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Background Fetal cardiovascular magnetic resonance (CMR) imaging may provide a valuable adjunct to fetal echocardiography in the evaluation of congenital cardiovascular pathologies. However, dynamic fetal CMR is difficult due to the lack of direct in-utero cardiac gating. The aim of this study was to investigate the effectiveness of a newly developed Doppler ultrasound (DUS) device in humans for fetal CMR gating. Methods Fifteen fetuses (gestational age 30–39 weeks) were examined using 1.5 T CMR scanners at three different imaging sites. A newly developed CMR-compatible DUS device was used to generate gating signals from fetal cardiac motion. Gated dynamic balanced steady-state free precession images were acquired in 4-chamber and short-axis cardiac views. Gating signals during data acquisition were analyzed with respect to trigger variability and sensitivity. Image quality was assessed by measuring endocardial blurring (EB) and by image evaluation using a 4-point scale. Left ventricular (LV) volumetry was performed using the single-plane ellipsoid model. Results Gating signals from the fetal heart were detected with a variability of 26 ± 22 ms and a sensitivity of trigger detection of 96 ± 4%. EB was 2.9 ± 0.6 pixels (4-chamber) and 2.5 ± 0.1 pixels (short axis). Image quality scores were 3.6 ± 0.6 (overall), 3.4 ± 0.7 (mitral valve), 3.4 ± 0.7 (foramen ovale), 3.6 ± 0.7 (atrial septum), 3.7 ± 0.5 (papillary muscles), 3.8 ± 0.4 (differentiation myocardium/lumen), 3.7 ± 0.5 (differentiation myocardium/lung), and 3.9 ± 0.4 (systolic myocardial thickening). Inter-observer agreement for the scores was moderate to very good (kappa 0.57–0.84) for all structures. LV volumetry revealed mean values of 2.8 ± 1.2 ml (end-diastolic volume), 0.9 ± 0.4 ml (end systolic volume), 1.9 ± 0.8 ml (stroke volume), and 69.1 ± 8.4% (ejection fraction). Conclusion High-quality dynamic fetal CMR was successfully performed using a newly developed DUS device for direct fetal cardiac gating. This technique has the potential to improve the utility of fetal CMR in the evaluation of congenital pathologies.

Background Accurate quantification of iron load is of importance in tailoring the therapy for patients with iron load disease. Magnetic resonance (MR) imaging is commonly used to assess iron load in different organs by calculating the T2* value. Estimation of precision and uncertainty of the obtained T2* value may be useful for determining changes in iron load between follow-up scans and for titration of treatment. Therefore, the purpose of this study was to develop and validate a new T2* analysis method, providing certainty estimates for quantification of iron load in heart and liver. Methods The proposed method is ar egion of interest (ROI)based algorithm which changes curve-fitting procedure based on the results from an initial T2* estimate using a 3-parameter, noise-corrected model. The certainty estimate, presented as the T2* value confidence interval, is derived from multiple sub-regions within the selected ROI. Except for ROI delineation, the proposed method does not require any user interaction. Phantom imaging was performed on a 1.5T system, with two clinically available multi-echo gradient-recalled echo sequences for cardiac and liver imaging. Phantoms were constructed to cover the clinically important range of T2*. A T2* single-echo gradient-echo sequence with TR set to 6 × T1 and a 50° flip angle was used as reference standard. Computer simulations were performed to assess accuracy and precision from 2 000 repetitions at SNR=15. Inter- and intra-observer variability was obtained in patients (n=22) by one experienced and one inexperienced observer.

Background Quantitative blood flow and aspects of regional myocardial function such as myocardial displacement and strain can be measured using phase-contrast cardiovascular magnetic resonance (PC-CMR). Since a gadolinium-based contrast agent is often used to measure myocardial infarct size, we sought to determine whether the contrast agent affects measurements of aortic flow and myocardial displacement and strain. Phase-contrast data pre and post contrast agent was acquired during free breathing using 1.5T PC-CMR. Results For aortic flow and regional myocardial function 12 and 17 patients were analysed, respectively. The difference pre and post contrast agent was 0.03 ± 0.16 l/min for cardiac output, and 0.1 ± 0.5 mm for myocardial displacement. Linear regression for myocardial displacement (MD) after and before contrast agent (CA) showed MDpostCA = 0.95MDpreCA+0.05 (r = 0.95, p < 0.001). For regional myocardial function, the contrast-to-noise ratios for left ventricular myocardial wall versus left ventricular lumen were pre and post contrast agent administration 7.4 ± 3.3 and 4.4 ± 8.9, respectively (p < 0.001). The contrast-to-noise ratios for left ventricular myocardial wall versus surrounding tissue were pre and post contrast agent administration -16.9 ± 22 and -0.2 ± 6.3, respectively (p < 0.0001). Conclusions Quantitative measurements of aortic flow yield equal results both in the absence and presence of gadolinium contrast agent. The total examination time may thereby be reduced when assessing both viability and quantitative flow using PC-CMR, by assessing aortic flow post contrast agent administration. Phase-contrast information for myocardial displacement is also assessable both in the absence and presence of contrast agent. However, delineation of the myocardium may be difficult or impossible post contrast agent due to the lower image contrast. Acquisition of myocardial displacement should therefore be performed pre contrast agent using current PC-CMR sequences.

Introduction In the situation of acute coronary occlusion, the myocardium supplied by the occluded vessel is subject to ischemia and is referred to as the myocardium at risk (MaR). It has previously been shown that cardiac magnetic resonance (CMR) imaging can be used for the assessment of MaR employing a T2-weighted edema sequence. Recently, it has been suggested that the endocardial extent of hyperenhancement as assessed by contrast enhanced CMR can also be used to quantify the MaR.

Background The time course of infarct evolution, i.e. how fast myocardial infarction (MI) develops during coronary artery occlusion, is well known for several species, whereas no direct evidence exists on the evolution of MI size normalized to myocardium at risk (MaR) in man. Despite the lack of direct evidence, current literature often refers to the "golden hour" as the time during which myocardial salvage can be accomplished by reperfusion therapy. Therefore, the aim of the present study was to investigate how duration of myocardial ischemia affects infarct evolution in man in relation to previous animal data. Consecutive patients with clinical signs of acute myocardial ischemia were screened and considered for enrollment. Particular care was taken to assure uniformity of the patients enrolled with regard to old MI, success of revascularization, collateral flow, release of biochemical markers prior to intervention etc. Sixteen patients were ultimately included in the study. Myocardium at risk was assessed acutely by acute Myocardial Perfusion Single photon emission computed tomography (MPS) and by T2 imaging (T2-STIR) cardiovascular magnetic resonance (CMR) after one week in 10 of the 16 patients. Infarct size was measured by late gadolinium enhancement (LGE) at one week. Results The time to reach 50% MI of the MaR (T50) was significantly shorter in pigs (37 min), rats (41 min) and dogs (181 min) compared to humans (288 min). There was no significant difference in T50 when using MPS compared to T2-STIR (p = 0.53) for assessment of MaR (288 ± 23 min vs 310 ± 22 min, T50 ± standard error). The transmural extent of MI increased progressively as the duration of ischemia increased (R2 = 0.56, p < 0.001). Conclusion This is the first study to provide direct evidence of the time course of acute myocardial infarct evolution in relation to MaR in man with first-time MI. Infarct evolution in man is significantly slower than in pigs, rats and dogs. Furthermore, infarct evolution assessments in man are similar when using MPS acutely and T2-STIR one week later for determination of MaR, which significantly facilitates future clinical trials of cardioprotective therapies in acute coronary syndrome by the use of CMR.

To assess reperfusion therapy, it is necessary to determine how much myocardium is salvaged by measuring the final infarct size in relation to the initial myocardium at risk (MaR) of the left ventricle (LV). T2 weighted MRI has recently been shown to be able to identify MaR but has not been validated against an independent method in humans.

Introduction Based on animal studies, it is currently accepted that duration of ischemia is a major determinant of the ability to salvage jeopardized myocardium by restoring the coronary blood flow and myocardial perfusion. In experimental animal studies it is possible to determine the exact time of occlusion as well as to ensure complete, persistent ischemia during the time of coronary occlusion. In humans, however, it is impossible to determine either the exact time of acute occlusion or whether spontaneous reperfusion and re-occlusion has occurred prior to the time of reperfusion therapy.

Quantification of myocardial and liver iron load has become a mainstay of guiding therapy in thalassaemia patients. However, current quantification methods are user dependent for data-point exclusion before curve fitting, and do not report the T2* certainty. Recently, an automatic inline maximum likelihood estimate (MLE) method with k-space Rician noise correction was validated against the reference standard manual truncation method. We now present a vendor-independent offline tool for fully automatic post processing and T2* quantification with certainty estimates, tested in computer simulations and patients with iron overload.

Background In the situation of acute coronary occlusion, the myocardium supplied by the occluded vessel is subject to ischemia and is referred to as the myocardium at risk (MaR). Single photon emission computed tomography has previously been used for quantitative assessment of the MaR. It is, however, associated with considerable logistic challenges for employment in clinical routine. Recently, T2-weighted cardiovascular magnetic resonance (CMR) has been introduced as a new method for assessing MaR several days after the acute event. Furthermore, it has been suggested that the endocardial extent of infarction as assessed by late gadolinium enhanced (LGE) CMR can also be used to quantify the MaR. Hence, we sought to assess the ability of endocardial extent of infarction by LGE CMR to predict MaR as compared to T2-weighted imaging. Methods Thirty-seven patients with early reperfused first-time ST-segment elevation myocardial infarction underwent CMR imaging within the first week after percutaneous coronary intervention. The ability of endocardial extent of infarction by LGE CMR to assess MaR was evaluated using T2-weighted imaging as the reference method. Results MaR determined with T2-weighted imaging (34 ± 10%) was significantly higher (p < 0.001) compared to the MaR determined with endocardial extent of infarction (23 ± 12%). There was a weak correlation between the two methods (r2 = 0.17, p = 0.002) with a bias of -11 ± 12%. Myocardial salvage determined with T2-weighted imaging (58 ± 22%) was significantly higher (p < 0.001) compared to myocardial salvage determined with endocardial extent of infarction (45 ± 23%). No MaR could be determined by endocardial extent of infarction in two patients with aborted myocardial infarction. Conclusions This study demonstrated that the endocardial extent of infarction as assessed by LGE CMR underestimates MaR in comparison to T2-weighted imaging, especially in patients with early reperfusion and aborted myocardial infarction.

Introduction. Manual delineation of the left ventricle is clinical standard for quantification of cardiovascular magnetic resonance images despite being time consuming and observer dependent. Previous automatic methods generally do not account for one major contributor to stroke volume, the long-axis motion. Therefore, the aim of this study was to develop and validate an automatic algorithm for time-resolved segmentation covering the whole left ventricle, including basal slices affected by long-axis motion. Methods. Ninety subjects imaged with a cine balanced steady state free precession sequence were included in the study (training set , test set ). Manual delineation was reference standard and second observer analysis was performed in a subset (). The automatic algorithm uses deformable model with expectation-maximization, followed by automatic removal of papillary muscles and detection of the outflow tract. Results. The mean differences between automatic segmentation and manual delineation were EDV −11 mL, ESV 1 mL, EF −3%, and LVM 4 g in the test set. Conclusions. The automatic LV segmentation algorithm reached accuracy comparable to interobserver for manual delineation, thereby bringing automatic segmentation one step closer to clinical routine. The algorithm and all images with manual delineations are available for benchmarking.