Search Results (235)

Background/Objectives: Nowadays, intravascular lithotripsy (IVL) has emerged as a novel technique for treatment of vascular calcifications, first in coronary and then in peripheral arteries. In the current literature there is little evidence that describes IVL as an effective and safe solution in treating severe aortic and aorto-iliac calcifications. The aim of this study is to report current available data about the use of IVL in treating aortic and aorto-iliac calcified lesions and its application in facilitating other endovascular procedures. Methods: the present review was conducted and reported in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) Guidelines. Preliminary searches were conducted on MEDLINE and Pubmed from January 2015 to February 2025. Studies were divided into 3 main categories depending on the location of calcifications and the type of treatment: IVL in visceral and infrarenal obstructive disease (group 1), IVL in aorto-iliac obstructive disease (group 2), IVL used to facilitate other endovascular procedures. Main primary outcomes in the perioperative period were technical and clinical successes and perioperative complications. Primary outcomes at 30 days and mid-term (2 years) were overall survival, limb salvage rate, primary patency, primary assisted patency, secondary patency, and residual stenosis. Results: Sixteen studies were identified for a total of 1674 patients. Technical and clinical successes were 100%, with low rates of perioperative complications. Dissection rate reaches up to 16.1% in some studies, without any differences compared to plain old balloon angioplasty (POBA) alone (22.8%; p = 0.47). At 30 days, limb salvage and survival rates were 100%. At 2 years, primary patency, assisted primary patency, and secondary patency were 95%, 98%, and 100%, respectively, with no difference compared to IVL + stenting. Conclusions: IVL has emerged as a novel approach to treat severe calcified lesions in visceral and aorto-iliac atherosclerotic disease and to facilitate other endovascular procedures. This technique seems to offer satisfactory early and mid-term outcomes in terms of primary, primary assisted patency, and secondary patency with low complication rates. Full article

Background: Delirium is a common, underdiagnosed neuropsychiatric syndrome in older adults, associated with high mortality and functional decline. Given its multifactorial nature and overlap with frailty, radiological markers may improve risk stratification in the emergency department (ED). Methods: We conducted a retrospective study on a small sample of 30 patients diagnosed with delirium in the emergency department who had recently undergone brain, thoracic, or abdominal CT scans for unrelated clinical indications. Using post-processing software, we analyzed radiological markers, including coronary artery calcifications (to estimate vascular age), cerebral atrophy (via the Global Cortical Atrophy scale), and cachexia (based on abdominal fat and psoas muscle volumetry). Results: Five domains were identified as significant predictors of 12-month mortality in univariate Cox regression: vascular age, delirium etiology, cerebral atrophy, delirium subtype (hyperactive vs. hypoactive), and cachexia. Based on these domains, we developed an exploratory 10-point delirium score. This score demonstrated acceptable diagnostic accuracy for mortality prediction (sensitivity 0.93, specificity 0.73, positive predictive value 0.77, negative predictive value 0.91) in this limited cohort. Conclusions: While preliminary and based on a small, retrospective sample of 30 patients, this multidimensional approach integrating clinical and radiological data may help improve risk stratification in elderly patients with delirium. Radiological phenotyping, particularly in terms of vascular aging and sarcopenia/cachexia, offers objective insights into patient frailty and could inform more personalized treatment pathways from the ED to safe discharge home, pending further validation. Full article

Background and Objectives: Galectin-3 (Gal-3), a pro-inflammatory cytokine, has been implicated in atherosclerosis and adverse cardiovascular outcomes. While its role in coronary artery disease (CAD) is increasingly recognized, its association with systemic atherosclerosis remains underexplored. Objective: To investigate serum Gal-3 levels in patients with CAD and evaluate correlations between CAD severity and extra-coronary atherosclerotic involvement (carotid, femoral, and radial territories). Materials and Methods: We prospectively enrolled 56 patients with CAD undergoing coronary angiography (42.8% with acute-ACS; 57.2% with chronic coronary syndromes-CCS). Gal-3 levels were measured within 24 h of admission. Atherosclerosis severity was assessed angiographically and through vascular ultrasound of the carotid, femoral, and radial arteries. Patients were stratified by median Gal-3 levels, and clinical follow-up was performed at 1 and 3 months. Results: Gal-3 levels were significantly higher in CAD vs. controls (20.7 vs. 10.1 ng/mL; p < 0.00001) and in ACS vs. CCS (22.18. vs. 17.93 ng/mL; p = 0.019). Gal-3 correlated positively with culprit lesion diameter stenosis (DS) (R = 0.30; p = 0.023) and maximum severity of additional treated lesions (R = 0.62; p = 0.006). Gal-3 also correlated positively with carotid plaque thickness (R = 0.32; p = 0.016), while patients with Gal-3 levels above the median showed increased median values for femoral plaque thickness (32.4 vs. 26.45 mm, p = 0.046). No correlation was found with radial artery calcification. Gal-3 showed moderate discrimination for ACS (AUC = 0.685; cut-off 20.18 ng/mL). On multivariate analysis age, DS, and ACS presentation were independent predictors of Gal-3 above 19.07 ng/mL. Conclusions: Gal-3 levels are elevated in ACS and correlate with atherosclerotic burden, particularly in coronary, carotid, and femoral territories. These findings support Gal-3 as a potential marker of lesion severity and systemic vascular involvement, highlighting its possible role in risk stratification and the monitoring of atherosclerotic disease progression. This study provides integrated insights into the impact of Gal-3 across multiple vascular beds by assessing them concurrently within the same patient cohort. Full article

Background/Objectives: Bisphosphonates may influence vascular calcification and atheroma formation via farnesyl pyrophosphate synthase inhibition in the mevalonate pathway regulating bone and lipid metabolism. However, the clinical impact of NCB use on cardiovascular outcomes remains uncertain, largely due to methodological heterogeneity in prior studies. We aimed to evaluate the association between nitrogen-containing bisphosphonate (NCB) therapy and coronary artery calcium (CAC) progression, as well as the incidence of cardiovascular disease (CVD) and coronary heart disease (CHD) events. Methods: From 6814 participants in MESA Exam 1, we excluded males (insufficient male NCB users in the MESA cohort), pre-menopausal women, baseline NCB users, and users of hormone replacement therapy, raloxifene, or calcitonin. Among 166 NCB initiators and 1571 non-users with available CAC measurements, propensity score matching was performed using the available components of FRAX, namely age, race, BMI, LDL cholesterol, alcohol, smoking, and steroid use, and baseline CAC yielded 165 NCB initiators matched to 473 non-users (1:3 ratio). Linear mixed-effects models evaluated CAC progression, and Cox models analyzed incident CVD and CHD events. Results: In the overall cohort, NCB use was not significantly associated with CAC progression (annual change: −0.01 log Agatston units; 95% CI: −0.05 to 0.01). However, among participants with a baseline estimated glomerular filtration rate (eGFR) < 65 mL/min/1.73 m², NCB use was associated with attenuated CAC progression compared with non-users (−0.06 log Agatston units/year; 95% CI: −0.12 to −0.007). No significant association was observed between NCB use and incident CVD events in the overall cohort (HR: 0.90; 95% CI: 0.60−1.36) or within kidney function subgroups. Conclusions: Incident NCB use among postmenopausal women with mild or no CAC at baseline was associated with reduced CAC progression only in women with impaired kidney function. However, this association did not correspond to a decreased risk of subsequent cardiovascular events, suggesting that the observed imaging benefit may not translate into meaningful clinical association. Full article

Background/Objectives: Patients with chronic kidney disease (CKD) are associated with a significantly elevated cardiovascular risk. The incidence and prevalence of mediated cardiac disorders and major adverse cardiac events (MACEs), such as heart failure, arrhythmias, acute coronary syndrome (ACS) based on coronary artery disease (CAD), stroke, venous thromboembolism, and peripheral artery disease, are significantly higher in CKD patients as compared with the general population. Methods: This narrative review summarizes the current clinical understanding, the pathophysiological mechanisms, and the clinical consequences in the context of cardiovascular risk and disease in CKD. Results: The impact of CKD on mediated cardiovascular disorders and elevated MACE prevalence is complex and multifactorial. The underlying mechanisms involve various traditional cardiovascular risk factors, such as arterial hypertension, smoking, dyslipidemia, and diabetes. Furthermore, CKD-specific molecular and pathophysiological factors, such as chronic inflammation and associated oxidative stress and endothelial cell dysfunction, pro-coagulatory status, uremic toxins and uremic lipids, progressive vascular calcification, and alterations in the regulation of the renin–angiotensin–aldosterone system (RAAS) and sympathetic activation cause an increased cardiovascular risk. Conclusions: Understanding the complex disease mechanisms between CKD and elevated cardiovascular risk might contribute to optimizing individual patients’ risk stratification and result in individualized diagnostic and treatment strategies via appropriate clinical biomarker application and individualized anti-inflammatory approaches. Full article

Mitral annular calcification (MAC) is usually considered an incidental, benign, age-related finding without serious complications in patients evaluated for cardiovascular or pulmonary disease with imaging studies that may result in mitral regurgitation or stenosis when severe. Therefore, it is usually not considered a significant alteration. However, there is accumulating evidence that it is associated with a higher risk of cardiovascular events, such as atherosclerotic coronary artery disease, aortic artery disease, carotid artery disease, peripheral artery disease, stroke, atrial fibrillation, atrioventricular and/or intraventricular conduction disturbance, systemic embolization, infective endocarditis, heart failure and mortality. The presence of MAC also significantly influences the outcome of mitral valve transcatheter and surgical interventions. Several conditions may predispose to MAC. MAC is strongly related to cardiovascular risk factors, such as hypertension, diabetes, smoking and cardiovascular atherosclerosis, and inflammation may also play a role in the pathogenesis of MAC. Also, conditions that increase mitral valve stress, such as hypertension, aortic stenosis and hypertrophic cardiomyopathy, predispose to accelerated degenerative calcification of the mitral annulus area. Congenital disorders, e.g., Marfan syndrome and Hurler syndrome, are also associated with MAC, due to an intrinsic abnormality of the connective tissue composing the annulus. Full article

Calcium (Ca²⁺) signaling is a fundamental regulatory mechanism controlling essential processes in the endothelium, vascular smooth muscle cells (VSMCs), and the extracellular matrix (ECM), including maintaining the endothelial barrier, modulation of vascular tone, and vascular remodeling. Cytosolic free Ca²⁺ concentration is tightly regulated by a balance between Ca²⁺ mobilization mechanisms, including Ca²⁺ release from the intracellular stores in the sarcoplasmic/endoplasmic reticulum and Ca²⁺ entry via voltage-dependent, transient-receptor potential, and store-operated Ca²⁺ channels, and Ca²⁺ elimination pathways including Ca²⁺ extrusion by the plasma membrane Ca²⁺-ATPase and Na⁺/Ca²⁺ exchanger and Ca²⁺ re-uptake by the sarco(endo)plasmic reticulum Ca²⁺-ATPase and the mitochondria. Some cell membranes/organelles are multifunctional and have both Ca²⁺ mobilization and Ca²⁺ removal pathways. Also, the individual Ca²⁺ handling pathways could be integrated to function in a regenerative, capacitative, cooperative, bidirectional, or reciprocal feed-forward or feed-back manner. Disruption of these pathways causes dysregulation of the Ca²⁺ signaling dynamics and leads to pathological cardiovascular conditions such as hypertension, coronary artery disease, atherosclerosis, and vascular calcification. In the endothelium, dysregulated Ca²⁺ signaling impairs nitric oxide production, reduces vasodilatory capacity, and increases vascular permeability. In VSMCs, Ca²⁺-dependent phosphorylation of the myosin light chain and Ca²⁺ sensitization by protein kinase-C (PKC) and Rho-kinase (ROCK) increase vascular tone and could lead to increased blood pressure and hypertension. Ca²⁺ activation of matrix metalloproteinases causes collagen/elastin imbalance and promotes vascular remodeling. Ca²⁺-dependent immune cell activation, leukocyte infiltration, and cholesterol accumulation by macrophages promote foam cell formation and atherosclerotic plaque progression. Chronic increases in VSMCs Ca²⁺ promote phenotypic switching to mesenchymal cells and osteogenic transformation and thereby accelerate vascular calcification and plaque instability. Emerging therapeutic strategies targeting these Ca²⁺-dependent mechanisms, including Ca²⁺ channel blockers and PKC and ROCK inhibitors, hold promise for restoring Ca²⁺ homeostasis and mitigating vascular disease progression. Full article

Background/Objectives: In 2024, Lithuania developed a national lung cancer screening program (the Program), targeting individuals aged 50 to 70 years, regardless of their smoking history, with screenings conducted once every three years. The Program aims not only to actively detect lung nodules (lung cancer) but also to identify clinically significant concomitant findings. The pilot study aimed to evaluate the screening process’s feasibility and organizational efficiency of the screening process, as well as its potential clinical effectiveness. Methods: Three family medicine centers were selected for participation. The Coordinating Center contacted individuals aged 50 to 70 sequentially and invited them to participate, regardless of smoking status. In total, 1014 individuals were prospectively enrolled and underwent low-dose chest computed tomography (LDCT) screening between 26 September 2024 and 14 February 2025. Results: Of the individuals invited, 76.1% agreed to participate. Lung-RADS v2022 category 4 nodules were identified in 1.4% of participants (n = 14), including six smokers and eight non-smokers. Additionally, one participant with a Lung-RADS category 2 nodule was diagnosed with squamous cell carcinoma originating from peripheral lung changes. Newly identified significant incidental findings were detected in 25.9% of participants: 5.1% had pulmonary or mediastinal findings (most commonly emphysema, interstitial lung changes, and bronchiectasis), 18.7% had cardiovascular findings (usually coronary artery calcification, aortic valve calcification, and aorta dilation), and 2.1% had other clinically relevant conditions (e.g., thyroid nodules, diaphragmatic changes). Following assessment by family physicians, 17.6% of all participants were referred to medical specialists, including pulmonologists, cardiologists, and others. Conclusions: This pilot study demonstrated that the Lithuanian lung cancer screening model is feasible, well-organized, and clinically valuable. The findings support the Program’s readiness for broader implementation at the national level. Full article

Background/Objectives: Given the conflicting results and limited published data on the correlation of vitamin A, E, and D, parathyroid hormone (PTH), and thyroid-stimulating hormone (TSH) levels, the triglyceride to high-density lipoprotein (TG/HDL) ratio, and glucose levels with the coronary artery calcium score (CAC score) in individuals at risk of coronary artery disease (CAD), this relationship requires extensive investigation. Therefore, our study aimed to investigate the correlations between the aforementioned metrics and the CAC score in individuals at risk of CAD in Saudi Arabia. Methods: This analytical cross-sectional study was conducted at the Department of Physiology, College of Medicine at King Saud University Medical City (KSUMC), King Saud University, Riyadh, Saudi Arabia, between November 2024 and April 2025, targeting patients at risk of CAD. After recruiting patients from cardiology and primary care clinics, data regarding blood vitamin A, E, and D and PTH and TSH levels and CAC scores were collected from each patient’s electronic medical records. A score of 10 points was used as a cutoff between low and high CAC scores. Results: Our sample size was 172 patients. The majority of the patients were male (62.2%), and 37.8% were female. The mean age of the sample was 59.98 ± 9.26 years, with an age range spanning 40 years. Serum vitamin A levels had a significant negative correlation with CAC scores, (odds ratio (OR) = 0.147, p-value = 0.002), whereas vitamin D and E, PTH, and TSH levels did not correlate with this score. The TG/HDL ratio was positively and significantly correlated with CAC scores (OR = 1.654, p-value = 0.030). The analysis model showed that a patient’s mean serum glycated hemoglobin (HbA1c) level positively and significantly influenced their odds of having a high CAC score (OR = 1.364, p-value = 0.018). Patient ethnicity was not significantly associated with the CAC score (CAC ≥ 10 points) (p = 0.749). Similarly, BMI did not correlate with the CAC score (p = 0.722). However, male patients were 3.42 times more likely than females to have a high CAC score (CAC ≥ 10 points), a statistically significant difference (p = 0.005). No significant differences were observed between males and females in terms of their mean vitamin A (1.74 ± 0.58 vs. 1.80 ± 0.52, p = 0.633), vitamin E (41.41 ± 15.99 vs. 37.61 ± 11.78, p = 0.189), or vitamin D levels (80.35 ± 31.07 vs. 77.16 ± 26.15, p = 0.479). Additionally, the patient’s age was significantly positively associated with the likelihood of having a high CAC score, with OR = 1.102 times (p < 0.001). Conclusions: The findings of our study indicate the strong impact of vitamin A, the TG/HDL ratio, and HbA1c on CAC scores, among other factors affecting CAC scores, and they need more concern and attention. Understanding the cellular mechanism of vitamin A correlation with calcification is of great clinical value. The TG/HDL ratio is emerging as a novel index for CVD when compared to other lipid profile parameters. Intensive large-scale studies are needed to explore the interpretations as well as cutoff values of this valuable index. Males are more prone to CVD due to their high correlation with CAC scores. Therefore, vitamin A administration and strict HbA1c and TG/HDL ratio monitoring could help as prophylactic measures to prevent cardiovascular disease in these patients. These findings could influence specific preventive measures or screening strategies for cardiovascular disease in high-risk populations. A lifestyle medicine approach that involves caregivers as well as patients should be implemented to minimize the incidence and complications of detrimental diseases. Full article

Background and Objectives: To examine individual-level sex differences in traditional and non-traditional risk factors and their potential effects on the severity of coronary artery disease (CAD). Materials and Methods: A cross-sectional analysis was performed on 208 patients with a low-to-intermediate pretest probability of CAD, referred to a Coronary CT angiography (CCTA) at the Department of Radiology, Maribor University Medical Centre, from January 2022 to January 2024. CCTA-derived EAT (epicardial adipose tissue) attenuation and CAC (coronary artery calcification) values were measured. The association between CAD, EAT, and risk factors was analyzed by sex, using correlation analysis and multivariate regression. Results: In the results obtained using the univariate logistic regression model, age (OR 1.122, p < 0.001) and hypertension (OR 4.087, p = 0.048) were significantly associated with the presence of obstructive CAD in women, while in men, age (OR 1.052, p = 0.008), hypercholesterolemia (OR 3.765, p = 0.042), and EAT attenuation (OR 1.053, p = 0.011) were significant factors. In results obtained using the multivariable logistic regression analysis model, EAT attenuation was found to be significantly associated with the presence of obstructive CAD in men (OR 1.087, p = 0.012), and age was a significant factor in women (OR =1.108, p = 0.033), while hypertension, body mass index (BMI), diabetes, hypercholesterolemia, angina pectoris, and smoking were not. Conclusions: In the sex-specific multivariable logistic regression analysis model, EAT attenuation was significantly associated with obstructive CAD in men, while in women, it was associated with age. EAT may function as a beneficial alternative indicator in identifying patients with CAD. Full article

Globally, cardiovascular disease is a leading cause of disability and early death, affecting 422.7 million people and causing 17.9 million deaths (31% of global deaths) in 2015. Peripheral arterial disease, previously overlooked compared to coronary artery disease, is now recognised as a major contributor to cardiovascular morbidity and mortality, with distinct characteristics. After noninvasive methods, the femoropopliteal segment is frequently treated with revascularisation, which is recommended for claudication and chronic limb-threatening ischemia (CLTI). Challenges such as mechanical stresses, chronic occlusions, extensive plaque, and calcification affect procedural success and vessel patency. Innovations were needed to address these issues, and vascular drug delivery devices have become integral to endovascular treatment. We review the current literature concerning a diverse range of these devices in clinical use and their role in managing symptomatic patients. Full article

Background/Objectives: High-risk coronary plaques (HRP), identified through coronary CT angiography (CCTA), are closely linked to cardiovascular events. Nutritional status and systemic inflammation may play a critical role in the development of HRP. The Naples Prognostic Score (NPS), which integrates markers of nutritional status and systemic inflammation, has emerged as a potential predictor of outcomes in various cardiovascular conditions. This study aimed to investigate the association between NPS and HRP as assessed by CCTA. Methods: A retrospective analysis was performed on 753 patients with chronic coronary syndrome (CCS) who underwent CCTA. The patients were categorized into two groups: those with high-risk plaques (HRP present), and those without (HRP absent). Additionally, they were further stratified based on their NPS. Univariable and multivariable logistic regression analyses were conducted to identify the most relevant clinical factors and the role of NPS in relation to HRP and the need for revascularization. Results: The study population had a mean age of 56.9 ± 10.7 years, with 40% being female. The NPS was significantly higher in the HRP-present group compared to the HRP-absent group (p = 0.001). Stratification by NPS groups revealed that higher NPS groups were associated with increased coronary artery calcification scores (CAC) and revascularization rates (p < 0.001 and p = 0.003, respectively). Multivariable regression analysis demonstrated a significant association between NPS and HRP (OR = 1.228, 95% CI: 1.013–1.489, p = 0.036). Conclusions: The NPS is independently associated with the presence of high-risk coronary plaques in patients with chronic coronary syndrome. NPS may serve as a complementary risk stratification tool by reflecting systemic inflammation and nutritional status. Further prospective studies are needed to validate its prognostic value. Full article

Objective: Patients with chronic inflammatory rheumatic diseases (CIRDs) have a higher incidence of coronary artery disease (CAD) due to accelerated atherogenesis. This study aimed to assess the extent and location of CAD lesions in CIRD patients compared to non-CIRD patients. Methods: A retrospective study was conducted on CIRD patients (rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis) who underwent coronary angiography at Hospital Fundación Jiménez Díaz (Madrid, Spain) between 2018 and 2022. For each CIRD patient, at least two frequency-matched controls were selected based on sex, age (±2 years), diabetic status, and clinical indication for coronary angiography. The indications for coronary angiography in both groups were chronic coronary syndrome and acute coronary syndrome with or without ST elevation. Results: A total of 66 CIRD patients were included, with 42 (63.6%) women, and a median age of 66.6 years (range: 58.3–75.2). Compared to the controls, CIRD patients had a higher number of affected coronary arteries (2.03 vs. 1.56, p = 0.03). The mid-anterior descending artery and the right posterior descending artery were more frequently involved in CIRD patients than in controls (odds ratio [OR] of 2.45 and 3.53, respectively, p ≤ 0.02 for both comparisons). The frequency of coronary calcification was higher in CIRD patients, though the difference did not reach statistical significance (5 of 66 in CIRD patients vs. 3 of 140 in non-CIRD controls, OR of 3.74, p = 0.06). Revascularization was more commonly performed in patients with CIRD (50 of 66 vs. 85 of 140 in those without CIRD (OR: 2.02 [95% CI: 1.01–4.18]; p = 0.03). Conclusions: Patients with CIRD exhibit more extensive CAD, with a higher propensity for involvement inthe mid-anterior descending and right posterior descending arteries compared to patients without CIRD. These findings highlight the need for closer cardiovascular monitoring and early risk stratification in CIRD patients to improve the detection and management of CAD. Full article

People with HIV (PWH) have an increased risk of developing cardiovascular disease (CVD). Our recent data demonstrated that the multi-isoform proinflammatory cytokine IL-32 is upregulated in PWH and is associated with arterial stiffness and subclinical atherosclerosis. However, the mechanisms by which IL-32 contributes to the pathogenesis of these diseases remain unclear. Here, we show that while the less expressed IL-32α isoform induces the differentiation of human classical monocytes into the calcium-resorbing osteoclast cells, the dominantly expressed isoforms IL-32β and IL-32γ suppress this function through the inhibition of TGF-β and induce the differentiation of monocytes into the calcium-depositing osteocalcin+ osteoblasts. These results aligned with the increase in plasma levels of osteoprotegerin, a biomarker of vascular calcification, and its association with the presence of coronary artery subclinical atherosclerosis and calcium score in PWH. These findings support a novel role for the proinflammatory cytokine IL-32 in the pathophysiology of CVD by increasing vascular calcification in PWH. Full article

Background: Patients with heterozygous familial hypercholesterolemia (HeFH) are at a high risk of atherosclerotic cardiovascular disease. The coronary artery calcification (CAC) score by the Ct-scan Agatston calcium score (ACS) > 100 classifies FH at a higher risk. The echocardiographic calcium score (ECS) evaluates aortic valve calcifications and is considered a good predictor of the atherosclerotic burden and cardiovascular outcome. Objective: To test the ECS as a predictor of ACS > 100 in a HeFH cohort. Methods: A coronary calcium CT scan with the calculation of ACS and an at rest-transthoracic echocardiogram with ECS evaluation were performed in 81 HeFH patients. Patients were divided into two groups according to the ACS: high-risk ACS patients (High-ACS) with Agatston value > 100 and low risk ACS patients (Low-ACS) with Agatston value ≤ 100. Patients were stratified according to ECS = 0 or ECS > 0. Results: High-ACS patients were older than Low-ACS patients; BMI, waist circumference, and blood systolic pressure were significantly higher (p < 0.001) in High-ACS patients. The ECS predicted an ACS > 100 with sensitivity = 0.84, specificity = 0.89, accuracy = 0.86, and precision = 0.76. Conclusions: The ECS could be a good surrogate of a coronary calcium CT scan for ACS evaluation in the specific subset of HeFH patients. Full article