Search

Background Left ventricular (LV) remodeling in patients with severe aortic valve stenosis (AS) is a complex process that goes beyond hypertrophic response and may involve reparative/replacement fibrosis. Currently, cardiac magnetic resonance (CMR) is the gold-standard imaging technique for detecting focal myocardial fibrosis through late gadolinium enhancement (LGE). However, myocardial fibrosis prevalence and distribution is quite variable among series. Our goal was to assess LGE prevalence and distribution pattern in severe symptomatic high-gradient AS. Methodology Single-center prospective cohort of 132 patients with severe symptomatic high-gradient AS (mean age 73±11 years; 48% male, mean valvular transaortic gradient 60±20 mmHg; mean aortic valve area 0.7±0.2 cm2/m2; mean LV ejection fraction by 2D echocardiogram 58±9%), all with normal flow (except one) undergoing surgical aortic valve replacement. Those with previous history of acute myocardial infarction, ischemic cardiomyopathy or other cardiomyopathy were excluded. All patients performed 1.5T CMR assessment with LV myocardium tissue characterization prior to surgery. Segmental LGE presence was assessed by two independent operators and classified according to the AHA 16 segment model, using 5-standard deviations from remote myocardium as the signal intensity cut-off for LGE identification and quantification. Results Overall, 96 patients (74%) had non-ischemic LGE (median LGE mass 3.2 g [IQR 0.2–8.3] g; median percentage of LGE myocardial mass 2.5% [IQR 0.1–6.1]%); 22 patients [17%] with exclusively junctional LGE); in one patient an incidental ischemic scar (subendocardial distribution) was identified. No cases of subepicardial distribution were found. Intramyocardial LGE was most frequently observed in basal and mid-anterior and inferior interventricular septum – see Figure 1. In these segments, LGE was most often junctional at right-ventricular insertion points (54%), followed by mid-wall LGE (32%) or both sites involvement (14%). Conclusion LGE is frequent in symptomatic high-gradient AS patients with preserved left ventricular ejection fraction, most often presenting as junctional enhancement in basal/mid-anterior and inferior interventricular septum. Future studies may address whether distinct LGE patterns may impact patient prognosis. Funding Acknowledgement Type of funding sources: None.

Background Left ventricular (LV) hypertrophy is a common expected finding in aortic stenosis (AS) patients. Cardiac magnetic resonance (CMR) plays an important role as a non-invasive method for determining LV mass and volume, and to characterize the LV remodeling response in AS. Aim To assess the prevalence, to describe the patterns and evolution of LV remodeling (by CMR) in AS patients referred for surgical aortic valve replacement (AVR). Methods Single-center prospective cohort of 132 consecutive patients (73 years [68–77 years], 49% men] with severe AS: mean transaortic pressure gradient (AVmean): 61±1.5 mmHg; aortic valve area (AVA): 0.7±0.1 cm2, referred for surgical AVR, with no previous history of ischemic cardiomyopathy. Before surgery, all patients underwent electrocardiogram, complete transthoracic echocardiogram (TTE) and CMR for LV assessment and tissue characterization (mean LV indexed mass [LVMi]: 80.3±26.5 g/m2; mean end-diastolic LV indexed volume [LVEDVi]: 84.4±24.5 mL/m2 and median geometric remodeling ratio [M/V]: 0.95 g/mL [IQR 0. 81–1.08 g/mL]). Patterns of LV remodeling were investigated before and after AVR by CMR measurements of LVMi, LVEDVi and M/V. Besides normal LV ventricular structure, four other patterns were considered: concentric remodeling, concentric hypertrophy, eccentric hypertrophy, and adverse remodeling (Figure 1). Results Overall, 43% (n=58) of the patients had concentric hypertrophy, 30% (n=40) concentric remodeling, 22% (n=29) normal ventricular geometry, 4% (n=5) eccentric hypertrophy and in two patients we observed an adverse remodeling pattern. AVR was performed in 80 patients. At the 3rd to 6th month post-AVR assessment, LV remodeling changed to: normal ventricular geometry in 46%, concentric remodeling in 31%, concentric hypertrophy in 19%, eccentric hypertrophy in 3% and adverse remodeling in only one patient (Figure 1). Conclusions In this group of patients with severe aortic stenosis, concentric hypertrophy was not the sole pattern of LV remodeling and two out of every five still presented a normal ventricular geometry and mass as assessed by CMR. LV response was dynamic after AVR which stands for complex and multifactorial interaction in these group of patients despite similar valvular pathophysiology and therapeutic intervention. Funding Acknowledgement Type of funding sources: None.

Background Left ventricular (LV) hypertrophy is a known compensatory mechanism to pressure overload in aortic stenosis (AS) patients. However, by cardiac magnetic resonance (CMR) different patterns of LV adaptation are seen in this group of patients. Aim To describe the patterns of LV adaptation (by CMR) and to analyze its structure and function indexes in AS patients referred for surgical aortic valve replacement (AVR). Methods We prospectively studied 134 consecutive patients (age: 73y [IQR 68–77y], 49% men) with severe symptomatic AS - mean transaortic pressure gradient (AVmean): 61±1.5 mmHg; mean aortic valve area: AVA): 0.7±0.1 cm2, referred for surgical AVR with no previous history of ischemic cardiomyopathy or other. All patients underwent electrocardiogram, 2D transthoracic echocardiogram (TTE) and cardiac magnetic resonance (CMR) before surgery for LV assessment and tissue characterization. Five patterns of LV structure were considered: normal ventricular structure (normal LV mass/volume ratio [M/V], normal LVMi and normal indexed LV end-diastolic volume (LVEDVi); concentric remodeling: increased M/V, normal LVMi; concentric hypertrophy: increased M/V and LVMi; eccentric hypertrophy: increased LVMi and LVEDVi, normal M/V and ejection fraction; and adverse remodeling: dilated left ventricle, increased LVMi and normal M/V in the context of an impaired ejection fraction. Echocardiogram and CMR structural and functional indexes were compared between these groups. Results At baseline study, at CMR: mean LV indexed mass [LVMi]: 80.3±26.5 g/m2; mean end-diastolic LV indexed volume [LVEDVi]: 84.4±24.5 mL/m2 and median geometric remodeling ratio [M/V]: 0.95 g/mL [IQR 0. 81–1.08 g/mL]. Overall, 22% patients had normal LV structure, 30% concentric remodeling ventricular geometry, and two patients had an adverse remodeling pattern. LV hypertrophy was the most prevalent pattern and occurred in 48% of subjects (concentric 43%; eccentric 4%). In our cohort, the severity of AS (AVmean (p Conclusions In our cohort, AS patients presented several distinct patterns of LV remodeling. Disease severity, functional repercussion and loading conditions are distinct between them. Funding Acknowledgement Type of funding sources: None.

Background In patients with severe aortic stenosis (AS), left ventricular (LV) remodeling is believed to be a compensatory adaptive process which should reverse after aortic valve intervention. However, this is not always the rule and remodeling persistence may negatively impact post-procedural outcomes and survival. Aim To assess the prevalence and predictors of morphological LV reverse remodeling in severe symptomatic AS patients after surgical aortic valve replacement (AVR). Methods We prospectively studied 75 patients (72y [68–77y], 45% male) with severe symptomatic AS - mean gradient (AVM): 61±17mmHg; mean indexed aortic valve area (AVAi) 0.41±0.10 cm2/m2 with no previous history of ischemic cardiomyopathy, all with high gradient, 4 with low-flow, 81% with hypertension, 27% with type 2 diabetes mellitus and 35% patients with stage 3 chronic kidney disease: median MDR creat clearance: 70.4mL/min [40–102]. All patients performed pre-operative cardiac magnetic resonance (CMR) at a mean period of 3.4 months (0–17 months) before AVR and at the 3–6th months after AVR, for LV reverse remodeling assessment. It was defined as at least the occurrence of one of the following: >15% reduction in LVEDVi; >15% reduction in LVMi by CMR; >10% reduction in geometric remodeling ratio. Clinical, AV severity data, preoperative functional LV and tissue characterization data were analyzed at multivariate regression to predict the occurrence of LV reverse remodeling. Results Overall, at pre-operative CMR: mean LV indexed mass (LVMi): 82±28.9 g/m2; mean end-diastolic LV indexed volume (LVEDVi): 87.4±26.6 mL/m2; mean geometric remodeling (LV mass/end-diastolic volume): 0.92±0.2 g/mL. After AVR, at echocardiographic evaluation, no patient had prosthetic obstruction or prosthetic patient mismatch: median LV-Ao gradient 12mmHg [9.1–14 mmHg]; 5 of them had mild paravalvular regurgitation. LV reverse remodeling occurred in 65 patients (88%) (Figure 1A) and these were younger, had significantly smaller preoperative AVAi and higher valvular gradients (Figure 1B). At multivariate analysis, only preoperative AVAi remained an independent predictor (odds ratio 0.85, 95% CI 0.735–0.984, p=0.029). Conclusions In this prospective cohort of patients LV reverse remodeling after surgical AVR was highly frequent, occurring in almost nine out of every ten patients. Funding Acknowledgement Type of funding sources: None.

Background Myocardial fibrosis (MF) is a common finding and a potential adverse prognostic marker in several cardiac diseases, including in severe aortic stenosis (AS). While histological analysis obtained through endomyocardial biopsy remains the gold-standard for MF assessment, non-invasive cardiac imaging may offer surrogate biomarkers for fibrosis. We tried to assess the correlation between MF quantification at histopathology and cardiac magnetic resonance (CMR)-derived tissue characterization data in patients with severe AS. Methodology Single-center prospective cohort enrolling 71 patients with severe symptomatic high-gradient AS undergoing surgical aortic valve replacement (SAVR) (mean age 71±9 years; 49% male, mean valvular transaortic gradient 60±20 mmHg; mean left ventricle [LV] ejection fraction 58±9%). Those with past history of myocardial infarction or cardiomyopathy were excluded. All patients underwent pre-operative CMR study with LV tissue characterization and quantification. Normal T1 mapping value was defined as >1021ms as per center protocol. Myocardial tissue was obtained during SAVR either through myocardial biopsy at basal LV septum or harvested from surgical myectomy specimens. Masson's trichrome stain was used for collagen/fibrosis assessment. Automatic quantification was obtained at QuPathTM digital pathology software after applying a dedicated artificial intelligence algorithm on ultra-high-resolution digital slide scanning images. Results Histology-confirmed MF was observed in all patients (median percentage of fibrotic myocardial tissue 15% [IQR 9–22%]). Median global T1 mapping and extracellular volume (ECV) percentage was 1048ms (IQR 1027–1078) and 24% (IQR 20–30%), respectively. Late gadolinium enhancement (LGE) with a non-ischemic pattern was present in 42 patients (59%) with a median LGE mass of 5.8g [IQR 1.0–10.2]; median percentage of 3.7% [IQR 0.6–10.4]. While neither T1 mapping (global or basal LV septum), ECV nor LGE had any significant correlation with histology-confirmed MF (Figure 1) the vast majority had significantly elevated global and basal LV septum T1 mapping – 81% and 92%, respectively. Conclusion In this single-center prospective study, microscopic MF was present in all patients with severe symptomatic high-gradient AS, was accompanied by elevated T1 mapping values but no correlation was found between myocardial fibrosis at histopathology analysis and CMR-derived LV tissue characterization parameters. This may not only stem from sampling (single point biopsy vs. whole myocardial tissue assessment) but also from distinct evaluation of different types of fibrosis by different methods. Funding Acknowledgement Type of funding sources: None.

Background Relative apical sparing (RAS) of left ventricular (LV) longitudinal strain (LS) is a red flag marker for the suspicion of amyloid cardiomyopathy. However, it has also been described in patients with severe aortic stenosis (AS). Aim To assess the prevalence of RAS in patients with severe symptomatic AS referred for surgical aortic valve replacement (AVR), to evaluate its clinical significance and assess its presence after surgery. Methods We prospectively studied 135 consecutive patients (age: 73 y [IQR 68–77 y], 49% men) with severe symptomatic AS – mean transaortic pressure gradient (AVmean): 60.9±17.7 mmHg; mean aortic valve area: 0.7±0.2 cm2, referred for surgical AVR with no previous history of ischemic cardiomyopathy or other. Beyond 12 lead-ECG and transthoracic echocardiography (TTE), all patients underwent cardiac magnetic resonance (CMR) before surgery. RAS was defined by the ratio >1 of average LS at apical segments/sum of the average basal and mid LS at speckle tracking analysis. AVR with septal myocardial biopsy, for investigational purposes, was performed in 80 patients. AS severity indexes, LV remodeling and tissue characterization parameters were compared in both groups of patients, with and without RAS. LS deformation pattern was reassessed at 3–6 months after AVR. Results RAS was present in 24 patients (18%). In the whole cohort there were neither pseudoinfarct pattern or low voltage ECG criteria, nor infiltration suspicion from CMR (native T1 value 1053 ms [IQR 1025–1071 ms] for institutional reference values: 972–1070 ms; ECV 24% [IQR 21–27%]). None of the patients had amyloid deposition at histopathology. Overall, mean CMR LV ejection fraction (LVEF) was 59.6±10.5% and 98 patients (74%) had non-ischemic delayed enhancement, with a median fibrosis fraction of 4.1% [IQR 1.6–7.8%]. RAS cohort had a significantly higher AVmean gradient, relative wall thickness, maximum septal thickness, peak systolic dispersion, with lower global LS at TTE, as well as higher LV mass and lower LVEF at CMR. RAS group has also higher NT-proBNP ambulatory values (Table 1). Follow-up evaluation after AVR revealed RAS disappearance in 19 patients (79.2%). Conclusions RAS occurs in almost one-fifth of the patients in this cohort despite the absence of signs of myocardial infiltration. This deformation pattern elapses with worse indexes of LV remodeling consistent with a more advanced stage of the disease, being reversible after AVR, which stands for the absence of concomitant myocardial infiltration. Funding Acknowledgement Type of funding sources: None.

Background Left ventricular myocardial work (LVMW) is a novel method to evaluated left ventricular (LV) function using pressure-strain loops. It might correct global longitudinal strain (GLS) for afterload, being eventually useful to assess whether GLS reduction is due to reduced contractility (reflected as reduced myocardial work) or increased afterload (reflected as increased myocardial work). Aim To describe indices of LVMW in a group of patients with severe symptomatic aortic stenosis (AS). Methods We prospectively studied 104 consecutive patients (age: 71 years [IQR 66.5–75.5] years, 51% men) with severe symptomatic high gradient AS: mean transaortic pressure gradient: 56.5mmHg [IQR 46.8–67.8]; aortic valve area: 0.73cm2 [IQR 0.61–0.88]; indexed stroke volume: 47.7±1.3 mL/m2 (11 patients with low-flow AS), preserved LV ejection fraction (EV) (LVEF: 56.0% [51.0–61.3]; GLS: −14.5% [IQR −16.1 to −10.6]), with no previous coronary artery disease and no history of cardiomyopathy. Beyond complete transthoracic echocardiography, all patients underwent cardiac magnetic resonance for LV myocardium tissue characterization. As proposed for AS, LV systolic pressure was corrected adding the mean transaortic pressure gradient to non-invasive systolic blood pressure cuff measurement in the echocardiographic algorithm. Four LVMW indices were collected in 83 patients (patients excluded for atrial fibrillation, left bundle branch block or absence of non-invasive blood pressure registration) and correlated to LV function indexes, LV hypertrophy and remodeling, myocardial tissue characterization, BNP and troponin levels (Pearson or Spearman correlation). These same indexes were compared in patients with LV ejection fraction (EF) below and above 50%, normal and reduced flow and presence of replacement fibrosis. Results Global constructive work (GCW) (2658.6±76.4mmHg%), global myocardial work (GMW) (2218.7±74.9mmHg%) and global wasted work (GWE) (262.0mmHg% [198.8–339.5]) were high above normal with concomitant lower work efficiency (WE) (88.0% [83.2–91.8]. Weak correlations were found between LVMW indexes and parameters describing aortic valve severity, flow and LV function (table). Except for significant differences of LVMI in patients with reduced LV ejection fraction (GCW 2770.3±687.4 vs 2056.0±380.7mmHg%, p=0,014 and GMW 2362.5±657.9 vs 1621.3±319.9, p=0,021 in patients with LV EF>50% vs. LV EF Conclusions Global constructive and myocardial work are increased in these patients with severe aortic stenosis. This might reflect an increased afterload predominance rather than a LV functional impairment, particularly relevant in this group of patients with exclusive high gradient disease and preserved LVEF. Funding Acknowledgement Type of funding sources: None. Correlations between LVMI – LV function

Background Right ventricular (RV) function in aortic stenosis (AS) has been largely neglected. Recently it was demonstrated that right ventricular impairment may be influenced by left ventricular (LV) function and afterload, well before overt pulmonary hypertension development. Aim To describe the prevalence of RV dysfunction in a group of patients with severe symptomatic aortic stenosis (AS) and its relation to LV function parameters and afterload. Methods We prospectively studied 93 consecutive patients (age: 73 years [IQR 68–77] years, 55% women) with pure severe symptomatic high gradient aortic stenosis: mean transaortic pressure gradient: 57.0mmHg [IQR 46.9–71.1]; aortic valve area: 0.72cm2 [IQR 0.61–0.88]; indexed stroke volume: 48.8±1.5 mL/m2 (11 patients with low-flow AS), preserved LV ejection fraction (EV) (LVEF: 56.0% [51.0–61.3]; GLS: −14.5% [IQR −16.1 to −10.6]), with no previous coronary artery disease and no history of cardiomyopathy. Beyond complete transthoracic echocardiography, all patients underwent cardiac magnetic resonance (CMR) for LV myocardium tissue characterization (late gadolinium enhancement and extracellular volume). Normal RV function was defined according to TAPSE ≥17mm, tricuspid annular systolic velocity ≥12cm/s, mean free wall longitudinal strain ≤−20%. Patients were divided into four groups: (0) – all three RV parameters below normal (1.1%), (1) – 1 normal parameter (12.9%), (2) – 2 normal parameters (44.1%), (3) – 3 normal parameters (41.9%). Indexes of LV systolic and diastolic function, CMR derived LV geometric remodeling, hypertrophy and tissue characterization, aortic valve disease severity and afterload were compared across the 4 groups of patients. We tried to identify predictors of RV dysfunction (group 0, 1, 2 vs. group 3) at multivariate regression analysis. Results Left ventricular performance parameters, diastolic and myocardial work indexes were significantly different across the groups (Figure). Neither AV severity indexes nor LV tissue characterization were distinct. At multivariate analysis only global constructive work was an independent predictor of RV dysfunction. Conclusion RV dysfunction is common in this group of patients with severe high gradient aortic stenosis and preserved ejection fraction. RV impairment is significantly related to several LV systolic and diastolic parameters and also to LV afterload, probably accounting for RV-LV interdependence. Funding Acknowledgement Type of funding sources: None.

Methods We assessed 238 consecutive patients (154 male, mean age 64+/11 years) undergoing adenosine stress cardiac MR in a single center between January 2012 and July 2014. Significant incidental results were defined as any previously unknown non ischemic finding with potential clinical and/or therapeutic implications (all patients had an previous cardiac ultrasound done within the previous 5 months). The exams were performed on a 1.5T MR equipment and according to the SCMR guidelines for a adenosine stress cardiac MR. Interpretation was done by agreement between a Radiologist and a Cardiologist with level III equivalent certification.

Risk stratification has become increasingly important in the management of patients with suspected or known ischaemic heart disease (IHD). Recent guidelines recommend that these patients have their care driven by risk assessment. The purpose of this position statement is to sum- marize current evidence on the value of cardiac single-photon emission computed tomography, positron emission tomography, and hybrid imaging in risk stratifying asymptomatic or symptomatic patients with suspected IHD, patients with stable disease, patients after coronary revas- cularization, heart failure patients, and specific patient population. In addition, this position statement evaluates the impact of imaging results on clinical decision-making and thereby its role in patient management. The document represents the opinion of the European Association of Nuclear Medicine (EANM) Cardiovascular Committee and of the European Association of Cardiovascular Imaging (EACVI) and intends to stimu- late future research in this field.

Mesenchymal/stromal stem cells (MSC) have unique properties favorable to their future use in clinical practice and have been studied for cardiac repair. MSC are larger than coronary microvessels and there is controversy about the risk of embolization and microinfarctions, which could compromise the intracoronary route for their delivery. The index of microcirculatory resistance (IMR) is an invasive method for quantitatively assessing the coronary microcirculation status and could be applied for evaluation of the acute effects of MSC intracoronary infusion providing new insights for this open question. Our purpose was to examine heart microcirculation effects after MSC intracoronary injection with IMR. Methods and Results: Eighteen healthy swine were randomized to receive 30 x 106 MSC or saline by intracoronary infusion. In the heart catheterization laboratory hemodynamic, electrocardiographic and coronary flow parameters were monitored and there were no differences between groups. Thermodilution-derived coronary flow reserve (CFR) and IMR were assessed at baseline, 5 and 30 minutes post-delivery using a coronary pressure wire. CFR had a small although not significant decrease in animals receiving MSC. After cell infusion, IMR increased at 5 and 30 minutes with a significant difference from the control group at 30 minutes (Table). Conclusion: Intracoronary delivery of MSC is possible without a significant negative impact on hemodynamic parameters, electrical stability and epicardial coronary flow status. However, this study provides definitive evidence of microcirculatory disruption upon intracoronary administration of MSC, in a large animal model closely resembling human cardiac physiology, function and anatomy. | | CONTROL | MSC | p | || | Baseline CFR | 3.8 ± 1 | 4 ± 2 | 0.7 | | Baseline IMR (U) | 8.1 ± 1 | 6.7 ± 0.6 | 0.3 | | Post-delivery CFR - 5 min. | 3.6 ± 1 | 3 ± 2 | 0.5 | | Post-delivery CFR - 30 min. | 3.8 ± 2 | 2.3 ± 1.5 | 0.064 | | Post-delivery IMR - 5 min. (U) | 9.8 ± 1 | 15.3 ± 2.8 | 0.08 | | Post-delivery IMR - 30 min. (U) | 8.8 ± 1 | 13.2 ± 1.8 | 0.02 | * Coronary flow reserve (CFR), index of microcirculatory resistance (IMR) CFR and IMR mean values

Purpose: To assess and compare the prognostic value of coronary CT angiography (CCTA) and exercise ECG (ExECG) in patients with suspected stable angina pectoris. Methods: Patients with suspected coronary artery disease (CAD) who had undergone both ECG exercise stress testing (ExECG) and CCTA (within 180 days) were identified retrospectively in a single center registry. The presence of 50% or greater coronary stenosis was assessed with CCTA. ExECG results were classified as normal, ischemic, or nondiagnostic. Patients were followed-up for major adverse cardiac events (MACE), defined as cardiac death, nonfatal myocardial infarction, unstable angina requiring hospitalization, and revascularization >90 days after index CCTA. Univariable and multivariable Cox regression analysis was used to determine the prognostic values, and discriminative power was assessed with continuous net reclassification improvement (cNRI). Results: Follow-up was completed for 467 patients (88%), with a median duration of 2.6 years (IQR 2.0-3.8). A total of 23 patients experienced MACE, including 3 deaths and 2 non-fatal myocardial infarctions. In the univariable model, modified CAD Consortium 2 score (HR 1.05, 95% CI 1.02-1.08), non-obstructive CAD (HR 5.63, 95% CI 1.25-25.43) and obstructive CAD (HR 15.43 CI 3.38-70.45) were predictors of MACE. In the multivariable model, only CCTA findings remained independently predictive of MACE. Addition of CCTA results to the clinical and ExECG model yielded a cNRI of 70% (222 reclassified upward, 245 downward). ![Figure][1] Conclusions: CCTA findings are strongly predictive of MACE. Its prognostic power seems superior and incremental to clinical and exercise ECG data. [1]: pending:yes

Purpose: To evaluate the performance of classic risk factors, alone or associated in scores, in identifying a higher than expected coronary atherosclerotic burden. Methods: We assessed 2069 consecutive patients (56% men, mean age 58±11 years) undergoing coronary CT angiography (CCTA) with Calcium Score (CaSc) for suspected coronary artery disease. A higher than expected atherosclerotic burden was defined as a CaSc >75th percentile (CaSc>p75) according to age and sex-adjusted nomograms. The ability of traditional risk factors to predict a CaSc>p75 was assessed in a customized logistic regression model (clinical score) and by the calculation of the HeartScore. The Population Attributable Risk (PAR) of the various risk factors for CaSc>p75 was also calculated. Results: The median CaSc was 3.0 [IQR 0.0-98.0], with 362 patients (17.5%) having CaSc>p75. The median HeartScore was 3.0 [IQR 1.0-4.0]. With the exception of hypertension, all classic risk factors were independent predictors of CaSc>p75: diabetes mellitus, dyslipidemia, smoking and family history (all OR 1.3-2.2, p≤ 0.026). The areas under the ROC curves to predict CaSc>p75 were 0.64 for the clinical score (95% CI 0.61-0.67, p p75 were in the two lower quartiles of the clinical score (Figure). Altogether, the various classical risk factors seem to explain only 56% of the prevalence of CaSc>p75 (adjusted PAR 0.56). Conclusion: Despite the statistical association of CV risk factors with a higher than expected atherosclerotic burden, they seem to justify only half of its prevalence. Even when integrated in scores, the predictive power of these risk factors is relatively modest, exposing the limitations of a risk stratification based solely on demographic and clinical risk factors.