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Delayed enhancement (DE) MRI is an important tool in diagnosis of cardiovascular disease as it can reveal different characteristics of the myocardium scars including infarction and no-reflow. Automatic segmentation of different regions has the advantage of improved accuracy and reduced inter-observer variability in quantifying key imaging biomarkers such as percentage of scars. In recent years deep learning has led to drastic performance improvement in automatic segmentation tasks using the UNet architecture. Cardiac MRI segmentation is a challenging task due to the high variability in imaging contrast, orientation and signal-to-noise ratio; specifically, for short-axis views, as they are double-oblique slices, due to the different orientations of the heart and operator choice, the overall appearance of the image can vary significantly, which poses a challenge to the neural networks as they cannot learn a consistent global anatomy. In this paper we developed a rotation-based augmentation to address this issue in both training and testing steps by eliminating the variance in orientations and demonstrated its effectiveness. 2D dilated UNet was used as the backbone network structure. On the test dataset, Dice scores of 0.933 for LV blood pool, 0.824 for myocardium, 0.578 for infarction and 0.697 for no re-flow regions were archived using the proposed framework.

Delayed enhancement (DE) MRI is an important tool in diagnosis of cardiovascular disease as it can reveal different characteristics of the myocardium scars including infarction and no-reflow. Automatic segmentation of different regions has the advantage of improved accuracy and reduced inter-observer variability in quantifying key imaging biomarkers such as percentage of scars. In recent years deep learning has led to drastic performance improvement in automatic segmentation tasks using the UNet architecture. Cardiac MRI segmentation is a challenging task due to the high variability in imaging contrast, orientation and signal-to-noise ratio; specifically, for short-axis views, as they are double-oblique slices, due to the different orientations of the heart and operator choice, the overall appearance of the image can vary significantly, which poses a challenge to the neural networks as they cannot learn a consistent global anatomy. In this paper we developed a rotation-based augmentation to address this issue in both training and testing steps by eliminating the variance in orientations and demonstrated its effectiveness. 2D dilated UNet was used as the backbone network structure. On the test dataset, Dice scores of 0.933 for LV blood pool, 0.824 for myocardium, 0.578 for infarction and 0.697 for no re-flow regions were archived using the proposed framework.

After a reperfused myocardial infarction (MI), dynamic tissue changes occur (edema, inflammation, microvascular obstruction, hemorrhage, cardiomyocyte necrosis, and ultimately replacement by fibrosis). The extension and magnitude of these changes contribute to long-term prognosis after MI. Cardiac magnetic resonance (CMR) is the gold-standard technique for noninvasive myocardial tissue characterization. CMR is also the preferred methodology for the identification of potential benefits associated with new cardioprotective strategies both in experimental and clinical trials. However, there is a wide heterogeneity in CMR methodologies used in experimental and clinical trials, including time of post-MI scan, acquisition protocols, and, more importantly, selection of endpoints. There is a need for standardization of these methodologies to improve the translation into a real clinical benefit. The main objective of this scientific expert panel consensus document is to provide recommendations for CMR endpoint selection in experimental and clinical trials based on pathophysiology and its association with hard outcomes. The CNIC is supported by the ISCiii, MICINN, and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (award SEV-2015-0505). This research was supported (in part) by the Intramural Research Program of the National Institutes of Health, National Heart, Lung, and Blood Institute. BI received funding for work in the topic of this review from the Carlos III Institute of Health–Fondo de Investigacion Sanitaria- and the European Regional Development Fund (ERDF/FEDER) (PI13/01979, DTS17/00136), the Spanish Ministry of Science, Innovation and Universities (MICINN) and ERDF/FEDER SAF2013-49663-EXP, Red Madrileña de nanomedicina en imagen molecular (RENIM-CM Ref# B2017/BMD-3867), H2020 ERA-CVD (JTC2016/APCIN-ISCIII-2016/AC16/00021), and Fundación BBVA 2016. CBD is supported by the NIHR Biomedical Research Centre at University Hospitals Bristol NHS Foundation Trust and the University of Bristol. The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the National Institute for Health Research or the Department of Health and Social Care. RF-J is a recipient of funding from the European Union Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement No. 707642. DGD was supported by the Instituto de Salud Carlos III, CIBERCV-Instituto de Salud Carlos III, Spain (grant CB16/11/00479), co-funded with European Regional Development Fund-FEDER contribution), and grants PIE/ 2013-00047 and PI 17/1397. DJH was supported by the British Heart Foundation (CS/14/3/31002), the National Institute for Health Research University College London Hospitals Biomedical Research Centre, Duke-National University Singapore Medical School, Singapore Ministry of Health’s National Medical Research Council under its Clinician Scientist-Senior Investigator scheme (NMRC/CSA-SI/0011/2017) and Collaborative Centre Grant scheme (NMRC/CGAug16C006), and the Singapore Ministry of Education Academic Research Fund Tier 2 (MOE2016-T2-2-021). This article is based upon work from COST Action EU-CARDIOPROTECTION CA16225 supported by COST (European Cooperation in Science and Technology). CB funding from British Heart Foundation (BHF) (RE/18/6134217) and Institute of Health Efficacy Mechanism and Evaluation Programme (12/170/45). PC was supported by the RHU MARVELOUS (ANR-16-RHUS-0009) of Université Claude Bernard Lyon 1 (UCBL), within the program "Investissements d'Avenir“ operated by the French National Research Agency (ANR). RD is funded by NIH (R01 HL136578 and R01 HL133407). MS received research support from Siemens Healthineers, and NIH R01 HL131919-01A1. HA was funded by the Swedish Heart-Lung Foundation, Lund University, Lund Sweden and Region of Scania, Sweden. EDA is funded by the British Heart Foundation (FS/13/71/30378). Sí

Altres ajuts: The CNIC is supported by the ISCiii, MICINN, and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (award SEV-2015-0505). This research was supported (in part) by the Intramural Research Program of the National Institutes of Health, National Heart, Lung, and Blood Institute. Agencies supporting the research of coauthors are acknowledged in the Online Appendix. The authors appreciate the scientific commitment of the sponsor unrelated to industrial interests. Dr. Arai has a U.S. Government Cooperative Research and Development Agreement with Siements; has a U.S. Government Cooperative Research and Development Agreement (Clinical Trial Agreement) with Bayer; and has a U.S. Government official duty (unpaid consultant) with Circle CVI (licensed software developed at the National Institutes of Health). Dr. Arheden is a shareholder in Imacor AB. Dr. Bax has received speaker fees from Abbott Vascular and Boehringer Ingelheim; and his institution has received unrestricted research grants from Medtronic, Boston Scientific, Biotronik, Edwards Lifesciences, and GE Healthcare. Dr. Berry has institutional agreements between the University of Glasgow (employer) and Abbott Vascular, AstraZeneca, Coroventis, DalCor, GlaxoSmithKline, HeartFlow, Novartis, Philips, and Siemens Healthcare. Dr. Bucciarelli-Ducci has served as a consultant for Circle Cardiovascular Imaging. Dr. Dharmakumar has a research agreement with Siemens Healthcare. Dr. Friedrich has served as a board member and advisor for Circle Cardiovascular Imaging. Dr. Kim has received an educational grant from Siemens Healthineers; and is cofounder of HeartIT LLC. Dr. Salerno has received research support from Siemens Healthineers. Dr Croisille's institution holds a research agreement with Siemens Healthcare, Circle Cardiovascular Imaging, and Olea Medical. Dr. Sánchez-González is an employee of Philips. After a reperfused myocardial infarction (MI), dynamic tissue changes occur (edema, inflammation, microvascular obstruction, hemorrhage, cardiomyocyte necrosis, and ultimately replacement by fibrosis). The extension and magnitude of these changes contribute to long-term prognosis after MI. Cardiac magnetic resonance (CMR) is the gold-standard technique for noninvasive myocardial tissue characterization. CMR is also the preferred methodology for the identification of potential benefits associated with new cardioprotective strategies both in experimental and clinical trials. However, there is a wide heterogeneity in CMR methodologies used in experimental and clinical trials, including time of post-MI scan, acquisition protocols, and, more importantly, selection of endpoints. There is a need for standardization of these methodologies to improve the translation into a real clinical benefit. The main objective of this scientific expert panel consensus document is to provide recommendations for CMR endpoint selection in experimental and clinical trials based on pathophysiology and its association with hard outcomes.

Supplemental material, 10.1177_1358863X19859072_supplementary_material for A randomized, placebo-controlled trial of canakinumab in patients with peripheral artery disease by Kerry S Russell, Denise P Yates, Christopher M Kramer, Andrea Feller, Ping Mahling, Laurence Colin, Timothy Clough, Tianke Wang, Lucy LaPerna, Alpa Patel, Holger Lawall, Mustafa M Shennak, James Fulmer, Sigrid Nikol, William B Smith, Oliver J Müller, Elizabeth V Ratchford and Craig T Basson in Vascular Medicine

Aims Myocardial fibrosis as detected by late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) is a powerful prognostic marker in hypertrophic cardiomyopathy (HCM) and may be progressive. The precise mechanisms underlying fibrosis progression are unclear. We sought to assess the extent of LGE progression in HCM and explore potential causal mechanisms and clinical implications. Methods and results Seventy-two HCM patients had two CMR (CMR1-CMR2) at an interval of 5.7 ± 2.8 years with annual clinical follow-up for 6.3 ± 3.6 years from CMR1. A combined endpoint of heart failure progression, cardiac hospitalization, and new onset ventricular tachycardia was assessed. Cine and LGE imaging were performed to assess left ventricular (LV) mass, function, and fibrosis on serial CMR. Stress perfusion imaging and cardiac energetics were undertaken in 38 patients on baseline CMR (CMR1). LGE mass increased from median 4.98 g [interquartile range (IQR) 0.97–13.48 g] to 6.30 g (IQR 1.38–17.51 g) from CMR1 to CMR2. Substantial LGE progression (ΔLGE ≥ 4.75 g) occurred in 26% of patients. LGE increment was significantly higher in those with impaired myocardial perfusion reserve (≺MPRI 1.40) and energetics (phosphocreatine/adenosine triphosphate ≺1.44) on baseline CMR (P ≤ 0.01 for both). Substantial LGE progression was associated with LV thinning, increased cavity size and reduced systolic function, and conferred a five-fold increased risk of subsequent clinical events (hazard ratio 5.04, 95% confidence interval 1.85–13.79; P = 0.002). Conclusion Myocardial fibrosis is progressive in some HCM patients. Impaired energetics and perfusion abnormalities are possible mechanistic drivers of the fibrotic process. Fibrosis progression is associated with adverse cardiac remodelling and predicts an increased risk of subsequent clinical events in HCM.

Cardiovascular disease remains a leading cause of morbidity and mortality globally. Changing natural history of the disease due to improved care of acute conditions and ageing population necessitates new strategies to tackle conditions which have more chronic and indolent course. These include an increased deployment of safe screening methods, life-long surveillance, and monitoring of both disease activity and tailored-treatment, by way of increasingly personalized medical care. Cardiovascular magnetic resonance (CMR) is a non-invasive, ionising radiation-free method, which can support a significant number of clinically relevant measurements and offers new opportunities to advance the state of art of diagnosis, prognosis and treatment. The objective of the SCMR Clinical Trial Taskforce was to summarizes the evidence to emphasize where currently CMR-guided clinical care can indeed translate into meaningful use and efficient deployment of resources results in meaningful and efficient use. The objective of the present initiative was to provide an appraisal of evidence on analytical validation, including the accuracy and precision, and clinical qualification of parameters in disease context, clarifying the strengths and weaknesses of the state of art, as well as the gaps in the current evidence This paper is complementary to the existing position papers on standardized acquisition and post-processing ensuring robustness and transferability for widespread use. Themed imaging-endpoint guidance on trial design to support drug-discovery or change in clinical practice (part II), will be presented in a follow-up paper in due course. As CMR continues to undergo rapid development, regular updates of the present recommendations are foreseen.

ObjectivesThe aim of this study was to describe associations of the presence of lipid-rich necrotic core (LRNC) in the proximal superficial femoral artery (SFA) with lower extremity peripheral artery disease (PAD) event rates and systemic cardiovascular event rates.BackgroundLRNC in the coronary and carotid arteries is associated with adverse outcomes but has not been studied previously in lower extremity arteries.MethodsParticipants with ankle-brachial index (ABI) values0.15, and revascularization at 47-month follow-up (hazard ratio: 2.18; 95% confidence interval: 1.27 to 3.75; p= 0.005). The association of SFA LRNC with PAD events was maintained even when this combined outcome excluded lower extremity revascularization (hazard ratio: 2.58; 95% confidence interval: 1.25 to 5.33; p= 0.01). LRNC in the SFA was not associated with all-cause mortality, acute coronary events, or stroke.ConclusionsAmong patients with PAD, LRNC in the SFA was associated with higher rates of clinical PAD events, and thisassociation was independent of ABI. Further study is needed to determine whether interventions that reduce SFA LRNCprevent PAD events.

ObjectivesWe studied associations of magnetic resonance imaging measurements of plaque area and relative percent lumen reduction in the proximal superficial femoral artery with functional performance among participants with peripheral arterial disease.BackgroundThe clinical significance of directly imaged plaque characteristics in lower extremity arteries is not well established.MethodsA total of 454 participants with an ankle brachial index

We hypothesized that stress-rest perfusion imaging of skeletal muscle in the lower extremity with contrast-enhanced ultrasound (CEU) could evaluate the severity of peripheral arterial disease (PAD).Perfusion imaging may provide valuable quantitative information on PAD, particularly in patients with diabetes in whom microvascular functional abnormalities are common.Study subjects included 26 control subjects and 39 patients with symptomatic PAD, 19 of whom had type 2 diabetes mellitus. A modified treadmill exercise test was performed to determine exercise time to development of claudication. Multilevel pulse-volume recordings and ankle-brachial index (ABI) at rest and post-exercise ABI were measured in both extremities. Microvascular blood flow in the gastrocnemius and soleus muscles was measured at rest and after 2 min of calibrated plantar-flexion exercise.During exercise, claudication did not occur in normal subjects and occurred earlier in PAD patients with diabetes than without (median time 1.2 min [95% confidence interval (CI) 0.6 to 2.5] vs. 3.0 min [95% CI 2.1 to 6.0], p0.01). Compared to control subjects, patients with PAD had lower skeletal muscle blood flow during plantar-flexion exercise and lower flow reserve on CEU. After adjusting for diabetes, the only diagnostic tests that predicted severity of disease by claudication threshold were CEU exercise blood flow and flow reserve (odds ratios 0.67 [95% CI 0.51 to 0.88; p = 0.003] and 0.64 [95% CI 0.46 to 0.89, p = 0.008], respectively). A quasi-likelihood information analysis incorporating all non-invasive diagnostic tests indicated that the best models for predicting severity of disease were the combination of diabetes and either exercise blood flow or flow-reserve on CEU.Perfusion imaging of limb skeletal during exercise and measurement of absolute flow reserve can provide valuable information on the severity PAD. This strategy may be useful for evaluating the total impact of disease in patients with complex disease or those with coexisting functional abnormalities of flow regulation.

ObjectivesThis study sought to perform a systematic review and meta-analysis to understand the role of stress cardiac magnetic resonance imaging (CMR) in assessing cardiovascular prognosis in patients with known or suspected coronary artery disease (CAD).BackgroundAlthough stress CMR is excellent for the diagnosis of obstructive CAD, the prognostic value of stress CMR has been less well described.MethodsPubMed, Cochrane CENTRAL, and metaRegister of Controlled Trials were searched for stress CMR studies with >6 months of prognostic data. Primary endpoints were cardiovascular death, myocardial infarction (MI), and a composite outcome of cardiovascular death or MI during follow-up. Summary effect estimates were generated with random-effects modeling, and annualized event rates were assessed.ResultsNineteen studies (14 vasodilator, 4 dobutamine, and 1 that used both) involved a total of 11,636 patients with a mean follow-up of 32 months. Patients had a mean age of 63 ± 12 years, 63% were male, and 26% had previous MI; mean left ventricular ejection fraction was 61 ± 12%; and late gadolinium enhancement was present in 29% and ischemia in 32%. Patients with ischemia had a higher incidence of MI (odds ratio [OR]: 7.7; p < 0.0001), cardiovascular death (OR: 7.0; p < 0.0001), and the combined endpoint (OR: 6.5; p < 0.0001) compared with those with a negative study. The combined outcome annualized events rates were 4.9% for a positive versus 0.8% for a negative stress CMR (p < 0.0001), 2.8% versus 0.3% for cardiovascular death (p < 0.0001), and 2.6% versus 0.4% for MI (p < 0.0005). The presence of late gadolinium enhancement was also significantly associated with a worse prognosis.ConclusionsA negative stress CMR study is associated with very low risk of cardiovascular death and MI. Stress CMR has excellent prognostic characteristics and may help guide risk stratification of patients with known or suspected CAD.

AIMS: Myocardial fibrosis as detected by late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) is a powerful prognostic marker in hypertrophic cardiomyopathy (HCM) and may be progressive. The precise mechanisms underlying fibrosis progression are unclear. We sought to assess the extent of LGE progression in HCM and explore potential causal mechanisms and clinical implications. METHODS AND RESULTS: Seventy-two HCM patients had two CMR (CMR1-CMR2) at an interval of 5.7 ± 2.8 years with annual clinical follow-up for 6.3 ± 3.6 years from CMR1. A combined endpoint of heart failure progression, cardiac hospitalization, and new onset ventricular tachycardia was assessed. Cine and LGE imaging were performed to assess left ventricular (LV) mass, function, and fibrosis on serial CMR. Stress perfusion imaging and cardiac energetics were undertaken in 38 patients on baseline CMR (CMR1). LGE mass increased from median 4.98 g [interquartile range (IQR) 0.97-13.48 g] to 6.30 g (IQR 1.38-17.51 g) from CMR1 to CMR2. Substantial LGE progression (ΔLGE ≥ 4.75 g) occurred in 26% of patients. LGE increment was significantly higher in those with impaired myocardial perfusion reserve (