Prognostic assessment following acute myocarditis requires convalescent scanning: neither peak troponin nor index scan T2 signal predicts convalescent late gadolinium enhancement

Funding Acknowledgements Type of funding sources: None. Background Cardiovascular magnetic resonance (CMR) is a key diagnostic investigation in acute myocarditis (1) and permits quantification of late gadolinium enhancement (LGE) and myocardial oedema. Follow-up CMR imaging is recommended to check for persistence of scar and oedema (2). Persistent late gadolinium enhancement is associated with a worse prognosis (3). It is not known whether all patients require follow-up scanning or whether the initial scan can provide useful information to identify which patients need convalescent assessment. Purpose In this study we considered whether extent of troponin elevation, extent of T2 elevation and initial late gadolinium enhancement burden predicted long-term late gadolinium enhancement at follow-up. Methods Index and follow-up CMR scans of consecutive patients presenting with a diagnosis of acute myocarditis between 2019 and 2020 across three hospitals were included. Inclusion criteria were: follow-up scan within 9 months of the index scan, CMR with LGE imaging and T2 mapping, and acute myocarditis being the primary diagnosis of the index scan. Myocardial T2 values in the area affected by myocarditis and percentage of LV myocardium showing late enhancement (using a threshold-based full height half width or manual region of interest strategy) were extracted. Results 20 patients were included in the study (80% male; mean age 37 years). Mean interval between the index and follow-up scan was 4.1 months. Peak troponin level during the acute illness was not associated with the proportion of LV myocardium affected by LGE in the index scan (R^2 <0.01) (Figure 1A). Myocardial T2 values in the first scan were not associated with the proportional resolution in LGE between the index and follow-up scans (R^2 0.02) (Figure 1B). The mean change in LGE was -61.7% (+/-22.8%) but the initial LGE burden did not predict the proportional degree of improvement in LGE between scans (R^2 <0.01)(Figure 1C). Conclusions The extent of troponin elevation and initial CMR phenotype was not a good predictor of the burden of long-term late gadolinium enhancement. Although most cases showed improvement in LGE scar burden between index and follow-up imaging, neither peak troponin level during the acute episode, nor T2 values at the first CMR scan were predictive of initial or change in scar burden. Serial CMR assessment is required to identify those patients who have residual long-term scarring.

Left atrial scar burden in sinus rhythm differs from atrial fibrillation using automated voltage analysis during radiofrequency ablation for atrial fibrillation

Funding Acknowledgements Type of funding sources: None. Introduction Scar burden in atrial fibrillation (AF) can be overestimated due to many factors. Scar burden has prognostic value and substrates considered for ablation by some electrophysiologists. We compared left atrial (LA) scar voltage in AF to sinus rhythm (SR) using voltage histogram analysis (VHA) of those undergoing pulmonary vein isolation (PVI) for persistent AF (PeAF). We believe this is the first study analysing LA scar location in SR and AF using VHA. Methods We retrospectively analysed 120 anatomical segments (AS) and whole LA voltages (N= 10 patients, mean age 68 ± 7, 4 females) in SR and AF. Fast anatomical maps (FAM) were grouped into 6 AS in AF and SR: Anterior, Posterior, Roof, Floor, Septal and Lateral AS, which were analysed via VHA (Figure 1) in 10 voltage ranges between 0mV-0.5mV. Total LA area in each voltage aliquot was recorded in SR and AF, taking diseased LA as 0.2-0.5mV and dense LA scar as <0.2mV. The pulmonary veins, mitral annulus and trans-septal puncture sites were excluded from analyses. We included patients over age 18 with PeAF who had de novo PVI with no extra ablation lines, maps with >1000 voltage points in both rhythms and uniform procedure involving initial mapping in AF then remapping in SR after PVI. Statistical analyses conducted with IBM SPSS v.26. Results Total LA scar burden was greater in AF (Mean 142.76 mm², SD ± 138.78mm²) than SR (Mean 109mm², SD ± 107.8mm²), p= <0.0001, Table 1. Scar correlation in SR and AF had a good relationship, R = 0.416 (p= <0.001). Every 1mm² of scar identified during SR yielded a mean of 1.54mm² in AF, (p= <0.001). Conclusions AF was associated with higher scar burden in the Roof, Anterior, Lateral and Posterior AS. Dense LA scar (≤ 0.2mV) on the Posterior AS was significantly higher in AF, while in other AS was comparable to SR. Mapping substrate in AF, especially the posterior wall, may be misleading as scar burden may be overestimated when compared to SR. Table 1Voltage< 0.02 mV (mean area ± SD mm2)0.2-0.5mV (mean area mm2)RhythmSRAFp-valueSRAFp-valueEntire LA115.89 ± 113.61143.41 ± 144.230.02*105.78 ± 103.73144.00 ± 135.24<0.0001*Roof82.72 ± 117.3283.68 ± 113.560.95115 ± 77.14150.61 ± 93.170.01*Anterior131.8 ± 169.53126.5 ± 154.570.85158.53 ± 99.22220.87 ± 173.070.002*Lateral70.5 ± 80.0090.57 ± 117.990.3687.52 ± 66.82137.05 ± 104.990.0002*Septal80.99 ± 89.0380.99 ± 89.030.6899.123 ± 73.62115.37 ± 84.830.18Floor105.1 ± 134.91106.42 ± 148.670.96117.62 ± 85.41151.2 ± 110.070.052Posterior102.14 ± 157.47159.03 ± 194.650.02*138.27 ± 112.28234 ± 150.45<0.0001*LA scar distribution in SR and AF, *denotes significant results.Abstract Figure 1

Novel dark-blood versus conventional bright-blood late gadolinium enhancement CMR: A pilot study comparing impact on myocardial ischaemic burden

Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): British Heart Foundation Background In patients with coronary artery disease (CAD), increasing myocardial ischaemic burden (MIB) is a strong predictor of adverse events. When measured by cardiovascular magnetic resonance (CMR), a MIB ≥12.5% is considered significant and often used as a threshold to guide revascularisation. Ischaemic scar can cause stress perfusion defects which do not represent ischaemia and should be excluded from the MIB calculation. Conventional bright-blood late gadolinium enhancement (LGE) is able to identify ischaemic scar but can suffer from poor scar-to-blood contrast, making accurate assessment of scar volume difficult. Dark-blood LGE methods increase scar-to-blood contrast and improve scar conspicuity which may impact the calculated scar burden and consequently the estimation of MIB when read in conjunction with perfusion images. Purpose To evaluate the impact of dark-blood LGE versus conventional bright-blood LGE on the estimation of MIB in patients with CAD. Methods 37 patients with suspected or known CAD who had evidence of CMR stress perfusion defects and ischaemic scar on LGE imaging were recruited. Patients underwent adenosine stress perfusion imaging followed by dark-blood LGE then conventional bright-blood LGE imaging at 3T. For dark-blood LGE, phase sensitive inversion recovery imaging with a shorter inversion time to null the LV blood-pool was used without any additional magnetization preparation. For each patient, three short-axis LGE slices were selected to match the three perfusion slice locations. Images were anonymised and analysed in random order. Ischaemic scar burden (ISB) was quantified for both LGE methods using a threshold >5 standard deviations above remote myocardium. Perfusion defect burden (PDB) was quantified by manual contouring of perfusion defects. MIB was calculated by subtracting the ISB from the PDB. Results MIB calculated using dark-blood LGE was 19% less compared to bright-blood LGE (15.7 ± 15.2% vs 19.4 ± 15.2%, p < 0.001). There was a strong positive correlation between the two LGE methods (rs = 0.960, p < 0.001, Figure 1A). Bland-Altman analysis revealed a significant fixed bias (mean bias = -3.6%, bias 95% CI: -2.6 to -4.7%, 95% limits of agreement: -9.8 to 2.5%) with no proportional bias (Figure 1B). MIB was calculated ≥12.5% and <12.5% by both LGE methods in 19 (51%) and 12 (32%) patients respectively. In 6 patients (16%), MIB was ≥12.5% using bright-blood LGE and <12.5% using dark-blood LGE (Figure 1A – orange data points). Overall, when used to classify MIB as <12.5% or ≥12.5%, there was only substantial agreement between the two LGE methods (κ=0.67, 95% CI: 0.45 to 0.90). Conclusions The use of dark-blood LGE in conjunction with perfusion imaging results in a lower estimate of MIB compared to conventional bright-blood LGE. This can cause disagreement around the threshold of clinically significant ischaemia which could impact clinical management in patients being considered for coronary revascularisation. Abstract Figure. Linear regression with corresponding B&A

Septal scar predicts non-response to cardiac resynchronization therapy

Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): South-Eastern Norway Regional Health Authority Norwegian Health Association Background Scar in the left ventricular (LV) posterolateral wall is associated with poor response to cardiac resynchronization therapy (CRT). The impact of septal scar, however, has been less thoroughly investigated. As recovery of septal function seems to be an important effect of CRT, we hypothesized that CRT response depends on septal viability. Aim The aim of the present study was to investigate the association between septal scar and volumetric response to CRT, and to compare the impact of scar located in septum to scar located in the posterolateral wall. Methods 128 patients with symptomatic heart failure undergoing CRT implantation based on current guidelines (ejection fraction 30 ± 8%, QRS-width 164 ± 17 ms) were included in the study. Volumes and ejection fraction were measured by echocardiography using the biplane Simpson’s method at baseline and six months follow up. Non-response was defined as less than 15% reduction in end-systolic volume. Scar was assessed by late gadolinium enhancement cardiac magnetic resonance, and reported as percentage scar per regional myocardial volume. Numbers are given in [median ;10-90% percentile]. Results Scar was present in 62 patients (48%). Scar burden was equal in septum [0% ;0-34%] and the posterolateral wall [0% ;0-36%], p = 0.10. 31 patients (24%) did not respond to CRT. The non-responders had higher scar burden than the responders in both septum [16% ;0-57% vs 0% ;0-23%, p < 0.001] and the posterolateral wall [6% ;0-74% vs 0% ;0-22%, p < 0.001]. In univariate regression analysis both septal and posterolateral scars correlated with non-response to CRT (r = 0.51 and r = 0.33, respectively). However, combined in a multivariate model only septal scar remained a significant marker of non-response (p < 0.001), while posterolateral scar did not (p = 0.23). Septal scar ≥ 7.1% predicted non-response with a specificity of 81% and a sensitivity of 70% by receiver operating characteristic curve analyses. The area under the curve was 0.79 (95% confidence interval 0.70 – 0.89) (Figure). Conclusions Septal scar is more closely associated with volumetric non-response to CRT than posterolateral scar. Future studies should explore the correlation between regional scar burden and different functional parameters, and how they relate to CRT response. Abstract Figure. Septal scar predicts non-response to CRT