Myocardial Perfusion Imaging After Severe COVID-19 Infection Demonstrates Regional Ischemia Rather Than Global Blood Flow Reduction.

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.

Aerosolised fluorescein can quantify FFP mask faceseal leakage: a cost-effective adaptation to the existing point of care fit test.

BACKGROUND: A qualitative fit test using bitter-tasting aerosols is the commonest way to determine filtering face-piece (FFP) mask leakage. This taste test is subjective and biased by placebo. We propose a cheap, quantitative modification of the taste test by measuring the amount of fluorescein stained filter paper behind the mask using image analysis. METHODS: A bitter-tasting fluorescein solution was aerosolised during mask fit tests, with filter paper placed on masks' inner surfaces. Participants reported whether they could taste bitterness to determine taste test 'pass' or 'fail' results. Filter paper photographs were digitally analysed to quantify total fluorescence (TF). RESULTS: Fifty-six healthcare professionals were fit tested; 32 (57%) 'passed' the taste test. TF between the taste test 'pass' and 'fail' groups was significantly different (p<0.001). A cut-off (TF = 5.0 × 106 units) was determined at precision (78%) and recall (84%), resulting in 5/56 participants (9%) reclassified from 'pass' to 'fail' by the fluorescein test. Seven out of 56 (12%) reclassified from 'fail' to 'pass'. CONCLUSION: Fluorescein is detectable and sensitive at identifying FFP mask leaks. These low-cost adaptations can enhance exiting fit testing to determine 'pass' and 'fail' groups, protecting those who 'passed' the taste test but have high fluorescein leak, and reassuring those who 'failed' the taste test despite having little fluorescein leak.

Patterns of myocardial injury in recovered troponin-positive COVID-19 patients assessed by cardiovascular magnetic resonance.

BACKGROUND: Troponin elevation is common in hospitalized COVID-19 patients, but underlying aetiologies are ill-defined. We used multi-parametric cardiovascular magnetic resonance (CMR) to assess myocardial injury in recovered COVID-19 patients. METHODS AND RESULTS: One hundred and forty-eight patients (64 ± 12 years, 70% male) with severe COVID-19 infection [all requiring hospital admission, 48 (32%) requiring ventilatory support] and troponin elevation discharged from six hospitals underwent convalescent CMR (including adenosine stress perfusion if indicated) at median 68 days. Left ventricular (LV) function was normal in 89% (ejection fraction 67% ± 11%). Late gadolinium enhancement and/or ischaemia was found in 54% (80/148). This comprised myocarditis-like scar in 26% (39/148), infarction and/or ischaemia in 22% (32/148) and dual pathology in 6% (9/148). Myocarditis-like injury was limited to three or less myocardial segments in 88% (35/40) of cases with no associated LV dysfunction; of these, 30% had active myocarditis. Myocardial infarction was found in 19% (28/148) and inducible ischaemia in 26% (20/76) of those undergoing stress perfusion (including 7 with both infarction and ischaemia). Of patients with ischaemic injury pattern, 66% (27/41) had no past history of coronary disease. There was no evidence of diffuse fibrosis or oedema in the remote myocardium (T1: COVID-19 patients 1033 ± 41 ms vs. matched controls 1028 ± 35 ms; T2: COVID-19 46 ± 3 ms vs. matched controls 47 ± 3 ms). CONCLUSIONS: During convalescence after severe COVID-19 infection with troponin elevation, myocarditis-like injury can be encountered, with limited extent and minimal functional consequence. In a proportion of patients, there is evidence of possible ongoing localized inflammation. A quarter of patients had ischaemic heart disease, of which two-thirds had no previous history. Whether these observed findings represent pre-existing clinically silent disease or de novo COVID-19-related changes remain undetermined. Diffuse oedema or fibrosis was not detected.

The effect of concomitant COVID-19 infection on outcomes in patients hospitalized with heart failure.

AIMS: Patients with cardiovascular disease appear particularly susceptible to severe COVID-19 disease, but the impact of COVID-19 infection on patients with heart failure (HF) is not known. This study aimed to quantify the impact of COVID-19 infection on mortality in hospitalized patients known to have HF. METHODS AND RESULTS: We undertook a retrospective analysis of all patients admitted with a pre-existing diagnosis of HF between 1 March and 6 May 2020 to our unit. We assessed the impact of concomitant COVID-19 infection on in-hospital mortality, incidence of acute kidney injury, and myocardial injury. One hundred and thirty-four HF patients were hospitalized, 40 (29.9%) with concomitant COVID-19 infection. Those with COVID-19 infection had a significantly increased in-hospital mortality {50.0% vs. 10.6%; relative risk [RR] 4.70 [95% confidence interval (CI) 2.42-9.12], P < 0.001} and were more likely to develop acute kidney injury [45% vs. 24.5%; RR 1.84 (95% CI 1.12-3.01), P = 0.02], have evidence of myocardial injury [57.5% vs. 31.9%; RR 1.81 (95% CI 1.21-2.68), P < 0.01], and be treated for a superadded bacterial infection [55% vs. 32.5%; RR 1.67 (95% CI 1.12-2.49), P = 0.01]. CONCLUSIONS: Patients with HF admitted to hospital with concomitant COVID-19 infection have a very poor prognosis. This study highlights the need to regard patients with HF as a high-risk group to be shielded to reduce the risks of COVID-19 infection.