The pathophysiology behind thrombus formation in paroxysmal atrial fibrillation (AF) patients is very complex. This can be due to left atrial (LA) flow changes, remodeling, or both. We investigated... Show moreThe pathophysiology behind thrombus formation in paroxysmal atrial fibrillation (AF) patients is very complex. This can be due to left atrial (LA) flow changes, remodeling, or both. We investigated differences for cardiovascular magnetic resonance (CMR)-derived LA 4D flow and remodeling characteristics between paroxysmal AF patients and patients without cardiac disease. In this proof-of-concept study, the 4D flow data were acquired in 10 patients with paroxysmal AF (age=61 +/- 8 years) and 5 age/gender matched controls (age=56 +/- 1 years) during sinus rhythm. The following LA and LA appendage flow parameters were obtained: flow velocity (mean, peak), stasis defined as the relative volume with velocities<10 cm/s, and kinetic energy (KE). Furthermore, LA global strain values were derived from b-SSFP cine images using dedicated CMR feature-tracking software. Even in sinus rhythm, LA mean and peak flow velocities over the entire cardiac cycle were significantly lower in paroxysmal AF patients compared to controls [(13.12.4 cm/s vs. 16.7 +/- 2.1 cm/s, p=0.01) and (19.3 +/- 4.7 cm/s vs. 26.8 +/- 5.5 cm/s, p=0.02), respectively]. Moreover, paroxysmal AF patients expressed more stasis of blood than controls both in the LA (43.2 +/- 10.8% vs. 27.8 +/- 7.9%, p=0.01) and in the LA appendage (73.3 +/- 5.7% vs. 52.8 +/- 16.2%, p=0.04). With respect to energetics, paroxysmal AF patients demonstrated lower mean and peak KE values (indexed to maximum LA volume) than controls. No significant differences were observed for LA volume, function, and strain parameters between the groups. Global LA flow dynamics in paroxysmal AF patients appear to be impaired including mean/peak flow velocity, stasis fraction, and KE, partly independent of LA remodeling. This pathophysiological flow pattern may be of clinical value to explain the increased incidence of thromboembolic events in paroxysmal AF patients, in the absence of actual AF or LA remodeling. Show less
Amier, R.P.; Marcks, N.; Hooghiemstra, A.M.; Nijveldt, R.; Buchem, M.A. van; Roos, A. de; ... ; Heart-Brain Connection Consortium 2021
OBJECTIVES This study sought to investigate the extent of hypertensive exposure as assessed by cardiovascular magnetic resonance imaging (MRI) in relation to cerebral small vessel disease (CSVD)... Show moreOBJECTIVES This study sought to investigate the extent of hypertensive exposure as assessed by cardiovascular magnetic resonance imaging (MRI) in relation to cerebral small vessel disease (CSVD) and cognitive impairment, with the aim of understanding the role of hypertension in the early stages of deteriorating brain health.BACKGROUND Preserving brain health into advanced age is one of the great challenges of modern medicine. Hypertension is thought to induce vascular brain injury through exposure of the cerebral microcirculation to increased pressure/pulsatility. Cardiovascular MRI provides markers of (subclinical) hypertensive exposure, such as aortic stiffness by puke wave velocity (PWV), left ventricular (LV) mass index (LVMi), and concentricity by mass-to-volume ratio.METHODS A total of 559 participants from the Heart-Brain Connection Study (431 patients with manifest cardiovascular disease and 128 control participants), age 67.8 +/- 8.8 years, underwent 3.0-T heart-brain MRI and extensive neuropsychological testing. Aortic PWV, LVMi, and LV mass-to-volume ratio were evaluated in relation to presence of CSVD and cognitive impairment. Effect modification by patient group was investigated by interaction terms; results are reported pooled or stratified accordingly.RESULTS Aortic PWV (odds ratio [OR]: 1.17; 95% confidence interval [CI]: 1.05 to 1.30 in patient groups only), LVMi (in carotid occlusive disease, OR: 5.69; 95% CI: 1.63 to 19.87; in other groups, OR: 1.30; 95% CI: 1.05 to 1.62]) and LV mass-to-volume ratio (OR: 1.81; 95% CI: 1.46 to 2.24) were associated with CSVD. Aortic PWV (OR: 1.07; 95% CI: 1.02 to 1.13) and LV mass-to-volume ratio (OR: 1.27; 95% CI: 1.07 to 1.51) were also associated with cognitive impairment. Relations were independent of sociodemographic and cardiac index and mostly persisted after correction for systolic blood pressure or medical history of hypertension. Causal mediation analysis showed significant mediation by presence of CSVD in the relation between hypertensive exposure markers and cognitive impairment.CONCLUSIONS The extent of hypertensive exposure is associated with CSVD and cognitive impairment beyond clinical brood pressure or medical history. The mediating role of CSVD suggests that hypertension may lead to cognitive impairment through the occurrence of CSVD. (C) 2021 Published by Elsevier on behalf of the American College of Cardiology Foundation. Show less
Purpose To compare cardiac magnetic resonance imaging (CMR) with [O-15]H2O positron emission tomography (PET) for quantification of absolute myocardial blood flow (MBF) and myocardial flow reserve ... Show morePurpose To compare cardiac magnetic resonance imaging (CMR) with [O-15]H2O positron emission tomography (PET) for quantification of absolute myocardial blood flow (MBF) and myocardial flow reserve (MFR) in patients with coronary artery disease (CAD). Methods Fifty-nine patients with stable CAD underwent CMR and [O-15]H2O PET. The CMR imaging protocol included late gadolinium enhancement to rule out presence of scar tissue and perfusion imaging using a dual sequence, single bolus technique. Absolute MBF was determined for the three main vascular territories at rest and during vasodilator stress. Results CMR measurements of regional stress MBF and MFR showed only moderate correlation to those obtained using PET (r = 0.39; P < 0.001 for stress MBF and r = 0.36; P < 0.001 for MFR). Bland-Altman analysis revealed a significant bias of 0.2 +/- 1.0 mL/min/g for stress MBF and - 0.5 +/- 1.2 for MFR. CMR-derived stress MBF and MFR demonstrated area under the curves of respectively 0.72 (95% CI: 0.65 to 0.79) and 0.76 (95% CI: 0.69 to 0.83) and had optimal cutoff values of 2.35 mL/min/g and 2.25 for detecting abnormal myocardial perfusion, defined as [O-15]H2O PET-derived stress MBF <= 2.3 mL/min/g and MFR <= 2.5. Using these cutoff values, CMR and PET were concordant in 137 (77%) vascular territories for stress MBF and 135 (80%) vascular territories for MFR. Conclusion CMR measurements of stress MBF and MFR showed modest agreement to those obtained with [O-15]H2O PET. Nevertheless, stress MBF and MFR were concordant between CMR and [O-15]H2O PET in 77% and 80% of vascular territories, respectively. Show less
Everaars, H.; Hoeven, N.W. van der; Janssens, G.N.; Leeuwen, M.A. van; Loon, R.B. van; Schumacher, S.P.; ... ; Nijveldt, R. 2020
OBJECTIVES This study sought to determine the agreement between cardiac magnetic resonance (CMR) imaging and invasive measurements of fractional flow reserve (FFR) in the evaluation of nonculprit... Show moreOBJECTIVES This study sought to determine the agreement between cardiac magnetic resonance (CMR) imaging and invasive measurements of fractional flow reserve (FFR) in the evaluation of nonculprit lesions after ST-segment elevation myocardial infarction (STEMI). In addition, we investigated whether fully quantitative analysis of myocardial perfusion is superior to semiquantitative and visual analysis.BACKGROUND The agreement between CMR and FFR in the evaluation of nonculprit lesions in patients with STEMI with multivessel disease is unknown.METHODS Seventy-seven patients with STEMI with at least 1 intermediate (diameter stenosis 50% to 90%) nonculprit lesion underwent CMR and invasive coronary angiography in conjunction with FFR measurements at 1 month after primary intervention. The imaging protocol included stress and rest perfusion, cine imaging, and late gadolinium enhancement. Fully quantitative, semiquantitative, and visual analysis of myocardial perfusion were compared against a reference of FFR. Hemodynamically obstructive was defined as FFR <= 0.80.RESULTS Hemodynamically obstructive nonculprit lesions were present in 31 (40%) patients. Visual analysis displayed an area under the curve (AUC) of 0.74 (95% confidence interval [CI]: 0.62 to 0.83), with a sensitivity of 73% and a specificity of 70%. For semiquantitative analysis, the relative upslope of the stress signal intensity time curve and the relative upslope derived myocardial flow reserve had respective AUCs of 0.66 (95% CI: 0.54 to 0.77) and 0.71 (95% CI: 0.59 to 0.81). Fully quantitative analysis did not augment diagnostic performance (all p > 0.05). Stress myocardial blood flow displayed an AUC of 0.76 (95% CI: 0.64 to 0.85), with a sensitivity of 69% and a specificity of 77%. Similarly, MFR displayed an AUC of 0.82 (95% CI: 0.71 to 0.90), with a sensitivity of 82% and a specificity of 71%.CONCLUSIONS CMR and FFR have moderate-good agreement in the evaluation of nonculprit lesions in patients with STEMI with multivessel disease. Fully quantitative, semiquantitative, and visual analysis yield similar diagnostic performance. (C) 2020 by the American College of Cardiology Foundation. Show less
BackgroundA velocity offset error in phase contrast cardiovascular magnetic resonance (CMR) imaging is a known problem in clinical assessment of flow volumes in vessels around the heart. Earlier... Show moreBackgroundA velocity offset error in phase contrast cardiovascular magnetic resonance (CMR) imaging is a known problem in clinical assessment of flow volumes in vessels around the heart. Earlier studies have shown that this offset error is clinically relevant over different systems, and cannot be removed by protocol optimization. Correction methods using phantom measurements are time consuming, and assume reproducibility of the offsets which is not the case for all systems. An alternative previously published solution is to correct the in-vivo data in post-processing, interpolating the velocity offset from stationary tissue within the field-of-view. This study aims to validate this interpolation-based offset correction in-vivo in a multi-vendor, multi-center setup.MethodsData from six 1.5T CMR systems were evaluated, with two systems from each of the three main vendors. At each system aortic and main pulmonary artery 2D flow studies were acquired during routine clinical or research examinations, with an additional phantom measurement using identical acquisition parameters. To verify the phantom acquisition, a region-of-interest (ROI) at stationary tissue in the thorax wall was placed and compared between in-vivo and phantom measurements. Interpolation-based offset correction was performed on the in-vivo data, after manually excluding regions of spatial wraparound. Correction performance of different spatial orders of interpolation planes was evaluated.ResultsA total of 126 flow measurements in 82 subjects were included. At the thorax wall the agreement between in-vivo and phantom was -0.20.6cm/s. Twenty-eight studies were excluded because of a difference at the thorax wall exceeding 0.6cm/s from the phantom scan, leaving 98. Before correction, the offset at the vessel as assessed in the phantom was -0.41.5cm/s, which resulted in a-5 +/- 16% error in cardiac output. The optimal order of the interpolation correction plane was 1st order, except for one system at which a 2nd order plane was required. Application of the interpolation-based correction revealed a remaining offset velocity of 0.1 +/- 0.5cm/s and 0 +/- 5% error in cardiac output.Conclusions p id=Par4 This study shows that interpolation-based offset correction reduces the offset with comparable efficacy as phantom measurement phase offset correction, without the time penalty imposed by phantom scans.Trial registration p id=Par5 The study was registered in The Netherlands National Trial Register (NTR) under TC 4865. Registered 19 September 2014. Retrospectively registered. Show less
Laan, A.M. van der; Hirsch, A.; Nijveldt, R.; Vleuten, P.A. van der; Giessen, W.J. van der; Doevendans, P.A.; ... ; Piek, J.J. 2012
