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BackgroundConventional transthoracic echocardiography (TTE) does often not accurately reveal pathologies in patients with acute myocarditis and preserved left ventricular ejection fraction (LVEEF). Therefore, we investigated the diagnostic value of two-dimensional (2D) speckle tracking echocardiography compared to late gadolinium enhancement (LGE) by cardiac magnetic resonance (CMR) imaging in patients with acute myocarditis and normal global LVEF.Methods and results31 patients (group 1) with the diagnosis of acute myocarditis confirmed by CMR according to the Lake Louise criteria and 20 healthy controls (group 2) were analyzed including global longitudinal strain (GLS) and regional longitudinal strain (RLS) derived by the bull’s eye plot. Although preserved LVEF was present in both groups, GLS was significantly lower in patients with acute myocarditis (group 1: GLS − 19.1 ± 1.8% vs. group 2: GLS − 22.1 ± 1.7%, p < 0.001). Compared to controls, lower RLS values were detected predominantly in the lateral, inferolateral, and inferior segments in patients with acute myocarditis. Additionally RLS values were significantly lower in segments without LGE.ConclusionIn patients with acute myocarditis and preserved LVEF, a significant reduction of GLS compared to healthy subjects was detected. Further RLS adds important information to the localization and extent of myocardial injury.Graphic abstract

Gas exchange in COVID-19 pneumonia is impaired and vessel obstruction has been suspected to cause ventilation-perfusion mismatch. Dual-energy CT (DECT) can depict pulmonary perfusion by regional assessment of iodine uptake. The purpose of this study was the analysis of pulmonary perfusion using dual-energy CT in a cohort of 27 consecutive patients with severe COVID-19 pneumonia. We retrospectively analyzed pulmonary perfusion with DECT in 27 consecutive patients (mean age 57 years, range 21-73; 19 men and 8 women) with severe COVID-19 pneumonia. Iodine uptake (IU) in regions-of-interest placed into normally aerated lung, ground-glass opacifications (GGO) and consolidations was measured using a dedicated postprocessing software. Vessel enlargement (VE) within opacifications and presence of pulmonary embolism (PE) was assessed by subjective analysis. Linear mixed models were used for statistical analyses. Compared to normally aerated lung 106/151 (70.2%) opacifications without upstream PE demonstrated an increased IU, 9/151 (6.0%) an equal IU and 36/151 (23.8%) a decreased IU. The estimated mean iodine uptake (EMIU) in opacifications without upstream PE (GGO 1.77 mg/mL; 95%-CI: 1.52-2.02; p = 0.011, consolidations 1.82 mg/mL; 95%-CI: 1.56-2.08, p = 0.006) was significantly higher compared to normal lung (1.22 mg/mL; 95%-CI: 0.95-1.49). In case of upstream PE, EMIU of opacifications (combined GGO and consolidations) was significantly decreased compared to normal lung (0.52 mg/mL; 95%-CI: -0.07-1.12; p = 0.043). The presence of VE in opacifications correlated significantly with iodine uptake (p<0.001). DECT revealed the opacifications in a subset of patients with severe COVID-19 pneumonia to be perfused non-uniformly with some being hypo- and others being hyperperfused. Mean iodine uptake in opacifications (both ground-glass and consolidation) was higher compared to normally aerated lung except for areas with upstream pulmonary embolism. Vessel enlargement correlated with iodine uptake: In summary, in a cohort of 27 consecutive patients with severe COVID-19 pneumonia, dual-energy CT demonstrated a wide range of iodine uptake in pulmonary ground-glass opacifications and consolidations as a surrogate marker for hypo- and hyperperfusion compared to normally aerated lung. Applying DECT to determine which pathophysiology is predominant might help to tailor therapy to the individual patient's needs.

COVID-19 is frequently complicated by venous thromboembolism (VTE). Computed tomography (CT) of the chest-primarily usually conducted as low-dose, non-contrast enhanced CT-plays an important role in the diagnosis and follow-up of COVID-19 pneumonia. Performed as contrast-enhanced CT pulmonary angiography, it can reliably detect or rule-out pulmonary embolism (PE). Several imaging characteristics of COVID-19 pneumonia have been described for chest CT, but no study evaluated CT findings in the context of VTE/PE. In our retrospective study, we analyzed clinical, laboratory and CT imaging characteristics of 50 consecutive patients with RT-PCR proven COVID-19 pneumonia who underwent contrast-enhanced chest CT at two tertiary care medical centers. All patients with RT-PCR proven COVID-19 pneumonia and contrast-enhanced chest CT performed at two tertiary care hospitals between March 1st and April 20th 2020 were retrospectively identified. Patient characteristics (age, gender, comorbidities), symptoms, date of symptom onset, RT-PCR results, imaging results of CT and leg ultrasound, laboratory findings (C-reactive protein, differential blood count, troponine, N-terminal pro-B-type natriuretic peptide (NT-proBNP), fibrinogen, interleukin-6, D-dimer, lactate dehydrogenase (LDH), creatine kinase (CK), creatine kinase muscle-brain (CKmb) and lactate,) and patient outcome (positive: discharge or treatment on normal ward; negative: treatment on intensive care unit (ICU), need for mechanical ventilation, extracorporeal membrane oxygenation (ECMO), or death) were analyzed. Follow-up was performed until May 10th. Patients were assigned to two groups according to two endpoints: venous thromboembolism (VTE) or no VTE. For statistical analysis, univariate logistic regression models were calculated. This study includes 50 patients. In 14 out of 50 patients (28%), pulmonary embolism was detected at contrast-enhanced chest CT. The majority of PE was detected on CTs performed on day 11-20 after symptom onset. Two patients (14%) with PE simultaneously had evidence of deep vein thrombosis. 15 patients (30%) had a negative outcome (need for intensive care, mechanical ventilation, extracorporeal membrane oxygenation, or death), and 35 patients (70%) had a positive outcome (transfer to regular ward, or discharge). Patients suffering VTE had a statistically significant higher risk of an unfavorable outcome (p = 0.028). In univariate analysis, two imaging characteristics on chest CT were associated with VTE: crazy paving pattern (p = 0.024) and air bronchogram (n = 0.021). Also, elevated levels of NT-pro BNP (p = 0.043), CK (p = 0.023) and D-dimers (p = 0.035) were significantly correlated with VTE. COVID-19 pneumonia is frequently complicated by pulmonary embolism (incidence of 28% in our cohort), remarkably with lacking evidence of deep vein thrombosis in nearly all thus affected patients of our cohort. As patients suffering VTE had an adverse outcome, we call for a high level of alertness for PE and advocate a lower threshold for contrast-enhanced CT in COVID-19 pneumonia. According to our observations, this might be particularly justified in the second week of disease and if a crazy paving pattern and / or air bronchogram is present on previous non-enhanced CT.

ObejctiveObstructive sleep apnoea (OSA) increases left ventricular transmural pressure more than central sleep apnoea (CSA) owing to negative intrathoracic pressure swings. We tested the hypothesis that the severity of OSA, and not CSA, is therefore associated with spheric cardiac remodelling after acute myocardial infarction.MethodsThis sub-analysis of a prospective observational study included 24 patients with acute myocardial infarction who underwent primary percutaneous coronary intervention. Spheric remodelling, calculated according to the sphericity index, was assessed by cardiac magnetic resonance imaging at baseline and 12 weeks after acute myocardial infarction. OSA and CSA [apnoea-hypopnoea index (AHI) ≥ 5/hour] were diagnosed by polysomnography. ResultsWithin 12 weeks after acute myocardial infarction, patients with OSA exhibited a significant increase in systolic sphericity index compared to patients without sleep-disordered breathing (no SDB) and patients with CSA (OSA vs. CSA vs. no SDB: 0.05 ± 0.04 vs. 0.01 ± 0.04 vs. − 0.03 ± 0.03, p = 0.002). In contrast to CSA, the severity of OSA was associated with an increase in systolic sphericity index after accounting for TIMI-flow before percutaneous coronary intervention, infarct size, pain-to-balloon-time and systolic blood pressure [OSA: B (95% CI) 0.443 (0.021; 0.816), p = 0.040; CSA: 0.193 (− 0.134; 0.300), p = 0.385].ConclusionIn contrast to CSA and no SDB, OSA is associated with spheric cardiac remodelling within the first 12 weeks after acute myocardial infarction. Data suggest that OSA-related negative intrathoracic pressure swings may contribute to this remodelling after acute myocardial infaction.Graphic abstract

Application of high power radiofrequency (RF) energy for a short duration (HPSD) to isolate pulmonary vein (PV) is an emerging technique. But power and duration settings are very different across different centers. Moreover, despite encouraging preclinical and clinical data, studies measuring acute effectiveness of various HPSD settings are limited. Twenty-five consecutive patients with symptomatic atrial fibrillation (AF) were treated with pulmonary vein isolation (PVI) using HPSD. PVI was performed with a contact force catheter (Thermocool SF Smart-Touch) and Carto 3 System. The following parameters were used: energy output 50 W, target temperature 43°C, irrigation 15 mL/min, targeted contact force of > 10 g. RF energy was applied for 6 to 10 s. Required minimal interlesion distance was 4 mm. Twenty minutes after each successful PVI adenosine provocation test (APT) was performed by administrating 18 mg adenosine to unmask dormant PV conduction. All PVs (100 PVs) were successfully isolated. RF lesions needed per patient were 131 ±  41, the average duration for each RF application was 8.1 ± 1.7 s. Procedure time was 138  ±  21 min and average of total RF energy duration was 16.3 ±  5.2 min and average amount of RF energy was 48209 ± 12808W s. APT application time after PVI was 31.1 ± 8.3 min for the left sided PVs and 22.2 ± 4.6 min (p = 0.005) for the right sided PVs. APT was transiently positive in 18 PVs (18%) in 8 (32%) patients. Pulmonary vein isolation with high power for 6-10 s is feasible and shortens the procedure and ablation duration. However, acute effectiveness of the HPSD seems to be lower than expected. Further studies combining other ablation parameters are needed to improve this promising technique.

Aims There is a lack of diagnostic and therapeutic options for patients with atrial cardiomyopathy and paroxysmal atrial fibrillation. Interestingly, an abnormal P‐wave terminal force in electrocardiogram lead V1 (PTFV1) has been associated with atrial cardiomyopathy, but this association is poorly understood. We investigated PTFV1 as a marker for functional, electrical, and structural atrial remodelling. Methods and results Fifty‐six patients with acute myocardial infarction and 13 kidney donors as control cohort prospectively underwent cardiac magnetic resonance imaging to evaluate the association between PTFV1 and functional remodelling (atrial strain). To further investigate underlying pathomechanisms, right atrial appendage biopsies were collected from 32 patients undergoing elective coronary artery bypass grafting. PTFV1 was assessed as the product of negative P‐wave amplitude and duration in lead V1 and defined as abnormal if ≥4000 ms*μV. Activity of cardiac Ca/calmodulin‐dependent protein kinase II (CaMKII) was determined by a specific HDAC4 pull‐down assay as a surrogate for electrical remodelling. Atrial fibrosis was quantified using Masson's trichrome staining as a measure for structural remodelling. Multivariate regression analyses were performed to account for potential confounders. A total of 16/56 (29%) of patients with acute myocardial infarction, 3/13 (23%) of kidney donors, and 15/32 (47%) of patients undergoing coronary artery bypass grafting showed an abnormal PTFV1. In patients with acute myocardial infarction, left atrial (LA) strain was significantly reduced in the subgroup with an abnormal PTFV1 (LA reservoir strain: 32.28 ± 12.86% vs. 22.75 ± 13.94%, P = 0.018; LA conduit strain: 18.87 ± 10.34% vs. 10.17 ± 8.26%, P = 0.004). Abnormal PTFV1 showed a negative correlation with LA conduit strain independent from clinical covariates (coefficient B: −7.336, 95% confidence interval −13.577 to −1.095, P = 0.022). CaMKII activity was significantly increased from (normalized to CaMKII expression) 0.87 ± 0.17 to 1.46 ± 0.15 in patients with an abnormal PTFV1 (P = 0.047). This increase in patients with an abnormal PTFV1 was independent from clinical covariates (coefficient B: 0.542, 95% confidence interval 0.057 to 1.027, P = 0.031). Atrial fibrosis was significantly lower with 12.32 ± 1.63% in patients with an abnormal PTFV1 (vs. 20.50 ± 2.09%, P = 0.006), suggesting PTFV1 to be a marker for electrical but not structural remodelling. Conclusions Abnormal PTFV1 is an independent predictor for impaired atrial function and for electrical but not for structural remodelling. PTFV1 may be a promising tool to evaluate patients for atrial cardiomyopathy and for risk of atrial fibrillation.

Background: Coronary collateral flow in angiography has been linked with lower mortality rates in patients with coronary artery disease. However, the relevance of the underlying mechanism is sparse. Therefore, we tested the hypothesis that in patients with acute myocardial infarction (AMI), relevant coronary collateral flow is associated with more salvaged myocardium and lower risk of developing heart failure. Methods and Results: Patients with first AMI who received a percutaneous coronary intervention within 24 h after symptom onset were classified visually by assigning a Cohen–Rentrop Score (CRS) ranging between 0 (no collaterals) and 3 (complete retrograde filling of the occluded vessel). All 36 patients included in the analysis underwent cardiac magnetic resonance examination within 3 to 5 days after myocardial infarction and after 12 weeks. Patients with relevant collateral flow (CRS 2–3) to the infarct-related artery had significantly smaller final infarct size compared to those without (7 ± 4% vs. 20 ± 12%, p < 0.001). In addition, both groups showed improvement in left ventricular ejection fraction early after AMI, whereas the recovery was greater in CRS 2–3 (+8 ± 5% vs. +3 ± 5%, p = 0.015). Conclusion: In patients with first AMI, relevant collateral flow to the infarct-related artery was associated with more salvaged myocardium at 12 weeks, translating into greater improvement of systolic left ventricular function. The protective effect of coronary collaterals and the variance of infarct location should be further investigated in larger studies.

Sleep disordered breathing (SDB) is known to cause left atrial (LA) remodeling. However, the relationship between SDB severity and LA dysfunction is insufficiently understood and may be elucidated by detailed feature tracking (FT) strain analysis of cardiac magnetic resonance images (CMR). After myocardial infarction (MI), both the left ventricle and atrium are subjected to increased stress which may be substantially worsened by concomitant SDB that could impair consequential healing. We therefore analyzed atrial strain in patients at the time of acute MI and 3 months after. 40 patients with acute MI underwent CMR and polysomnography (PSG) within 3-5 days after MI. Follow-up was performed 3 months after acute MI. CMR cine data were analyzed using a dedicated FT software. Atrial strain (ε) and strain rate (SR) for atrial reservoir ([ε ]; [SR ]), conduit ([ε ]; [SR ]) and booster function ([ε ]; [SR ]) were measured in two long-axis views. SDB was defined by an apnea-hypopnea-index (AHI) ≥15/h. Interestingly, LA ε and ε were significantly reduced in patients with SDB and correlated negative with AHI as a measure of SDB severity at both baseline and follow-up. Intriguingly, patients that exhibited a reduced AHI at follow-up were more likely to have developed improved atrial reservoir and conduit strain (linear regression, =0.08 for ε and ε ). Patients with improved SDB (ΔAHI < -5/h) exhibited a mean improvement of LA reservoir strain of +7.2 ± 8.4% whereas patients with SDB deterioration (ΔAHI> + 5/h) showed a mean decrease of -5.3 ± 11.0% ( = 0.0131). Similarly, the difference for LA conduit function was +4.8 ± 5.9% (ΔAHI < -5/h) vs -3.6 ± 8.8% (ΔAHI> +5/h). Importantly, conventional volumetric parameters for atrial function (LA area, LA volume index) did not correlate with AHI at baseline or follow-up. Our results show that LA function measured by CMR strain but not by volumetry is impaired in patients with SDB during acute cardiac injury. Consistent with a mechanistic association, improvement of SBD at follow-up resulted in improved LA strain. LA strain measurement might thus provide insight into atrial function in patients with SDB.

Left ventricular hypertrophy (LVH) is a hallmark of chronic pressure or volume overload of the left ventricle and is associated with risk of cardiovascular morbidity and mortality. The purpose was to evaluate different electrocardiographic criteria for LVH as determined by cardiovascular magnetic resonance (CMR). Additionally, the effects of concentric and eccentric LVH on depolarization and repolarization were assessed. 120 patients with aortic valve disease and 30 healthy volunteers were analysed. As ECG criteria for LVH, we assessed the Sokolow-Lyon voltage/product, Gubner-Ungerleider voltage, Cornell voltage/product, Perugia-score and Romhilt-Estes score. All ECG criteria demonstrated a significant correlation with LV mass and chamber size. The highest predictive values were achieved by the Romhilt-Estes score 4 points with a sensitivity of 86% and specificity of 81%. There was no difference in all ECG criteria between concentric and eccentric LVH. However, the intrinsicoid deflection (V6 37 ± 1.0 ms vs. 43 ± 1.6 ms, p < 0.05) was shorter in concentric LVH than in eccentric LVH and amplitudes of ST-segment (V5 -0.06 ± 0.01 vs. -0.02 ± 0.01) and T-wave (V5 -0.03 ± 0.04 vs. 0.18 ± 0.05) in the anterolateral leads (p < 0.05) were deeper. By calibration with CMR, a wide range of predictive values was found for the various ECG criteria for LVH with the most favourable results for the Romhilt-Estes score. As electrocardiographic correlate for concentric LVH as compared with eccentric LVH, a shorter intrinsicoid deflection and a significant ST-segment and T-wave depression in the anterolateral leads was noted.