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Aimsmyocardial oedema is largely represented in takotsubo syndrome (TTS) and may contribute to alter the myocardium morphology and function. The aim of the study is to describe relationships between oedema, mechanical, and electrical abnormalities in TTSMethods and resultsthe study included n = 32 hospitalized TTS patients and n = 23 controls. Cardiac magnetic resonance (CMR) with tissue mapping and feature tracking was performed with concomitant 12-lead electrocardiogram (ECG) recording. Mean age of TTS was 72 ± 12 years old, 94% women. Compared with controls, patients had higher left ventricular (LV) mass, worse systolic function, higher septal native T1 (1116 ± 73 msec vs. 970 ± 23 msec, P < 0.001), T2 (56 ± 5 msec vs. 46 ± 2 msec, P < 0.001), and extracellular volume (ECV) fraction (32 ± 5% vs. 24 ± 1%, P < 0.001). TTS patients had higher apicobasal gradient of T2 values (12 ± 6 msec vs. 2 ± 6 msec, P < 0.001); basal LV wall displayed higher native T1, T2, and ECV (all P < 0.002) but similar circumferential strain against controls (−23 ± 3% vs. −24 ± 4%, P = 0.351). In the TTS cohort, septal T2 values showed significant correlations with native T1 (r = 0.609, P < 0.001), ECV (r = 0.689, P < 0.001), left ventricular ejection fraction (r = −0.459, P = 0.008) and aVR voltage (r = −0.478, P = 0.009). Negative T-wave voltage and QTc length correlated with apicobasal T2 mapping gradient (r = 0.499, P = 0.007 and r = 0.372, P = 0.047, respectively) but not with other tissue mapping measurements.ConclusionsCMR T1 and T2 mapping demonstrated increased myocardial water content conditioning interstitial expansion in acute TTS, detected even outside areas of abnormal wall motion. Oedema burden and distribution associated with mechanical and electrocardiographic changes, making it a potential prognostic marker and therapeutic target in TTS.

Hematopoietic mutations in epigenetic regulators like DNA methyltransferase 3 alpha (DNMT3A) drive clonal hematopoiesis of indeterminate potential (CHIP) and are associated with adverse prognosis in patients with heart failure (HF). The interactions between CHIP-mutated cells and other cardiac cell types remain unknown.Here, we identify fibroblasts as potential interaction partners of CHIP-mutated monocytes using combined transcriptomic data from peripheral blood mononuclear cells of HF patients with and without CHIP and the cardiac tissue. We demonstrate that CHIP augments macrophage-to-cardiac fibroblasts interactions. Mechanistically, the secretome ofDNMT3A-silenced monocytes leads to myofibroblast activation, partially through epidermal growth factor (EGFR) signaling. Harboring DNMT3A CHIP-driver mutations is associated with increased cardiac interstitial fibrosis in mice and patients, and, thereby, may contribute to the poor outcome.These findings not only identify a novel pathway of DNMT3A CHIP-driver mutation-induced instigation and progression of HF, but may also provide a rationale for the development of new anti-fibrotic strategies.Graphical abstract

D-dimer testing is known to have a high sensitivity at simultaneously low specificity, resulting in nonspecific elevations in a variety of conditions.This retrospective study sought to assess diagnostic and prognostic features of D-dimers in cancer patients referred to the emergency department for suspected pulmonary embolism (PE) and deep vein thrombosis (DVT). In total, 526 patients with a final adjudicated diagnosis of PE (n = 83) and DVT (n = 69) were enrolled, whereas 374 patients served as the comparative group, in which venous thromboembolism (VTE) has been excluded.For the identification of VTE, D-dimers yielded the highest positive predictive value of 96% (95% confidence interval (CI), 85-99) at concentrations of 9.9 mg/L and a negative predictive value of 100% at .6 mg/L (95% CI, 97-100). At the established rule-out cut-off level of .5 mg/L, D-dimers were found to be very sensitive (100%) at a moderate specificity of nearly 65%. Using an optimised cut-off value of 4.9 mg/L increased the specificity to 95% for the detection of life-threatening VTE at the cost of moderate sensitivities (64%). During a median follow-up of 30 months, D-dimers positively correlated with the reoccurrence of VTE (p = .0299) and mortality in both cancer patients with VTE (p .0001) and without VTE (p = .0008).Although D-dimer testing in cancer patients is discouraged by current guidelines, very high concentrations above the 10-fold upper reference limit contain diagnostic and prognostic information and might be helpful in risk assessment, while low concentrations remain useful for ruling out VTE.

Aim To assess the prevalence and prognostic significance of NI-LGE in patients undergoing stress-CMR. Methods Stress-CMR with either dipyridamole or adenosine was performed in 283 patients (228 men, 81%) including perfusion imaging, wall motion evaluation and LGE. Follow-up was completed in all enrolled patients (median time: 1850 days; interquartile range: 1225-2705 days). Composite endpoint included cardiac death, ventricular tachycardia, myocardial infarction, stroke, hospitalization for cardiac cause and coronary revascularization performed beyond 90 days from stress-CMR scans. Results One hundred and twelve patients (40%) had negative LGE (no-LGE), 140 patients (49%) I-LGE and 31 patients (11%) NI-LGE. Twenty-five events occurred in the no-LGE group, 68 in I-LGE and 11 in the NI-LGE group. On survival curves, patients with NI-LGE had worse prognosis than patients with no-LGE regardless of the presence of inducible perfusion defects. No significant prognostic differences were found between I-LGE and NI-LGE. Conclusion NI-LGE can be detected in 11% of patients during stress-CMR providing a diagnosis of nonischemic cardiac disease. Patients with NI-LGE have worse prognosis than those with no-LGE.

The goal of this study was to examine prognostic relationships between cardiac imaging measures and cardiovascular outcome in people living with human immunodeficiency virus (HIV) (PLWH) on highly active antiretroviral therapy (HAART).PLWH have a higher prevalence of cardiovascular disease and heart failure (HF) compared with the noninfected population. The pathophysiological drivers of myocardial dysfunction and worse cardiovascular outcome in HIV remain poorly understood.This prospective observational longitudinal study included consecutive PLWH on long-term HAART undergoing cardiac magnetic resonance (CMR) examination for assessment of myocardial volumes and function, T1 and T2 mapping, perfusion, and scar. Time-to-event analysis was performed from the index CMR examination to the first single event per patient. The primary endpoint was an adjudicated adverse cardiovascular event (cardiovascular mortality, nonfatal acute coronary syndrome, an appropriate device discharge, or a documented HF hospitalization).A total of 156 participants (62% male; age [median, interquartile range]: 50 years [42 to 57 years]) were included. During a median follow-up of 13 months (9 to 19 months), 24 events were observed (4 HF deaths, 1 sudden cardiac death, 2 nonfatal acute myocardial infarction, 1 appropriate device discharge, and 16 HF hospitalizations). Patients with events had higher native T1 (median [interquartile range]: 1,149 ms [1,115 to 1,163 ms] vs. 1,110 ms [1,075 to 1,138 ms]); native T2 (40 ms [38 to 41 ms] vs. 37 ms [36 to 39 ms]); left ventricular (LV) mass index (65 g/mOur findings reveal important prognostic associations of diffuse myocardial fibrosis and LV remodeling in PLWH. These results may support development of personalized approaches to screening and early intervention to reduce the burden of HF in PLWH (International T1 Multicenter Outcome Study; NCT03749343).

Background: Endomyocardial biopsy (EMB) is the gold standard method for surveillance of acute cardiac allograft rejection (ACAR) despite its invasive nature. Cardiovascular magnetic resonance (CMR)–based myocardial tissue characterization allows detection of myocarditis. The feasibility of CMR-based surveillance for ACAR-induced myocarditis in the first year after heart transplantation is currently undescribed. Methods: CMR-based multiparametric mapping was initially assessed in a prospective cross-sectional fashion to establish agreement between CMR- and EMB-based ACAR and to determine CMR cutoff values between rejection grades. A prospective randomized noninferiority pilot study was then undertaken in adult orthotopic heart transplant recipients who were randomized at 4 weeks after orthotopic heart transplantation to either CMR- or EMB-based rejection surveillance. Clinical end points were assessed at 52 weeks. Results: Four hundred one CMR studies and 354 EMB procedures were performed in 106 participants. Forty heart transplant recipients were randomized. CMR-based multiparametric assessment was highly reproducible and reliable at detecting ACAR (area under the curve, 0.92; sensitivity, 93%; specificity, 92%; negative predictive value, 99%) with greater specificity and negative predictive value than either T1 or T2 parametric CMR mapping alone. High-grade rejection occurred in similar numbers of patients in each randomized group (CMR, n=7; EMB, n=8; P =0.74). Despite similarities in immunosuppression requirements, kidney function, and mortality between groups, the rates of hospitalization (9 of 20 [45%] versus 18 of 20 [90%]; odds ratio, 0.091; P =0.006) and infection (7 of 20 [35%] versus 14 of 20 [70%]; odds ratio, 0.192; P =0,019) were lower in the CMR group. On 15 occasions (6%), patients who were randomized to the CMR arm underwent EMB for clarification or logistic reasons, representing a 94% reduction in the requirement for EMB-based surveillance. Conclusions: A noninvasive CMR-based surveillance strategy for ACAR in the first year after orthotopic heart transplantation is feasible compared with EMB-based surveillance. Registration: HREC/13/SVH/66 and HREC/17/SVH/80. Australian New Zealand Clinical Trials Registry: ACTRN12618000672257.

The aim of this study is to provide a systematic assessment of the influence of the position on the arterial input function (AIF) for perfusion quantification. In 39 patients with a wide range of left ventricular function the AIF was determined using a diluted contrast bolus of a cardiac magnetic resonance imaging in three left ventricular levels (basal, mid, apex) as well as aortic sinus (AoS). Time to peak signal intensities, baseline corrected peak signal intensity and upslopes were determined and compared to those obtained in the AoS. The error induced by sampling the AIF in a position different to the AoS was determined by Fermi deconvolution. The time to peak signal intensity was strongly correlated (r2 > 0.9) for all positions with a systematic earlier arrival in the basal (− 2153 ± 818 ms), the mid (− 1429 ± 928 ms) and the apical slice (− 450 ± 739 ms) relative to the AoS (all p 2 > 0.9 for both) for all positions with a systematic overestimation in all positions relative to the AoS (all p

This review surveys the findings of the International Study of Comparative Health Effectiveness with Medical and Invasive Approaches (ISCHEMIA) trial and puts them into a clinical perspective regarding its effect of the role of cardiac magnetic resonance imaging (CMR) as a well-validated gatekeeper for invasive angiography and myocardial revascularization. Noninvasive stress testing of patients with intermediate-to-high pretest likelihood for obstructive coronary artery disease (CAD) using perfusion CMR provides excellent diagnostic accuracy in detecting ischemic myocardium, and additional information from tissue characterization can guide the management of patients with stable angina toward a more individualized therapy as other non-coronary underlying causes of chest pain can be detected. Since ISCHEMIA failed to show that an invasive strategy using percutaneous coronary intervention or coronary artery bypass grafting was associated with an improved prognosis compared with initial conservative medical therapy among stable patients with moderate-to-severe ischemia, CMR as a multifaceted diagnostic imaging approach to explain patients' symptoms should be preferred over anatomical and stress testing alone. Nevertheless, the exclusion of left main coronary artery stenosis either by coronary CT or MR angiography may be required. In conclusion, the results of the ISCHEMIA trial are in good accordance with those of the MR-INFORM trial recently published in the New England Journal of Medicine, as the noninvasive management of a large proportion of patients with CAD was shown to be noninferior to current invasive strategies. Recent outcome data from trials may therefore have an impact on future guidelines to further reduce the execution of unnecessary left heart catheterizations.

Human immunodeficiency virus (HIV) infection is a leading cause of mortality and morbidity worldwide. The introduction of antiretroviral therapy (ART) has significantly reduced the risk of developing acquired immune deficiency syndrome and increased life expectancy, approaching that of the general population. However, people living with HIV have a substantially increased risk of cardiovascular diseases despite long-term viral suppression using ART. HIV-associated cardiovascular complications encompass a broad spectrum of diseases that involve the myocardium, pericardium, coronary arteries, valves, and systemic and pulmonary vasculature. Traditional risk stratification tools do not accurately predict cardiovascular risk in this population. Multimodality imaging plays an essential role in the evaluation of various HIV-related cardiovascular complications. Here, we emphasize the role of multimodality imaging in establishing the diagnosis and aetiopathogenesis of various cardiovascular manifestations related to chronic HIV disease. This review also provides a critical appraisal of contemporary data and illustrative cases.

The purpose of this study is to ascertain agreement in measurements of the scar area between late gadolinium enhancement (LGE), native and post-contrast T1 mapping in patients with known ischemic heart disease. 132 patients (age 60 ± 11 yrs, male 82%) were included in the study. Corresponding 3 short axis slices images of LGE, native and post contrast T1 mapping were used. Scar area was evaluated semi- quantitatively with FWHM methods, in which scar is automatically determined by specialized post-processing software. Agreement per culprit vessel was also assessed. Concordance and inter- intraobserver reproducibility were assessed with Bland-Altman analysis. The results show that scar area amounted to 12.6% of myocardium for LGE, 9.1% for native (p 0.05) and 19.4% (p 0.05) for post-contrast T1 mapping. LAD and RCA territory infarcts showed statistical discrepancy for both T1 acquisitions. Intraobserver differences in infarct size were comparable at 0.39% ± 0.28, 2.93% ± 0.03 and 0.97% ± 0.01 respectively (p≫0.05). Interobserver differences were 5.56% ± 0.91 for LGE, 11.87% ± 3.21 (p 0.05) for native and 5.55% ± 2.87 (p≫0.05) for post-contrast T1 mapping. In conclusion, native T1 acquisitions systematically underestimated infarct size in comparison to LGE, while post-contrast T1 overestimated it. Variances in measurements were most pronounced for LAD and RCA territory infarcts. Intraobserver reproducibility was similar with both methods, whereas interobserver variability for native T1 mapping acquisition was worse.

Cardiac symptoms are increasingly recognized as late complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in previously well individuals with mild initial illness, but the underlying pathophysiology leading to long-term cardiac symptoms remains unclear. In this study, we conducted serial cardiac assessments in a selected population of individuals with Coronavirus Disease 2019 (COVID-19) with no previous cardiac disease or notable comorbidities by measuring blood biomarkers of heart injury or dysfunction and by performing magnetic resonance imaging. Baseline measurements from 346 individuals with COVID-19 (52% females) were obtained at a median of 109 days (interquartile range (IQR), 77–177 days) after infection, when 73% of participants reported cardiac symptoms, such as exertional dyspnea (62%), palpitations (28%), atypical chest pain (27%) and syncope (3%). Symptomatic individuals had higher heart rates and higher imaging values or contrast agent accumulation, denoting inflammatory cardiac involvement, compared to asymptomatic individuals. Structural heart disease or high levels of biomarkers of cardiac injury or dysfunction were rare in symptomatic individuals. At follow-up (329 days (IQR, 274–383 days) after infection), 57% of participants had persistent cardiac symptoms. Diffuse myocardial edema was more pronounced in participants who remained symptomatic at follow-up as compared to those who improved. Female gender and diffuse myocardial involvement on baseline imaging independently predicted the presence of cardiac symptoms at follow-up. Ongoing inflammatory cardiac involvement may, at least in part, explain the lingering cardiac symptoms in previously well individuals with mild initial COVID-19 illness.

Objective To develop a clinical risk score for individualized risk stratification of patients with clinically suspected myocardial inflammation. Background Myocardial inflammation is a prominent cause of non-ischaemic dilated cardiomyopathy, heart failure (HF) and sudden cardiac death. Methods This is a prospective multicentre longitudinal study of consecutive patients referred to cardiac magnetic resonance (CMR) with clinically suspected myocardial inflammation between October 2011 and December 2019 as a part of standard diagnostic pathway. Patients were followed up from the date of CMR. The outcome endpoints included major adverse cardiovascular event (MACE, cardiovascular mortality, sudden cardiac death, appropriate device discharge); or death or hospitalisation due to HF). A prognostic model was developed using Cox proportional hazards analysis and validated internally and externally. Results The final dataset included 722 subjects (50 years (40–61); males 422 (58%)). During a follow-up period of median 19 (15–23) months, there were 64 (9%) MACE and 130 (18%) HF events. Ten predictor variables qualified for entry into the prognostic model: age, sex, hematocrit, C-reactive protein, high-sensitive troponin-T (TNT), left and right ventricular ejection fraction, native T1 and T2, and late gadolinium enhancement (LGE). The final multivariable Cox regression model included native T2 (Figure 1A), TNT and LGE (Figure 1B) for the primary (Chi-square: 102.0, p Conclusions This is the first systematic assessment of outcomes in patients with clinically suspected myocardial inflammation, providing a non-invasive estimation of the probability of adverse events based on a score using readily available clinical parameters. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): DZHK