study.

PURPOSE: To determine and compare the imaging features of hepatic alveolar Echinococcosis using color Doppler US, CT, and MRI. MATERIAL AND METHODS: Abdominal CT and MRI with and without contrast agents and color Doppler US were performed on seven patients with hepatic alveolar Echinococcosis. The lesions were evaluated for location, features of echogenicity, intensity and density, calcification, and vascular, hilar, and perihepatic involvement. The diagnosis was confirmed histopathologically in all patients. RESULTS: Six patients had solitary lesions, and one displayed multiple lesions. The lesions were generally seen as heterogeneous and hyper- or hypoechoic when imaged with color Doppler US, hypodense with CT, and hypointense with MRI, in comparison with the liver parenchyma. Calcification, central necrosis, and small peripheral cysts were observed in six, seven, and four patients, respectively. Vascular flow or contrast enhancement was not observed in any of the cases. A look at the respective advantages of each method reveals that calcification was best rendered visible via CT, small peripheral cysts with T2-weighted MRI, central necrosis with CT and MRI, and perihepatic invasion with multiplanar MRI. Vascular involvement was revealed by all methods. CONCLUSION: Color Doppler US, CT, and MR imaging function extremely well as complementary methods in the diagnosis of HAE. Color Doppler US should be performed in these patients owing to its ability to efficiently detect the disease. Knowledge of imaging characteristics makes it possible to radiologically ascertain an early diagnosis.

Adult↗
PubMed2001

Calciphylaxis is associated with hyperphosphatemia and increased osteopontin expression by vascular smooth muscle cells.

Calciphylaxis or calcific uremic arteriolopathy (CUA) is a fatal disease in dialysis patients due to calcification of cutaneous blood vessels. The pathogenesis has been attributed to elevated parathyroid hormone (PTH). However, recent studies evaluating vascular calcification in nondialysis patients have found that the smooth muscle cells play an active role, including production of the bone matrix protein osteopontin. To examine the involvement of various clinical parameters and smooth muscle cells of CUA, we performed a case-control analysis comparing 10 CUA patients with our current dialysis patients. Available histologic sections were immunostained for osteopontin, markers of smooth muscle cells, endothelial cells, and macrophages. Compared with our current dialysis population, patients with CUA were more likely to be obese, white, and female (P < 0.02). Comparison of laboratory values found CUA patients with lower serum albumin, greater serum phosphorus, and greater calcium X phosphorus product (P < 0.01). In contrast, there was no difference in the concentration of PTH or calcium between the 2 groups. Immunostaining of calcified blood vessels showed that all calcified vessels stained positive for osteopontin, whereas all the noncalcifed vessels showed no osteopontin localization. Staining for smooth muscle alpha-actin decreased in the medial layer with calcification, with cells appearing to be sloughed off, leading to near occlusion of the vessel lumen. Our case-control study demonstrates that hyperphosphatemia and an elevated calcium X phosphorus product is associated with CUA. Histologic examination suggests that the calcification is associated with increased expression of osteopontin by smooth muscle cells.

Adult↗
PubMed2003

Coronary artery, aortic wall, and valvular calcification in nondialyzed individuals with type 2 diabetes and renal disease.

BACKGROUND: Individuals with end-stage renal disease (ESRD) have highly prevalent and severe vascular and valvular calcification. We undertook this study to test the hypothesis that vascular and valvular calcification begins and is often severe long before diabetic renal disease progresses to ESRD. METHODS: A total of 32 nondialyzed individuals with type 2 diabetes mellitus and diabetic renal disease (albumin excretion rate>30 microg/min) [mean glomerular filtration rate (GFR), 49.8 +/- 6.1 mL/min/1.73 m2] were identified and compared with a group of 18 normoalbuminuric diabetics. We used 3:1 matching to identify 95 nondiabetic controls without renal disease, matched for age, gender, ethnicity, and the presence/absence of dyslipidemia, hypertension, and known coronary artery disease (CAD). RESULTS: Using electron beam computed tomography (CT), the prevalence of coronary artery calcification was significantly greater among diabetic renal disease individuals (prevalence, 94% vs. 59%, P < 0.001; median score, 238 vs. 10, P < 0.001) than the nondiabetic controls. The coronary artery calcification scores were significantly more severe among diabetic renal disease individuals than either the diabetic or nondiabetic controls. Among individuals with diabetic renal disease, the coronary artery calcification and aortic wall calcification scores were several-fold greater among those with known CAD than among those without. There was also a significantly greater prevalence of aortic and mitral valve calcification among diabetic renal disease individuals than nondiabetic controls (aortic, 23% vs. 6%, P = 0.03; mitral, 25% vs. 2%, P < 0.001). Multivariate analysis using all three groups reproduced these findings and also consistently identified age and diabetic renal disease as additional predictors for the presence or severity of coronary artery and aortic wall calcification. CONCLUSION: In this first, systematic analysis among nondialyzed individuals with diabetic renal disease, these data demonstrate that vascular and valvular calcification is present and often severe long before the disease progresses to ESRD. The data also suggest that the coronary artery and aortic wall calcification may represent atherosclerosis.

Aortic Diseases↗
PubMedDate not supplied

[The clinical x-ray characteristics of the soft tissues of the lower extremities in diabetics].

The authors present the results of clinicoroentgenological and immunological investigations of the state of lower limb soft tissues in 117 patients with diabetes mellitus. Vascular wall calcification and soft tissue edema were noted practically in all the patients with a period of disease over 1 year. X-ray investigation permitted the detection of vascular lesion at early stages of complication development, in most of the patients even at the preclinical stage. A degree of lower limb vascular lesion is not related to a type of diabetes mellitus and the patients' age. There is direct correlation between the affection of the walls of medium size vessels and vessels of the fundus of the eye. The frequency and severity of lower limb vascular lesion, polyneuropathy and nephropathy grow significantly with an increase in a period of disease. A parallel decrease of immunoglobulins is noted. The affection of osseous tissue does not depend on a period of disease and shows insignificant correlation with a degree of vascular lesion.

Adolescent↗
PubMed1987

Ultrastructure of cardiocyte degeneration and myocardial calcification in the dystrophic hamster.

The myocardium of the Bio 14.6 cardiomyopathic hamster was examined with the electron microscope to identify cellular and organelle changes during the acute lesioning stage, a period typified by concomitant cardiocyte destruction and calcium elevation. Most cardiocytes retained their normal histologic and ultrastructural features, but scattered foci of altered and necrotic cells were observed in association with degenerative calcifying lesions. Prenecrotic alterations of myocytes included cellular edema; varying degrees of distension of sarcoplasmic reticulum and T-tubules; contraction bands and other myofibrillar abnormalities; mitochondrial clustering and hyperplasia; a wide spectrum of mitochondrial changes such as altered sizes, shapes, and cristal patterns, and increases in the number and size of osmiophilic matrix inclusions. Morphologic features consistent with substantial calcium excess were not observed in most altered but prenecrotic cells. Instead, calcium deposition within extruded mitochondria and upon degenerating organelle debris was observed only after cardiocyte disruption. Some calcifying cell remnants were phagocytized by macrophages, whereas large calcified plaques and other deposits remained in the interstitium. Mitochondrial calcification in vascular smooth muscle cells and fibroblasts was evident in highly calcified lesions. These observations suggest that most of the morphologically identifiable calcium deposition present in this cardiomyopathy results from secondary calcification subsequent to sarcolemmal disruption.

Age Factors↗
PubMed2005

Inducers and inhibitors of biomineralization: lessons from pathological calcification.

OBJECTIVES: Ectopic calcification is a common response to soft tissue injury and systemic mineral imbalance and can lead to devastating clinical consequences when present in joints, heart valves and blood vessels. We have hypothesized that mineralization of matrices in any tissue is normally controlled by a balance between procalcific and anticalcific regulatory proteins such that abnormal deposition of apatite is avoided. Alterations in this balance induced by injury, disease or genetic deficiency are postulated to induce ectopic mineral deposition. Over the past several years, we have developed in vitro and in vivo models of ectopic calcification to investigate potential inducers and inhibitors of this process. RESULTS: Osteopontin, a secreted phosphoprotein, has emerged as a major inhibitor of ectopic mineralization. Osteopontin is a potent inhibitor of vascular cell calcification in vitro and mice lacking osteopontin are highly susceptible to ectopic calcification. Furthermore, osteopontin treatment of biomaterials protected against ectopic mineralization. Our studies indicate that in addition to inhibiting apatite crystal initiation and growth, osteopontin stimulates resorption of ectopic calcification via peripheral macrophages and giant cells. In contrast, inorganic phosphate has emerged as a major inducer of mineralization in these systems. Elevated inorganic phosphate (Pi) was shown to induce smooth muscle cell matrix calcification with morphological properties similar to those observed in calcified human valves and atherosclerotic plaques. Furthermore, mineralization induced by inorganic phosphate was dependent on the activity of the sodium-dependent phosphate cotransporter, Pit-1. CONCLUSIONS: These studies implicate controlled, transcellular transport of Pi as a major requirement for matrix calcification.

Animals↗
PubMed2000

Vascular smooth muscle and arterial calcification.

Smooth muscle cultures can calcify under certain circumstances. As a model system these cultures therefore provide information on why calcification occurs in atherosclerotic plaques. Whether all smooth muscle cells (under certain conditions), or only specific populations, can produce this mineralization has not been resolved. Demer's group has cloned calcifying vascular cells from subcultured bovine aorta and studied them in detail. They have speculated on whether the cells are smooth muscle which have altered in phenotype, or whether they are derived from a stem cell population within the artery wall. The article argues that while the normal process of smooth muscle phenotypic modulation seen in arterial repair could account for the observations, this view may be two simplistic considering the complex nature of the artery wall. Certainly there is evidence for heterogeneity of smooth muscle cells in the artery wall and recent evidence suggests that stem cells can circulate in the blood and repopulate tissues. Further studies are required to resolve the important question as to the origin of cells which produce mineralization in atheroma.

Animals↗
PubMed2005

[Progress in research on function and mechanism of cardiac vascular system of taurine].

The function for cardiac vascular system of taurine is extensive, and the mechanism is complicated. Taurine protects the cells from the cell injury caused by ischemia etc. Through repressing apoptosis, prevents endothelial dysfunction caused by hyperglycemia, hypercholesterolemia, smoking and homocysteine; suppresses the proliferation and calcification in vascular smooth muscle cells, promotes metabolization and excretion of cholesterol in the animal models of hyperlipemia, and confers the resistance to an oxidant, hypochlorous acid, produced by neutrophil on cells, and taurine chrolamine to inhibit activation of NF-kappaB, which might be associated with anti-atherosclerotic effect. Taurine mainly acts inside the cell. However, taurine transport system becomes aberrant in pathological myocardial and vascular tissue. In addition, taurine improves cardiovascular function in fructose-induced hypertension and an iron-overload murine animal models.

Animals↗
PubMed1980

The origin and significance of thyroid psammoma bodies.

We have used ultrastructural techniques to study the pathogenesis of calcifications and psammoma bodies in human thyroid disorders. Particular attention was paid to psammoma bodies associated with papillary thyroid carcinoma which were found to represent the end stages of two different biologic events. The one event took place in the vascular stalk of the neoplastic papillae, starting with a thickening of the base lamina followed by a vascular thrombosis, calcification, and tumor cell necrosis. In the other, intralymphatic tumor thrombi in the thyroid adjacent to the main tumors or in the opposite thyroid lobe became necrotic and calcified. In some instances, destruction of the lymphy vessels led to fibrin exudation and perilymphatic fibrosis. The laminated bodies seen inside thyroid follicles in some nonneoplastic conditions were found to represent inspissated colloid and not considered to be true psammoma bodies. Like the amyloid calcifications seen in medullary carcinoma and the stromal calcospherites seen in several conditions, they seem to lack diagnostic importance. Our findings emphasize the biologic importance of the events leading to psammoma body formation and explain how they may contribute to the indolent course of this type of cancer.

Carcinoma↗
PubMed2001

Arterial calcifications, arterial stiffness, and cardiovascular risk in end-stage renal disease.

To test the predictive values of and independent contributions to cardiovascular and all-cause mortality of various arterial parameters exploring characteristics of the arterial wall at different sites, we studied prospectively 110 stable end-stage renal disease patients on hemodialysis. These parameters involved carotid diameter, carotid intima-media thickness, carotid compliance, carotid distensibility, carotid incremental elastic modulus, aortic diameter, aortic pulse wave velocity, and the presence of arterial calcifications measured at the sites of the carotid artery, abdominal aorta, iliofemoral axis, and legs. The presence of calcifications was analyzed semiquantitatively as a score (0 to 4) according to the number of arterial sites with calcifications. During a follow-up of 53+/-21 months (mean+/-SD), 25 cardiovascular and 14 noncardiovascular deaths occurred. In univariate analysis, the carotid incremental elastic modulus was the most closely related to prognosis. Risk of death increased with the number of vascular sites involved by calcifications. Moreover, information (in terms of prediction) given by carotid elastic incremental modulus was additive to the presence and extent of vascular calcification-related prediction value. Adjusted hazard ratios of all-cause and cardiovascular mortality for an increase of 1 unit in calcification score were 1.9 (95% confidence interval [CI], 1.4 to 2.6) and 2.6 (95% CI, 1.5 to 4.4), respectively (P<0.001 for both). Adjusted hazard ratios of all-cause and cardiovascular mortality for a 1-SD increase in carotid incremental elastic modulus were 1.6 (95% CI, 1.2 to 2.2) and 1.7 (95% CI, 1.2 to 2.4), respectively (P<0.01 for both). The results of this study showed that the presence and extent of vascular calcifications were strong predictors of cardiovascular and all-cause mortality. Carotid incremental elastic modulus gave additional predictive value.

Adult↗
PubMed2005

Evaluation and management of pain in patients with Klippel-Trenaunay syndrome: a review.

Klippel-Trenaunay syndrome (KTS) is a rare disorder that consists of a triad of capillary vascular malformation, venous malformations and/or varicose veins, and soft tissue and/or bony hypertrophy. Pain is a real and debilitating problem in these patients. We have observed 9 common causes of pain in KTS: (1) chronic venous insufficiency, (2) cellulitis, (3) superficial thrombophlebitis, (4) deep vein thrombosis, (5) calcification of vascular malformations, (6) growing pains, (7) intraosseous vascular malformation, (8) arthritis, and (9) neuropathic pain. The management of pain in patients with KTS depends on its cause. These patients are best evaluated initially in a center with an experienced multidisciplinary team that includes a primary health care provider, surgeons, and ancillary staff. The ongoing care of a patient with KTS often depends on a local provider who is more readily accessible to the patient but may not have the expertise of a large center to manage the complications of KTS. The purpose of this communication is to review the common causes of pain in these patients to provide local health care providers and patients and their families with appropriate management strategies.

Analgesics↗
PubMed2002

Carotid calcification on panoramic radiographs: an important marker for vascular risk.

OBJECTIVE: The objective of this study was to determine whether carotid calcifications are harbingers of future vascular events. STUDY DESIGN: Between 1986 and 2000, 71 patients were found to have carotid artery calcifications on routine panoramic films. Medical records were reviewed for vascular risk factors existing before and vascular end points subsequent to the radiographs. RESULTS: The mean age of our patients was 68 years. Sixty-one (86%) had preexisting vascular risk factors, 73% with multiple risk factors. Forty-one end points occurred in 29 patients. The average time to an end point was 2.7 years. The end points included myocardial infarction (8, 11%), stroke (5, 7%), death (11, 15%), revascularization procedures (8, 11%), transient ischemic attack (2, 3%), and angina (7, 10%). Twenty-three patients (34%) had major end points of myocardial infarction, stroke, or death. CONCLUSIONS: Carotid calcifications identified on panoramic radiographs are powerful markers for subsequent vascular events. Patients found to have carotid calcification on panoramic radiographs should be referred for cerebrovascular and cardiovascular evaluation and aggressive management of vascular risk factors.

Aged↗
PubMed2005

[The role of calcium ions in the pathomechanism of the artery calcification accompanying atherosclerosis].

Artery calcification occurring in atherosclerosis is connected with a high risk of cardiovascular events. Quantitative calcification evaluation using electron beam tomography indicated a correlation between artery calcification and well-known cardiovascular risk factors, i.e. smoking, obesity, and hyperlipidemia. Elevated calcium scores are especially observed in diabetic patients, which may even explain the higher mortality in this group. Calcification leads to increased blood vessel rigidity and, consequently, elevated arterial vascular resistance and left ventricular hypertrophy. An increased risk of plaque rupture in relation to calcium-rich atherosclerotic lesions was not proved. Plaque rupture and thromboembolitic complications are probably higher in the case of lipid-rich lesions. Atherosclerotic calcification is an active process in which many cells (monocytes/macrophages, vascular smooth muscle cells, and endothelial cells) participate. Many substances and transcription factors normally participating in the bone remodeling process are found in calcified atherosclerotic lesions (e.g. Cbfa-1, osteocalcin, alkaline phosphatase, BMP-2, osteopontin, osteoprotegrin, and RANKL). On monocytes, cells playing an important role in atherosclerosis progression, the presence of a calcium-sensing receptor (CaR) has been demonstrated. Increase in monocyte chemotaxis and increased interleukin 6 secretion in response to extracellular calcium were observed. Monocytes also directly and indirectly enhance vascular calcification. Immune cells and cytokines participating in vascular calcification are connected in one pathogenetic mechanism, i.e. atherosclerosis as an inflammatory disease and calcification.

Animals↗
PubMed1995

Matrix proteins associated with bone calcification are present in human vascular smooth muscle cells grown in vitro.

Atherosclerotic lesions are composed of cellular elements that have migrated from the vessel lumen and wall to form the cellular component of the developing plaque. The cellular elements are influenced by various growth-regulatory molecules, cytokines, chemoattractants, and vasoregulatory molecules that regulate the synthesis of the extracellular matrix composing the plaque. Because vascular smooth muscle cells (VSMC) constitute the major cellular elements of the atherosclerotic plaque and are thought to be responsible for the extracellular matrix that becomes calcified in mature plaques, immunostaining for collagenous and noncollagenous proteins typically associated with bone matrix was conducted on VSMC grown in vitro. VSMC obtained from human aorta were grown in chambers on glass slides and immunostained for procollagen type I, bone sialoprotein, osteonectin, osteocalcin, osteopontin, decorin, and biglycan. VSMC demonstrated an intense staining for procollagen type I, and a moderately intense staining for the noncollagenous proteins, bone sialoprotein and osteonectin, two proteins closely associated with bone mineralization. Minimal immunostaining was noted for osteocalcin, osteopontin, decorin, and biglycan. The presence in VSMC of collagenous and noncollagenous proteins associated with bone mineralization suggest that the smooth muscle cells in the developing atherosclerotic plaque play an important role in the deposition of the extracellular matrix involved in calcification of developing lesions.

Biglycan↗
PubMed2004

Observations from multidetector CT imaging of different types of renal artery stents.

PURPOSE: To present an optimized protocol for acquisition and reconstruction of multidetector computed tomographic angiographic (CTA) images of the stents most commonly used in renal arteries. TECHNIQUE: CTA was performed on a 16-detector row CT scanner using 0.75-mm collimation. Multiplanar reformatted images perpendicular to the stents and 2-dimensional curved reformatted images were displayed. Two different view windows ("vascular" and "stent") were used, each adapted to the stent density, the vascular wall density, and the aortic enhancement. Five different types of stainless steel balloon-expandable stents were examined; all caused discernable artifacts. These artifacts became more prominent as the stent density increased, becoming most significant when 2 stents were positioned one inside the other. The "stent" window allowed better appreciation of the stent shape and its position compared to the aortic wall and ostial calcifications. The "vascular" window afforded a better view of the vascular lumen, in addition to visualizing the stent in several planes. CONCLUSIONS: Multidetector CTA using dedicated acquisition and reconstruction protocols is capable of visualizing the vascular lumen of different types of renal stents while avoiding metallic artifacts.

Angiography↗
PubMed1984

Cell injury and calcification of rat aorta in vitro.

In order to study the mechanism of dystrophic calcification of vascular connective tissue as a result of cell injury, anoxic incubation and organ culture in CMRL 1066 of fresh and freeze thawed rat aorta and serum incubation of fresh rat aorta were performed. Calcium concentration of the culture medium was adjusted to 2.5mM and phosphate to 0.9mM. Calcium depletion from the culture medium continued for 3 weeks and then plateaued. In every experiment, calcification was seen predominantly in association with the membranous cellular degradation products derived from degenerated smooth muscle cells. These were morphologically similar to the matrix vesicles. In the areas of massive necrosis, particularly in the freeze thawed aortic tissue, massive calcification extending to collagen and elastic fibers was seen. Of the various membranous cellular degradation products, mitochondrial inner membrane also appeared to serve as one of the nidi of calcification. Influx of extracellular Ca2+, which results from suppression of ion pumps upon cell injury, to PO4(3-) rich cytosol is thought to play a pivotal role in dystrophic calcification. Phosphatidyl serine located along the inner surface of the plasma membrane or the membranous vesicle may serve as the substrate for heterogeneous nucleation of apatite. Calcification of the cellular degradation products which was more pronounced in freeze thawed aorta is apparently non-energy dependent. Calcification of the elastic and collagen fibers evidently occurs as an extension from the calcified cellular degradation products.

Animals↗
PubMed2026

Proteomic Mediators of Chronic Obstructive Pulmonary Disease Phenotypes and Coronary Artery Calcification Burden in Ever Smokers.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) increases cardiovascular disease risk. Coronary artery calcification (CAC) predicts cardiovascular events and mortality in COPD. We hypothesized that plasma proteins linked to pulmonary phenotypes mediate CAC burden. METHODS: Pulmonary function, emphysema, airway wall thickening, Agatston CAC scores (inverse normal transformed), and relative abundance of 1305 plasma proteins (log-transformed) were assessed in 989 Phase 1 COPDGene (Genetic Epidemiology of COPD) participants. Proteins associated with both pulmonary phenotypes (FEV1[forced expiratory volume in 1 second]%predicted, FVC [forced vital capacity], FEV1/FVC, emphysema, airway wall thickness, wall area percentage) and CAC (false discovery rate P&#x2264;0.20) were evaluated using multivariable mediation. Model adjustments included sex, age, race, body mass index, smoking, comorbidities, and medications. Adjustment for pulmonary artery-to-aortic diameter ratio-a marker of pulmonary vascular pressure-was also explored. The95% bootstrap CIs that excluded zero were considered significant. RESULTS: FEV1%predicted (P=0.026) and FEV1/FVC (P=0.010) were associated with CAC. After adjusting for FEV1, visual emphysema, and visual airway wall thickening remained associated with CAC. Five proteins (TSP2 [thrombospondin-2], renin, MMP-7 [matrix metalloproteinase-7], ERBB1 [epidermal growth factor receptor], MIC-1 [macrophage inhibitory cytokine-1]) mediated the FEV1%predicted and CAC association. All except MIC-1 mediated FEV1/FVC and CAC. All except renin mediated quantitative airway wall thickness or wall area percentage and CAC. Additionally, &#x3b1;2-antiplasmin (alpha-2 antiplasmin) mediated airway wall thickness and CAC. ERBB1 mediated visual paraseptal emphysema and CAC. Pulmonary artery-to-aortic diameter ratio adjustment reduced or eliminated some mediation effects. ERBB1 remained an independent mediator across multiple phenotypes. CONCLUSIONS: Six plasma proteins mediated associations between COPD phenotypes and CAC burden. These effects were partially influenced by pulmonary artery-to-aortic diameter ratio A, suggesting shared molecular pathways linking lung dysfunction to cardiovascular risk in COPD.

Humans↗
PubMed2026

Comparison of Performance of Publicly Available Polygenic Risk Scores to Predict Clinically Actionable Coronary Artery Calcium Scores: The BioHEART-CT Cohort.

AIM: Coronary artery disease (CAD) remains the leading cause of morbidity and mortality globally. Polygenic Risk Scores (PRS) have been trained against major adverse cardiovascular outcomes (MACE) in large cohorts. Few studies have examined the effectiveness of these CAD MACE PRS tools in detecting individuals with subclinical coronary calcification. An association would provide an opportunity for clinical translation and targeting of CT imaging to new patients at risk for subclinical disease. METHODS: An analysis of 53 publicly available CAD PRS tools was completed in participants of the BioHEART-CT Discovery 1000 cohort presenting for clinically referred CT coronary angiography (CCTA). Associations between PRS and two binary CACS outcomes reflecting clinically significant coronary calcification were assessed: a) Absolute CACS (CACS &#x2265;100 Agatston units [AU]; and b) Percentile CACS (CACS &#x2265;75th age-/sex-adjusted percentile). Models were adjusted for genetic principal components, modifiable cardiovascular risk factors, and age/sex (in Absolute CACS). A subgroup analysis was performed using Framingham Risk Score (FRS) at baseline. RESULTS: Among 803 BioHEART-CT Discovery 1000 participants, 487 (60.6%) had any detectable coronary calcium. Most PRS tools demonstrated significant association with CACS outcomes, particularly evident when PRS was modelled as a continuous predictor. For Percentile CACS, 94.3% of PRS tools were significantly associated after full adjustment (median OR per PRS SD 1.41 (IQR 1.23-1.60). Quintile-based analysis revealed that individuals in the Top Quintile PRS had up to 7.99-fold increased odds of Percentile CACS &#x2265;75th compared to those in the Bottom Quintile. Analysis by FRS group revealed positive performance, especially in individuals of Low FRS wherein incorporating a PRS increased pre-test probability from 14% to 26%. CONCLUSION: Whilst most CAD PRS tools have been developed against clinical events, we show their ability to predict clinically relevant coronary calcification. Utility appears strongest in individuals traditionally considered lower risk, presenting an opportunity for clinical translation for improved diagnosis in the primary prevention setting, with the potential to triage individuals into a CACS screening pathway.

coronary artery disease↗