16 research outputs found

    Diagnosis and treatment of vascular graft and endograft infections:a structured clinical approach

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    A vascular graft or endograft infection (VGEI) is a severe complication that can occur after vascular graft or endograft surgery and is associated with high morbidity and mortality rates. A multidisciplinary approach, consisting of a team of vascular surgeons, infectious diseases specialists, medical microbiologists, radiologists, nuclear medicine specialists, and hospital pharmacists, is needed to adequately diagnose and treat VGEI. A structured diagnostic, antibiotic, and surgical treatment algorithm helps clinical decision making and ultimately aims to improve the clinical outcome of patients with a VGEI

    Interpretation of pre-morbid cardiac 3T MRI findings in overweight and hypertensive young adults

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    In young adults, overweight and hypertension possibly already trigger cardiac remodeling as seen in mature adults, potentially overlapping non-ischemic cardiomyopathy findings. To this end, in young overweight and hypertensive adults, we aimed to investigate changes in left ventricular mass (LVM) and cardiac volumes, and the impact of different body scales for indexation. We also aimed to explore the presence of myocardial fibrosis, fat and edema, and changes in cellular mass with extracellular volume (ECV), T(1) and T(2) tissue characteristics. We prospectively recruited 126 asymptomatic subjects (51% male) aged 27–41 years for 3T cardiac magnetic resonance imaging: 40 controls, 40 overweight, 17 hypertensive and 29 hypertensive overweight. Myocyte mass was calculated as (100%–ECV) * height(2.7)-indexed LVM. Absolute LVM was significantly increased in overweight, hypertensive and hypertensive overweight groups (104 ± 23, 109 ± 27, 112 ± 26 g) versus controls (87 ± 21 g), with similar volumes. Body surface area (BSA) indexation resulted in LVM normalization in overweights (48 ± 8 g/m(2)) versus controls (47 ± 9 g/m(2)), but not in hypertensives (55 ± 9 g/m(2)) and hypertensive overweights (52 ± 9 g/m(2)). BSA-indexation overly decreased volumes in overweight versus normal-weight (LV end-diastolic volume; 80 ± 14 versus 92 ± 13 ml/m(2)), where height(2.7)-indexation did not. All risk groups had lower ECV (23 ± 2%, 23 ± 2%, 23 ± 3%) than controls (25 ± 2%) (P = 0.006, P = 0.113, P = 0.039), indicating increased myocyte mass (16.9 ± 2.7, 16.5 ± 2.3, 18.1 ± 3.5 versus 14.0 ± 2.9 g/m(2.7)). Native T(1) values were similar. Lower T(2) values in the hypertensive overweight group related to heart rate. In conclusion, BSA-indexation masks hypertrophy and causes volume overcorrection in overweight subjects compared to controls, height(2.7)-indexation therefore seems advisable

    Reference Cardiac MRI Values

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    Head-to-head com parison between echocardiography and cardiac MRI in the evaluation of the athlete's heart

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    Objective: Echocardiographic cut-off values are often used for cardiac MRI in athletic persons. This study investigates the difference between echocardiographic and cardiac MRI measurements of ventricular and atrial dimensions and ventricular wall thickness, and its effect on volume and wall mass prediction in athletic subjects compared with non-athletic controls. Methods: Healthy non-athletic (59), regular athletic (59) and elite athletic (63) persons, aged 18-39 years and training 2.5±1.9, 13.0±3.0 and 25.0±5.4 h/week, respectively (p< 0.001), underwent echocardiography and cardiac MRI consecutively. Left ventricular (LV) and right ventricular (RV) dimensions were measured on both modalities. LV and RV end-diastolic and end-systolic volumes and LV wall mass were determined on cardiac MRI. Echocardiographic M-mode LV volumes (Teichholz formula) and LV wall mass (American Society of Echocardiography formula) were calculated. Results: LV and RV dimensions were smaller on echocardiography (p< 0.001), and although the correlation with the cardiac MRI volume was good (p< 0.01), the difference in volume was large (LV end-diastolic volume difference 93±32 g, p< 0.001). LV wall thickness and calculated wall mass were significantly (p< 0.001) larger on echocardiography (wall mass difference -101±34 g, p< 0.001). Differences in absolute dimensions did not change significantly between non-athletic and athletic persons; however, the difference in echocardiographic estimations of LV volumes and wall mass did increase significantly with the larger athlete's heart, requiring possible correction of the standard echocardiographic formulas. Conclusions: Echocardiography shows systematically smaller atrial and ventricular dimensions and volumes, and larger wall thickness and mass, compared with cardiac MRI. Correction for the echocardiographic formulas can facilitate better intertechnique comparability. These findings should be taken into account in the interpretation of cardiac MRI findings in athletic subjects in whom cardiomyopathy is suspected on echocardiogr aphy

    Impact of revised Task Force Criteria: Distinguishing the athlete's heart from ARVC/D using cardiac magnetic resonance imaging

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    Background: Cardiac magnetic resonance (CMR) evaluation of athletes for arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is complicated by overlapping features such as right ventricular (RV) volume increase. The revised ARVC/D diagnostic Task Force Criteria (TFC) incorporate cut-off values for RV ejection fraction (EF) and RV end-diastolic volume (EDV) on CMR.Design: To distinguish ARVC/D patients from athletes we compared CMR ventricular volumes, function, TFC cut-off values, and LV/RV ratios since athletes show proportionate, and ARVC/D patients disproportionate, changes in LV and RV.Methods: Quantitative CMR parameters of 33 ARVC/D patients (64% male, mean age 45.4 years, diagnosed by revised TFC), 66 healthy athletes and 66 healthy non-athletes (sex and age matched) were compared using revised TFC and new cut-off values representing LV/RV balance.Results and conclusions: Absolute values for ARVC/D patients/athletes/non-athletes were: in males, RV EDV 149/133/106 ml/m2, ratio EDV LV/RV 0.70/0.91/0.93, RV EF 34/52/54%, LV EF 48/57/58%, ratio EF LV/RV 1.49/1.10/1.09; and in females, RV EDV 115/115/91 ml/m2, ratio EDV LV/RV 0.86/0.94/0.97, RV EF 43/54/58%, LV EF 52/57/61%, ratio EF LV/RV 1.23/1.08/1.04 (p-values < 0.05). Areas under the ROC-curve are 0.68 (RV EDV index), 0.84 (LV/RV EDV ratio) and 0.93 (RV EF), demonstrating significantly (p < 0.001) better performance of RV EF and LV/RV EDV ratio. If a wall motion abnormality is present (observed in 30 ARVC/D patients and not in healthy subjects), RV EF can help distinguish ARVC/D from physiological cardiac adaptation in athletes on CMR whereas RV EDV index cannot. A good alternative in athletes is the LV/RV EDV ratio, representing normal proportionate adaptation of both ventricles

    Native T1 reference values for nonischemic cardiomyopathies and populations with increased cardiovascular risk : A systematic review and meta-analysis

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    Background: Although cardiac MR and T1 mapping are increasingly used to diagnose diffuse fibrosis based cardiac diseases, studies reporting T1 values in healthy and diseased myocardium, particular in nonischemic cardiomyopathies (NICM) and populations with increased cardiovascular risk, seem contradictory. Purpose: To determine the range of native myocardial T1 value ranges in patients with NICM and populations with increased cardiovascular risk. Study Type: Systemic review and meta-analysis. Population: Patients with NICM, including hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM), and patients with myocarditis (MC), iron overload, amyloidosis, Fabry disease, and populations with hypertension (HT), diabetes mellitus (DM), and obesity. Field Strength/Sequence: (Shortened) modified Look–Locker inversion-recovery MR sequence at 1.5 or 3T. Assessment: PubMed and Embase were searched following the PRISMA guidelines. Statistical Tests: The summary of standard mean difference (SMD) between the diseased and a healthy control populations was generated using a random-effects model in combination with meta-regression analysis. Results: The SMD for HCM, DCM, and MC patients were significantly increased (1.41, 1.48, and 1.96, respectively, P < 0.01) compared with healthy controls. The SMD for HT patients with and without left-ventricle hypertrophy (LVH) together was significantly increased (0.19, P = 0.04), while for HT patients without LVH the SMD was zero (0.03, P = 0.52). The number of studies on amyloidosis, iron overload, Fabry disease, and HT patients with LVH did not meet the requirement to perform a meta-analysis. However, most studies reported a significantly increased T1 for amyloidosis and HT patients with LVH and a significant decreased T1 for iron overload and Fabry disease patients. Data Conclusions: Native T1 mapping by using an (Sh)MOLLI sequence can potentially assess myocardial changes in HCM, DCM, MC, iron overload, amyloidosis, and Fabry disease compared to controls. In addition, it can help to diagnose left-ventricular remodeling in HT patients. Level of Evidence: 2. Technical Efficacy: Stage 3. J. Magn. Reson. Imaging 2018;47:891–912

    Performance of visual, manual, and automatic coronary calcium scoring of cardiac 13N-ammonia PET/low dose CT

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    Background: Coronary artery calcium is a well-known predictor of major adverse cardiac events and is usually scored manually from dedicated, ECG-triggered calcium scoring CT (CSCT) scans. In clinical practice, a myocardial perfusion PET scan is accompanied by a non-ECG triggered low dose CT (LDCT) scan. In this study, we investigated the accuracy of patients’ cardiovascular risk categorisation based on manual, visual, and automatic AI calcium scoring using the LDCT scan. Methods: We retrospectively enrolled 213 patients. Each patient received a 13N-ammonia PET scan, an LDCT scan, and a CSCT scan as the gold standard. All LDCT and CSCT scans were scored manually, visually, and automatically. For the manual scoring, we used vendor recommended software (Syngo.via, Siemens). For visual scoring a 6-points risk scale was used (0; 1-10; 11-100; 101-400; 401-100; > 1 000 Agatston score). The automatic scoring was performed with deep learning software (Syngo.via, Siemens). All manual and automatic Agatston scores were converted to the 6-point risk scale. Manual CSCT scoring was used as a reference. Results: The agreement of manual and automatic LDCT scoring with the reference was low [weighted kappa 0.59 (95% CI 0.53-0.65); 0.50 (95% CI 0.44-0.56), respectively], but the agreement of visual LDCT scoring was strong [0.82 (95% CI 0.77-0.86)]. Conclusions: Compared with the gold standard manual CSCT scoring, visual LDCT scoring outperformed manual LDCT and automatic LDCT scoring

    Interpretation of pre-morbid cardiac 3T MRI findings in overweight and hypertensive young adults

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    In young adults, overweight and hypertension possibly already trigger cardiac remodeling as seen in mature adults, potentially overlapping non-ischemic cardiomyopathy findings. To this end, in young overweight and hypertensive adults, we aimed to investigate changes in left ventricular mass (LVM) and cardiac volumes, and the impact of different body scales for indexation. We also aimed to explore the presence of myocardial fibrosis, fat and edema, and changes in cellular mass with extracellular volume (ECV), T1 and T2 tissue characteristics. We prospectively recruited 126 asymptomatic subjects (51% male) aged 27-41 years for 3T cardiac magnetic resonance imaging: 40 controls, 40 overweight, 17 hypertensive and 29 hypertensive overweight. Myocyte mass was calculated as (100%-ECV) * height2.7-indexed LVM. Absolute LVM was significantly increased in overweight, hypertensive and hypertensive overweight groups (104 ± 23, 109 ± 27, 112 ± 26 g) versus controls (87 ± 21 g), with similar volumes. Body surface area (BSA) indexation resulted in LVM normalization in overweights (48 ± 8 g/m2) versus controls (47 ± 9 g/m2), but not in hypertensives (55 ± 9 g/m2) and hypertensive overweights (52 ± 9 g/m2). BSA-indexation overly decreased volumes in overweight versus normal-weight (LV end-diastolic volume; 80 ± 14 versus 92 ± 13 ml/m2), where height2.7-indexation did not. All risk groups had lower ECV (23 ± 2%, 23 ± 2%, 23 ± 3%) than controls (25 ± 2%) (P = 0.006, P = 0.113, P = 0.039), indicating increased myocyte mass (16.9 ± 2.7, 16.5 ± 2.3, 18.1 ± 3.5 versus 14.0 ± 2.9 g/m2.7). Native T1 values were similar. Lower T2 values in the hypertensive overweight group related to heart rate. In conclusion, BSA-indexation masks hypertrophy and causes volume overcorrection in overweight subjects compared to controls, height2.7-indexation therefore seems advisable
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