BACKGROUND:Carotid and coronary atherosclerosis are critical determinants of cardiovascular risk, yet their interrelationship in middle-aged populations is incompletely understood. This study assessed carotid plaque composition, risk-factor associations, coronary disease, and sex differences in a subclinical cohort. METHODS:Within the Swedish CArdioPulmonary bioImage Study, 533 asymptomatic individuals aged 50-64 years with carotid plaque ≥2.7 mm on ultrasound underwent 3T multi-contrast carotid cardiovascular magnetic resonance (CMR) and coronary computed tomography angiography. Carotid plaque characteristics were determined manually using established criteria on multi-contrast weighted carotid CMR. Bayesian regression models evaluated associations between cardiovascular risk factors and coronary atherosclerosis. RESULTS:Lipid-rich necrotic core (LRNC) was present in 60% (320/533) and intraplaque hemorrhage (IPH) in 5.4% (29/533); calcification occurred in 48.6% (259/533). Maximum carotid wall thickness was 1.8 (1.6-2.0) mm, and mean lumen area 31.3 (26.7-36.1) mm². Coronary atherosclerosis was present in 63.6% (339/533) of participants, with ≥50% stenosis in 12.9% (69/533), and coronary artery calcium score >400 in 12.8% (68/533). Men (N = 367) had larger carotid lumen area, mean wall area, and maximum wall thickness (all p < 0.001) than women (N = 166), differences that persisted after body-surface-area adjustment (all p < 0.01). LRNC was present in 66% (242/367) of men compared to 47% (78/166) of women (p < 0.001). LRNC presence was not associated with coronary atherosclerosis, whereas IPH was associated with coronary involvement. CONCLUSION:In middle-aged individuals, distinct cardiovascular risk factors were positively linked to the presence and volume of LRNC and calcified plaques. The substantial prevalence of high-risk plaque features, particularly LRNC and especially in men, highlights a significant subclinical carotid disease burden.

Background Aortic stenosis (AS) leads to left ventricular (LV) remodelling and fibrosis. Myocardial fibrosis can be focal and irreversible, associated with poor prognosis, or diffuse and potentially reversible after surgery. Cardiac magnetic resonance imaging (CMR) shows promise in quantifying diffuse myocardial fibrosis (DMF), but methods vary in precision. The aim of this study was to investigate the presence and distribution of DMF from myocardial biopsies and CMR tissue characteristics in severe AS. Secondarily, explore the association between DMF and LV function.Methods Forty-three patients with severe AS underwent CMR and transthoracic echocardiography within 1 week before surgical aortic valve replacement. CMR included balanced steady-state free-precession cine images, T1 relaxometry with Modified Look-Locker Inversion recovery and extracellular volume calculations. Endomyocardial biopsies were sampled.Results Histological analysis of 192 biopsies showed a median LV collagen volume fraction (CVF) of 19%, peaking in segment 1, according to the segment model recommended by the American Heart Association (AHA). There were significant moderate correlations between CVF and extracellular volume in AHA segments 1 (r² = 0.54, p<0.01) and 16 (r² = 0.44, p=0.03), where the DMF had the highest prevalence. Functional assessments demonstrated correlations between CVF and global circumferential and radial strain (r2 0.31, p=0.04 respectively r2−0.33, p=0.03), as well as LV ejection fraction (r2−0.34, p=0.03). T1 relaxation time correlated with GLS (r2 0.42, p<0.01), mitral annular plane systolic excursion (r2−0.39, p=0.01) and mean S’ LV (r2−0.45, p<0.01) from transthoracic echocardiography.Conclusion CVF varied across LV segments and was significantly highest at the base of the heart, suggesting the start location for fibrosis. Systolic functional data correlated with CVF and T1 relaxation time.

Aims To investigate the prevalence of diastolic dysfunction and associated risk factors in pre-diabetes and diabetes in the general population.Methods Diastolic function was assessed by transthoracic echocardiography in a cross-sectional sample of 3840 men and women aged 50–64 years from the Swedish CArdioPulmonary bioImage Study. Anthropometry, medical history, blood pressure, biochemistry and coronary atherosclerosis assessed by CT were recorded. Population-specific reference ranges were applied. Diastolic function was compared across glycaemic groups and analysed in relation to risk factors.Results Normoglycaemia was present in 82%, pre-diabetes in 12% and diabetes in 6%. Diastolic function was impaired (p<0.001) in pre-diabetes and diabetes, with higher prevalence of abnormal diastolic variables in pre-diabetes (30%) and diabetes (33%) than in normoglycaemia (21%). Among participants with pre-diabetes/diabetes, diastolic dysfunction was associated with hypertension and more severe coronary atherosclerosis (p<0.001). In multivariable analyses, waist circumference (OR 1.034, 95% CI 1.013 to 1.054) and high Coronary Artery Calcium Score (OR 2.897, 95% CI 1.373 to 6.113) were independently associated with diastolic dysfunction, also after exclusion of subjects with ischaemic heart disease. In those without coronary atherosclerosis and hypertension, systolic blood pressure was the only independent risk factor (OR 1.027, 95% CI 1.002 to 1.053).Conclusions Diastolic dysfunction was as common in pre-diabetes as in diabetes and was mainly associated with central adiposity, hypertension and coronary atherosclerosis. In individuals without coronary atherosclerosis or hypertension, systolic blood pressure was still the only independent predictor. These findings challenge the concept of a clinically relevant isolated diabetic cardiomyopathy and highlight the importance of early and comprehensive cardiometabolic risk factor control to prevent heart failure with preserved ejection fraction.

Background Heterogeneous myocardial contraction is common in myocardial disease and linked to ventricular arrhythmias, but its frequency and relevance in the general population remain unclear. This study aimed to investigate the frequency of increased left ventricular mechanical dispersion (LVMD) and to examine its clinical and imaging correlates in a population-based cohort.Methods LVMD was assessed using speckle-tracking echocardiography in 3997 participants aged 50–64 years (51% women) from the Swedish Cardiopulmonary Bioimage Study. The upper limit of normal (ULN) for LVMD was defined as the 95th percentile in a subgroup (n=1165) without cardiovascular disease or risk factors. In the full cohort, cardiovascular risk factors, including coronary artery calcium score (CACS) and left ventricular mass index (LVMI) from cardiac CT, were compared between subjects with and without high LVMD, and predictors of high LVMD were assessed using multivariable regression.Results The ULN for LVMD was 53 ms and LVMD>ULN was present in 11.8% of the full cohort. These individuals were older, more often male, had higher body mass index (BMI) and more frequently had hypertension, hyperlipidaemia and previous myocardial infarction. They also had higher LVMI (57±11 g vs 52±11 g, p<0.001). CACS ≥100 was present in 17.8% vs 10.3% (OR 1.90, 95% CI 1.46 to 2.48, p<0.001) in those with increased versus normal LVMD. Age, BMI, LVMI and heart rate were independently associated with LVMD.Conclusions LVMD above ULN was observed in 11.8% of this middle-aged general population sample and was associated with a more adverse cardiovascular risk profile and markers of cardiac remodelling, particularly higher LVMI and larger indexed left ventricular volumes.

Elevated troponin I (TnI) has been reported in patients with chronic obstructive pulmonary disease (COPD) without cardiovascular disease (CVD), suggesting non-ischaemic mechanisms. We assessed this association in a population-based cohort of 22 526 individuals without known CVD or significant coronary artery calcification. TnI showed no association with COPD (adjusted OR 0.87, 95% CI 0.60 to 1.26; highest category vs below limit of detection) or with forced expiratory volume in 1 s/forced vital capacity (adjusted difference 0.002, 95% CI -0.001 to 0.004). Median TnI was 2.2 ng/L in both obstructive and non-obstructive groups. These findings do not support a pulmonary source of TnI elevation in mild to moderate, stable COPD and suggest that TnI elevations should prompt cardiovascular evaluation rather than being attributed to pulmonary disease alone.

Heart failure (HF) and arterial hypertension (AH) are strongly associated with obesity, with a linear relationship to increasing body mass index (BMI). However, some individuals with obesity do not exhibit signs of HF or AH. This study aimed to compare, for the first time in a large population-based cohort, individuals with obesity who have normal left ventricular function and remodeling (LVFR) and no AH (ObNI) with those who have impaired LVFR or AH (ObI), and corresponding individuals without obesity (NObNI and NObI). A cross-sectional analysis was performed on 4 435 participants from the Swedish CArdioPulmonary bioImage Study (SCAPIS). Participants were grouped into four categories: (1) ObNI (n = 586), (2) ObI (n = 224), (3) NObNI (n = 3 041), and (4) NObI (n = 584). Descriptive analyses compared individuals with obesity with normal LVFR and no AH (ObNI) to the other three groups. Although no significant differences between the two subgroups with obesity could be seen regarding BMI (33.1 vs. 33.5 kg/m2, p = 0.095), there was significant differences in coronary artery calcification score (CACS) levels, where ObNI participants were more prone to show no or very low CACS in comparison with ObI participants (p < 0.001). Also compared to ObI participants, ObNI individuals had lower levels of HbA1c, fasting plasma glucose, triglycerides, and troponin I (all p < 0.001). Furthermore, significant differences were observed between the two groups regarding sedentary behavior (p = 0.041), where ObNI subjects showed a more active lifestyle. Compared with ObNI, individuals with ObI exhibited a higher left ventricular mass index (LVMI; p < 0.001) and lower diastolic function parameters (p < 0.001), while left ventricular ejection fraction (EF) did not differ significantly (p = 0.27). Relative to NObNI, ObNI participants demonstrated increased LVMI (p = 0.007), lower EF (p < 0.001), and impaired diastolic function (p < 0.001). Coronary artery calcification scores (CACS) were higher in ObI than in ObNI (p < 0.001), and ObNI also showed higher CACS than NObNI (p = 0.008). ObNI participants had lower CACS levels, more favorable metabolic profiles, better cardiac function, and greater physical activity than ObI individuals. However, compared to NObNI, they showed higher CACS, increased left ventricular mass, and reduced cardiac function, highlighting distinct cardiovascular risks across obesity phenotypes.

Post-systolic shortening (PSS) has emerged as a method for evaluating left ventricular dysfunction. We aimed to determine whether pathological PSS, alone or in combination with global longitudinal strain (GLS), is a prognostic factor for major adverse cardiovascular events (MACEs) in patients with type 2 diabetes. We prospectively investigated 364 patients with type 2 diabetes aged 55–65 years in the CARDIPP study. All patients underwent echocardiography between 2005 and 2009. PSS, measured by speckle tracking echocardiography, was defined as myocardial contraction after aortic valve closure. Pathological PSS was defined as a post-systolic index > 5

Aims The REDUCE-AMI trial showed that beta-blockers in patients with preserved left ventricular ejection fraction (LVEF) after acute myocardial infarction (AMI) had no effect on mortality or cardiovascular outcomes. The aim of this substudy was to evaluate whether global longitudinal strain (GLS) is a better prognostic marker than LVEF, and if beta-blockers have a beneficial effect in patients with decreased GLS.Methods and results REDUCE-AMI was a registry-based randomized clinical trial. Conventional echocardiographic parameters and GLS were obtained and a likelihood ratio test between models adjusted for age, sex, hypertension, smoking, diabetes, previous AMI, and multi-vessel disease was used to compare LVEF and GLS as prognostic methods. A Cox regression model evaluated the impact of beta-blocker treatment on the composite endpoint of death from any cause or new AMI. A total of 1436 patients (28.6% of the total population) were included in this substudy. Due to poor image quality or incompatible equipment, 324 (22.6%) patients were excluded from the analysis of GLS. The median GLS was 17.3%. The likelihood ratio test resulted in no difference (P = 0.56) when comparing the combination of GLS to LVEF. The results were robust when adding beta-blocker randomization status as an independent variable.Conclusion In patients after AMI with preserved LVEF, GLS did not add prognostic value regarding death from any cause or new AMI. In addition, beta-blocker treatment did not alter the prognostic information obtained from GLS. Consequently, this study does not support an additive value of GLS compared with standard echocardiographic measurement in this patient population.

BACKGROUND:Valvular heart disease (VHD) commonly leads to the development of turbulent blood flow. Turbulent kinetic energy (TKE), measured with 4D flow MRI, may be a complement to current metrics for early identification of VHD. PURPOSE:To investigate TKE as a marker of VHD in relation to flow velocity and cardiovascular geometry. STUDY TYPE:Retrospective observational cross-sectional. POPULATION:Twenty controls and 106 subjects with VHDs, including mitral regurgitation, aortic regurgitation, pulmonary regurgitation, tricuspid regurgitation, and aortic stenosis. FIELD STRENGTH/SEQUENCES:Four-dimensional flow MRI using a spoiled gradient-echo phase-contrast sequence with asymmetric 4-point motion encoding at 1.5 or 3 T. ASSESSMENT:Time-resolved segmentations of the left and right ventricles (LV, RV), atria (LA, RA), and aorta were performed. Total and maximum TKE, maximum and average velocity, and diameters were evaluated in each. Correlations between TKE, velocity, and diameter were assessed, along with group differences between VHD subjects and controls. STATISTICAL TESTS:Student's t-test, Wilcoxon rank-sum test, chi-squared test, Pearson's correlation, two-way analysis of covariance. A p value < 0.05 was considered significant. RESULTS:Total and maximum TKE correlated significantly with maximum velocity (r = 0.45-0.76) and averaged velocity (r = 0.22-0.44) and less strongly with diameters for aorta, LV, LA, and RV (r = 0.18-0.37). Compared to controls, total and maximum aortic TKE were significantly higher in aortic stenosis (3.8 vs. 1.6 mJ; 291.7 vs. 133.7 J/m3). Maximum LV TKE was significantly elevated in aortic regurgitation (106.6 vs. 91.8 J/m3). Total TKE was significantly elevated in LA for mitral regurgitation (1.1 vs. 0.6 mJ), in RA for tricuspid regurgitation (1.6 vs. 0.7 mJ), and in RV for pulmonary regurgitation (1.7 vs. 1.0 mJ). DATA CONCLUSION:TKE is elevated in mild VHD. When evaluated alongside velocity as a marker for VHD, TKE may be more discriminative. Consequently, it has potential to be a hemodynamic marker of early VHD conveying complementary information to velocity. EVIDENCE LEVEL:4. TECHNICAL EFFICACY:Stage 1.

BACKGROUND AND AIM:Cardiovascular disease (CVD) is the major cause of death in patients with type 2 diabetes mellitus (T2DM), making it of interest to attain efficient methods for prognostic purposes. We aimed to prospectively investigate the association between plasma copeptin and cardiovascular disease (CVD) in individuals with type 2 diabetes mellitus (T2DM), adjusting for mean 24-h ambulatory blood pressure, left ventricular mass index, and traditional cardio-metabolic risk factors. METHODS AND RESULTS:A cohort of 523 patients with T2DM with complete data on copeptin, age, sex, body mass index (BMI), smoking, total cholesterol, eGFR, HbA1c, 24-h ambulatory systolic blood pressure (24-h SBP), and left ventricular mass index (LVMI) was derived from the Cardiovascular Risk Factors in Patients with Diabetes - a Prospective Study in Primary Care (CARDIPP) study. The incidence of major adverse cardiovascular events (MACE) and all-cause mortality were obtained from the Swedish Cause of Death Registry and the Inpatient Register. A Cox-proportional hazard analysis was conducted. Over 15 years, 120 patients had MACE, while 122 died of any cause. Patients with a copeptin level of ≥5.6 pmol/L exhibited a 2.05 hazard ratio (HR) for MACE (95 % CI 1.24-3.37, p < 0.005). However, after adjustment, no significant association with all-cause mortality (HR 1.30, 95 % CI 0.84-2.02, p = 0.238) was noted. These findings were independent of traditional cardio-metabolic risk factors, 24-h SBP, and LVMI. CONCLUSIONS:Elevated copeptin levels (≥5.6 pmol/L) in patients with T2DM were independently associated with an increased risk of MACE. Measuring plasma copeptin may help identify high-risk T2DM patients. TRIAL REGISTRATION:ClinicalTrials.gov: NCT01049737.

Inter-arm blood pressure differences (IABPDs) can be caused by atherosclerosis. We investigated 29 921 men and women aged 50–64 years from the nationwide population-based Swedish CArdio Pulmonary bioImage Study (SCAPIS) to evaluate if IABPD is related to risk factors for atherosclerosis and can be used as a marker of atherosclerosis as evaluated by coronary artery calcium score, arterial segment involvement score on computed tomography, carotid ultrasound, and ankle-brachial index (ABI). The overall prevalence of systolic IABPD at least 10 mmHg was 2110/29 921 (7.1%). Individuals with IABPD at least 10 mmHg were significantly ( P < 0.001) older, more often women, had higher BMI, nonhigh-density lipoprotein cholesterol, triglycerides, SBP and DBPs, and were more likely to have diabetes. In unadjusted analyses, IABPD at least 10 mmHg was associated with presence of coronary atherosclerosis, with more carotid arteries with plaque, and with pathological ABI. These associations were largely attenuated after adjustment for cardiovascular risk factors (age, sex, nonhigh-density lipoprotein cholesterol, systolic BP, smoking, diabetes, and the use of BP lowering drugs). Only ABI retained significance after these adjustments. In conclusion, a systolic IABPD of at least 10 mmHg in middle aged men and women is common in the general population, and can be used as a screening tool for subclinical atherosclerotic changes in coronary, carotid, and lower extremity arteries. However, these relationships were largely explained by correlations between IABPD and traditional cardiovascular risk factors.

Coronary Computed Tomography Angiography (CCTA) is recommended as a first-line investigation to exclude significant coronary artery stenosis in case of low to intermediate pre-test probability (PTP). The aim was to investigate CCTA findings in relation to the PTP of patients referred directly from primary health care centres. In this retrospective cohort study consecutive primary care CCTA referrals in a Swedish county 1st of June 2021 until 30th Nov. 2022 were included. CCTA reports were obtained for 483 patients ≥ 30 years old, without known CAD and stratified as no CAD, with atheromatosis or with suspected significant stenosis. For the 381 patients with eligible PTP data, the mean age was 60 years and 70

INTRODUCTION:Children born with lower birth weight face an increased risk of developing cardiovascular disease later in life. We hypothesize that cardiovascular protein biomarkers in cord blood, associated with birth weight SDS and systolic cardiac function, may reveal mechanisms behind early programming of cardiovascular function. METHODS:We investigated the association between birth weight SDS and plasma levels of 184 circulating proteins determined by Proximity Extension Assay (PEA) in cord blood from 48 children. The birth weight-associated proteins were correlated with left ventricular longitudinal strain (LVLS) determined by echocardiography at birth and 3 months of age. RESULTS:We identified seven cardiovascular protein biomarkers associated with birth weight SDS: stem cell factor, leptin, elafin, insulin-like growth factor-binding protein-1, follastatin, paraoxonase, and epithelial cell adhesion molecule (Ep-CAM). Among these, Ep-CAM significantly correlated with LVLS at 3 months of age. CONCLUSION:PEA successfully identified both established and novel proteins associated with fetal growth and birth size, including one novel protein related to LVLS. This indicates that our approach is promising for uncovering biological pathways that may be involved in direct programming of cardiovascular function in children and affect the risk of cardiovascular disease in adulthood.

BACKGROUND:Cardiovascular autonomic neuropathy (CAN), a serious complication of type 1 diabetes mellitus (T1DM), requires early detection for timely prevention of disease progression. Although traditional autonomic function tests effectively identify advanced neuropathic abnormalities, they lack sensitivity for early-stage CAN in young individuals. Heart rate recovery (HRRec) and heart rate variability (HRV) following exercise are potential early markers of autonomic dysfunction in this group. METHODS:HRRec and HRV from Holter-ECG recordings after a standardized exercise test were compared between 43 individuals with T1DM, aged 10-30 years, subject to modern treatment with advanced technology and with moderate to good metabolic control (mean HbA1c 57 mmol/mol), and 43 healthy controls, matched for age and sex. HRV was additionally assessed on a reference Holter-ECG recording without prior exertion. RESULTS:Twice as many participants with T1DM (33%) compared to controls (16%) maintained a heart rate > 100 beats/min beyond two hours after the exercise test. HRV did not differ between groups on reference Holter-ECG without prior exertion, but nocturnal HRV was significantly lower in the T1DM group compared to controls after the standardized exercise test (p < 0.05), primarily among individuals with a lower physical capacity. Long-term HbA1c correlated negatively with nocturnal high-frequency HRV in T1DM participants (p < 0.05). CONCLUSION:Heart rate variability post-exercise may be a pertinent tool for the assessment of early autonomic cardiac dysfunction in young individuals with T1DM with moderate to good metabolic control.

Background: Arterial mechanics are crucial to cardiovascular functionality. The pressure–strain elastic modulus often delineates mechanical properties. Emerging methods use non-linear continuum mechanics and non-convex minimization to identify tissue-specific parameters in vivo. Reliability of these methods, particularly their accuracy in representing the in vivo stress state, is a significant concern. This study aims to compare the predicted stress state and the collagen-attributed load-bearing fraction with the stress state from in silico experiments. Methods: Our team has evaluated an in vivo parameter identification method through in silico experiments involving finite element models and demonstrated good agreement with the parameters of a healthy abdominal aorta. Results: The findings suggest that the circumferential stress state is well represented for an abdominal aorta with a low transmural stress gradient. Larger discrepancies are observed in the axial direction. The agreement deteriorates in both directions with an increasing transmural stress gradient, attributed to the membrane model’s inability to capture transmural gradients. The collagen-attributed load-bearing fraction is well predicted, particularly in the circumferential direction. Conclusions: These findings underscore the importance of investigating both isotropic and anisotropic aspects of the vessel wall. This evaluation advances the parameter identification method towards clinical application as a potential tool for assessing arterial mechanics.

AimTo investigate the association between Systematic Coronary Risk Evaluation 2 (SCORE2) and subclinical damage in two vascular beds: atherosclerosis in the coronary arteries and aortic arterial stiffness, in a large population-based cohort without cardiovascular disease or diabetes. MethodsDesign: A cross-sectional study based on Swedish CArdio Pulmonary bioImaging Study (SCAPIS) data. Study population: A population-based cohort of 3087 participants aged 50-64. OutcomePulse Wave Velocity (PWV) was measured, and aortic arterial stiffness was defined as PWV >= 10 m/s. Coronary artery calcium score (CACS) was determined by coronary computed tomography and clinically significant coronary calcification was defined as CACS > 100. ResultsThe prevalence of arterial stiffness was 6.6% in the low-moderate SCORE2 risk group, 31.0% in the high-risk group, and 53.3% in the very high-risk group. The prevalence of coronary calcification was 4.5%, 18.5% 23.0%, respectively. There was a modest overlap between arterial stiffness and coronary calcification in all SCORE2 risk groups. When comparing the high SCORE2 risk group with the low-moderate risk group, the Odds ratio (OR) was 6.4, 95% confidence interval (CI 5.1-8.0) for arterial stiffness and 4.8 (CI 3.7-6.3) for coronary calcification. When comparing the very high SCORE2 risk group to the low-moderate group, the OR was 16.2 (CI 11.3-23.1) for arterial stiffness and 6.4 (CI 4.2-9.7) for coronary calcification. ConclusionOur study shows that high cardiovascular risk according to SCORE2 is associated with increased arterial stiffness and significant coronary calcification in a population without prevalent cardiovascular disease or diabetes. This knowledge can be useful in primary care, where SCORE2 is frequently used as a risk prediction tool. The modest overlap between arterial stiffness and coronary calcification suggests that CACS and PWV describe different types of vascular damage. KEY POINTS center dot What is known? center dot arterial stiffness and coronary calcification are measures of subclinical vascular damage and predictors of poorer cardiovascular outcomes. center dot What is the knowledge gap? center dot there is limited data on the association between scORe2 and subclinical macrovascular damage. center dot What this study shows? center dot this study shows an association between scORe2 risk and arterial stiffness and subclinical coronary atherosclerosis. the higher the scORe2 risk the higher the prevalence of both arterial stiffness and coronary calcification. these two measures overlap, albeit to a small extent.

BACKGROUND:Thoracic aortic aneurysm is a life-threatening disease due to the risk for acute aortic syndromes, and subjects with dilated ascending aortas are recommended surveillance imaging to assess the need for preventive surgery. Our objectives were to investigate the progression of dilated ascending aortas and risk factors for rapid progression in a prospectively enrolled general population-based cohort of subjects aged 50-65 years. METHODS:From the 5058 subjects prospectively enrolled in the general population-based Swedish CArdioPulmonary bioImage Study (SCAPIS) in Linköping, we followed all 74 subjects (22% female, mean age 59±4 years) with ascending aortic dilation (≥40 mm) identified by CT angiography, thoracic CT or transthoracic echocardiography. Office and home blood pressure (BP), pulse wave velocity, coronary artery calcification and carotid plaques were assessed at baseline. Transthoracic echocardiography was used to follow ascending aortic diameters over time. RESULTS:Three subjects underwent acute or elective aortic repair before the first follow-up examination. Among the remaining subjects, the mean progression rate of ascending aortic diameter was 0.4 mm/year (range 0-1.8 mm/year) during a mean follow-up of 6.1±1.3 years. In 10 (14%) subjects, all men, no progression was seen. In multivariable analysis, higher 7-day home systolic BP was the only factor associated with faster progression rate. CONCLUSIONS:Progression of mild to moderate ascending aortic dilation was in general slow. Our findings emphasise the benefit of home BP measurements over office BP and underline the importance of BP control in subjects with a dilated ascending aorta.

BACKGROUND:Despite its potential to improve the assessment of cardiovascular diseases, four-dimensional (4D) flow cardiovascular magnetic resonance (CMR) is hampered by long scan times. 4D flow CMR is conventionally acquired with three motion encodings and one reference encoding, as the three-dimensional velocity data are obtained by subtracting the phase of the reference from the phase of the motion encodings. In this study, we aim to use deep learning to predict the reference encoding from the three motion encodings for cardiovascular 4D flow. METHODS:A U-Net was trained with adversarial learning (U-NetADV) and with a velocity frequency-weighted loss function (U-NetVEL) to predict the reference encoding from the three motion encodings obtained with a non-symmetric velocity-encoding scheme. Whole-heart 4D flow datasets from 126 patients with different types of cardiomyopathies were retrospectively included. The models were trained on 113 patients with a 5-fold cross-validation, and tested on 13 patients. Flow volumes in the aorta and pulmonary artery, mean and maximum velocity, total and maximum turbulent kinetic energy at peak systole in the cardiac chambers and main vessels were assessed. RESULTS:Three-dimensional velocity data reconstructed with the reference encoding predicted by deep learning agreed well with the velocities obtained with the reference encoding acquired at the scanner for both models. U-NetADV performed more consistently throughout the cardiac cycle and across the test subjects, while U-NetVEL performed better for systolic velocities. Comprehensively, the largest error for flow volumes, maximum and mean velocities was -6.031% for maximum velocities in the right ventricle for the U-NetADV, and -6.92% for mean velocities in the right ventricle for U-NetVEL. For total turbulent kinetic energy, the highest errors were in the left ventricle (-77.17%) for the U-NetADV, and in the right ventricle (24.96%) for the U-NetVEL, while for maximum turbulent kinetic energy were in the pulmonary artery for both models, with a value of -15.5% for U-NetADV and 15.38% for the U-NetVEL. CONCLUSION:Deep learning-enabled referenceless 4D flow CMR permits velocities and flow volumes quantification comparable to conventional 4D flow. Omitting the reference encoding reduces the amount of acquired data by 25%, thus allowing shorter scan times or improved resolution, which is valuable for utilization in the clinical routine.