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Background: Acute myocardial damage is common in severe COVID-19. Post-mortem studies have implicated microvascular thrombosis, with cardiovascular magnetic resonance (CMR) demonstrating a high prevalence of myocardial infarction and myocarditis-like scar. The microcirculatory sequelae are incompletely characterized. Perfusion CMR can quantify the stress myocardial blood flow (MBF) and identify its association with infarction and myocarditis. Objectives: To determine the impact of the severe hospitalized COVID-19 on global and regional myocardial perfusion in recovered patients. Methods: A case-control study of previously hospitalized, troponin-positive COVID-19 patients was undertaken. The results were compared with a propensity-matched, pre-COVID chest pain cohort (referred for clinical CMR; angiography subsequently demonstrating unobstructed coronary arteries) and 27 healthy volunteers (HV). The analysis used visual assessment for the regional perfusion defects and AI-based segmentation to derive the global and regional stress and rest MBF. Results: Ninety recovered post-COVID patients median age 64 [interquartile range (IQR) 54–71] years, 83% male, 44% requiring the intensive care unit (ICU) underwent adenosine-stress perfusion CMR at a median of 61 (IQR 29–146) days post-discharge. The mean left ventricular ejection fraction (LVEF) was 67 ± 10%; 10 (11%) with impaired LVEF. Fifty patients (56%) had late gadolinium enhancement (LGE); 15 (17%) had infarct-pattern, 31 (34%) had non-ischemic, and 4 (4.4%) had mixed pattern LGE. Thirty-two patients (36%) had adenosine-induced regional perfusion defects, 26 out of 32 with at least one segment without prior infarction. The global stress MBF in post-COVID patients was similar to the age-, sex- and co-morbidities of the matched controls (2.53 ± 0.77 vs. 2.52 ± 0.79 ml/g/min, p = 0.10 ), though lower than HV (3.00 ± 0.76 ml/g/min, p < 0.01 ). Conclusions: After severe hospitalized COVID-19 infection, patients who attended clinical ischemia testing had little evidence of significant microvascular disease at 2 months post-discharge. The high prevalence of regional inducible ischemia and/or infarction (nearly 40%) may suggest that occult coronary disease is an important putative mechanism for troponin elevation in this cohort. This should be considered hypothesis-generating for future studies which combine ischemia and anatomical assessment.

Heart failure (HF) is a debilitating and life-threatening condition, with 5-year survival rate lower than breast or prostate cancer. It is the leading cause of hospital admission in over 65s, and these admissions are projected to rise by more than 50% over the next 25 years. Transthoracic echocardiography (TTE) is the first-line step in diagnosis in acute and chronic HF and provides immediate information on chamber volumes, ventricular systolic and diastolic function, wall thickness, valve function and the presence of pericardial effusion, while contributing to information on aetiology. Dilated cardiomyopathy (DCM) is the third most common cause of HF and is the most common cardiomyopathy. It is defined by the presence of left ventricular dilatation and left ventricular systolic dysfunction in the absence of abnormal loading conditions (hypertension and valve disease) or coronary artery disease sufficient to cause global systolic impairment. This document provides a practical approach to diagnosis and assessment of dilated cardiomyopathy that is aimed at the practising sonographer.

BackgroundCardiac amyloidosis (CA) has been associated with a high prevalence of intracardiac thrombi, but this was reported in small cohorts of high risk patients (with a clinical indication for transoesophageal echocardiography). It is therefore not known whether such observations are applicable to the general CA population.PurposeTo assess the prevalence of intracardiac thrombi in patients with CA.Methods324 consecutive patients with CA were studied prospectively using a standard CMR protocol at 1.5T, including early and late gadolinium imaging and T1 mapping. Early gadolinium images (segmented imaging, trigger 2) of the left atrial appendage (LAA) were acquired using a 5 mm contiguous stack and a TI of 440 ms.ResultsThe study participants comprised 155 with light chain CA (AL), 166 with transthyretin amyloidosis (ATTR), 2 with Apo A-I, and 1 with Apo A-IV CA. The prevalence of intracardiac thrombi was 5.2% in AL, 7.2% in ATTR; 6.2% overall. 90% of thrombi were in the LAA. This was higher when there was atrial fibrillation (9.1% AL, 14.3% ATTR) but intracardiac thrombi were also present in sinus rhythm (SR) 3.1% (4.5% AL, 1.1% ATTR). In all patients with AF the thrombi were present despite long term anticoagulation. The presence of intracardiac thrombi was associated with a greater degree of systolic dysfunction and myocardial amyloid infiltration (higher native T1 and ECV).Abstract 21 Figure 1Acquisition of stack through the LAA. Early gadolinium ¡mages of the LAA (bottom row) acquired using a 5 mm contiguous stack through the LAA (top row) and an inversion time of 440 ms to confirm the presence or absence of thrombus vs normal pectinate muscle. The thrombus in the left atrial appendage can only be visualised in the last two images (red arrows in panel 4 and 5) and could have been missed with the acquisition of only one imageConclusionsThe prevalence of intracardiac thrombi in CA and AF is high despite long term anticoagulation, with significant thrombus prevalence even in SR, meriting vigilance for intracardiac thrombi in all. CMR with early gadolinium imaging of the LAA is a valuable screening tool for thrombi in the LAA and should be routine part of the clinical protocol when amyloidosis is suspected. Current guidelines for electrical cardioversion after prolonged anticoagulation without screening forthrombus in the LAA should not be applied to patients with CA.

A 55-year-old woman with a recent history of surgically and radioiodine treated thyroid cancer experienced a run of polymorphic ventricular tachycardia with hemodynamic perturbation during anaesthetic induction with propofol, fentanyl and rocuronium for elective surgical excision of right hip metastasis. Electrocardiography showed new T-wave inversion and QT prolongation that subsequently resolved. Cardiac enzymes were elevated but invasive coronary angiography showed unobstructed epicardial coronary arteries. Cardiovascular magnetic resonance showed not only normal biventricular size and systolic function but also a striking pattern of patchy myocardial oedema involving the basal-to-mid anterior, septal and inferior walls and some associated hypertrophy in the anteroseptum (representing focal myocardial swelling from the oedema) but no focal or diffuse myocardial fibrosis. All these abnormalities resolved on subsequent convalescent imaging. A diagnosis of multifactorial acquired long QT syndrome secondary to atypical variant stress-induced cardiomyopathy was made with the likely provoking factors in this case having been the female sex, understandable pre-operative anxiety, anaesthetic drugs, supraglottic airway placement and thyroid dysfunction. An implantable loop recorder during follow-up detected no further significant arrhythmias and she remains well and asymptomatic to date on a low dose of beta-blocker.

BackgroundConventional bright-blood late gadolinium enhancement (BB LGE) provides excellent contrast between areas of LGE and normal myocardium. Conversely, contrast between LGE and epicardial fat is frequently poor making the detection of sub-epicardial LGE difficult. Sub-epicardial LGE is a sensitive and specific pattern of LGE classically described in myocarditis. However, in practice, patients with a clinical presentation consistent with myocarditis often have no evidence of LGE. Fat water phase sensitive inversion recovery (PSIR) LGE (FW PSIR LGE) is a novel sequence that enables delineation of pericardial fat and may have a role in improving detection of sub-epicardial LGE.ObjectiveTo compare the diagnostic utility of the FW PSIR LGE sequence to standard BB LGE in patients with suspected myocarditis.MethodsThirty-one patients referred for clinical CMR for suspected myocarditis were studied. A full left ventricle short axis stack was performed using both techniques. Two experienced observers analyzed all BB LGE and FW PSIR LGE stacks. A scoring system was devised to quantify the presence and extent of gadolinium enhancement.ResultsAll patients (mean age 43±20 years) presented with chest pain and raised troponin (median high sensitivity troponin T 706 ng/L, interquartile range 104–1185 ng/L) and a normal coronary angiogram or very low probability of coronary artery disease. A total of 496 LV segments were analysed. Significantly more segments demonstrated sub-epicardial LGE using FW PSIR LGE compared to BB LGE (122/496 (25%) vs 44/496 (9%), p<0.01). Twelve patients (39%) with no BB LGE (classified as no myocarditis) were found to have sub-epicardial LGE on FW PSIR LGE (therefore reclassified as positive for myocarditis). There was good agreement between the two observers using both sequences (BB LGE: global agreement 80%, kappa 0.72; FW PSIR LGE: global agreement 80%, kappa 0.78, both p<0.001).Abstract 17 Figure 1Conventional bright blood late gadolinium enhancement images (left panels) and coffesponding separated fat water PSIR LGE and fusion imaging (left panels) of 2 different patients showing no definite evidence of subepicardial enhancement in conventional imaging and evidence of subepicardial LGE in separated fat water LGE (red arrows)ConclusionsFW PSIR LGE significantly increases sub-epicardial LGE detection in patients with suspected myocarditis compared to standard bright blood LGE and importantly changes the clinical diagnosis in a third of patients.

IntroductionCardiac involvement in immunoglobulin light chain (AL) amyloidosis is the major determinant of survival. Cardiac response to chemotherapy is conventionally assessed by serum brain natriuretic peptide (NT-proBNP) and echocardiography, but neither quantify amyloid burden. The aim of this study was to evaluate cardiac AL amyloid by CMR at 3 months, 6 months and 1 year post-chemotherapy.Methods78 patients with cardiac AL amyloidosis were studied serially using CMR with T1 mapping and extracellular volume at baseline and 3 months, 6 months and 12 months post-chemotherapy.ResultsAt 6 months, 60% of patients achieved a complete or very good partial haematological response, and 40% patients a partial response or no response. Amyloid regression was not detectable, however, amyloid progression was detectable in 30% patients at 6 months. Although this occurred in the PR group, it also occurred in the CR and VGPR groups (47%). At one year, 66% patients achieved a CR or VGPR. Regression of amyloid was seen in 32% patients, all with CR or VGPR and 0 patients in PR or NR (p<0.05). 46% patients with changes in ECV consistent with regression of amyloid had changes in LGE. Amyloid regression was associated with significant reduction in LV mass and increased LVEDV (p<0.05).ConclusionIn newly diagnosed and treated AL amyloidosis, CMR demonstrates the dynamic biology of infiltration: increasing rapidly, particularly if chemotherapy fails to switch off light chain production; regressing more slowly (by 1 year) if effective. Serial monitoring of myocardial infiltration has the potential for new AL amyloidosis therapeutic regimes based on myocardial organ response.