Rapid Recovery of Acute Giant Cell Myocarditis with Hypereosinophilia with Combined Immunosuppression and Benralizumab

Rapid Recovery of Acute Giant Cell Myocarditis with Hypereosinophilia with Combined Immunosuppression and Benralizumab

S64 Journal of Cardiac Failure Vol. 25 No. 8S August 2019 168 Rapid Recovery of Acute Giant Cell Myocarditis with Hypereosinophilia with Combined Immu...

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S64 Journal of Cardiac Failure Vol. 25 No. 8S August 2019 168 Rapid Recovery of Acute Giant Cell Myocarditis with Hypereosinophilia with Combined Immunosuppression and Benralizumab K. Salmond, H. Tazelaar, L. LeMond, R. Scott, B. Hardaway, D. Steidley, J. Rosenthal, D. Delgado; Mayo Clinic Arizona, Scottsdale, AZ Introduction: Myocarditis is often an elusive diagnosis as the clinical presentation can be nonspecific and definitive diagnosis can be challenging due to the low sensitivity of endomyocardial biopsy. Additionally, treatment of myocarditis is controversial with no guidelines and limited data available regarding efficacy. Nevertheless, recent studies have demonstrated a treatment benefit with immunosuppression, particularly in giant cell myocarditis (GCM). This report highlights a unique case of histologically confirmed GCM in which the patient also had a significant peripheral hypereosinophilia, and examines the response of combined immunosuppression with rabbit anti-thymocyte globulin (RATG), corticosteroids, cyclosporine, and benralizumaban interleukin-5 receptor antagonistthat resulted in rapid recovery. Case Report: A 25 year old woman with a history of asthma for 3 years and a recent diagnosis of heart failure with reduced ejection fraction (40%) presented with acute chest pain and worsening left ventricular (LV) dysfunction with a reduction of her left ventricular ejection fraction (LVEF) to 25-30% within 2 weeks. Laboratory studies revealed a 40% peripheral eosinophilia. Further workup was negative for infection, eosinophilic granulomatosis with polyangiitis, or malignancy. A cardiac MRI showed late-gadolinium enhancement and an endomyocardial biopsy confirmed significant eosinophilic tissue infiltration, myocyte necrosis, and the presence of giant cells. She was treated with a combined immunosuppression regimen of RATG induction, corticosteroids, cyclosporine, and benralizumab. Despite this regimen, she had a recurrence of peripheral eosinophilia during the course of her hospitalization. Nevertheless, she had significant clinical improvement in symptomatology, functional status, and hemodynamics. Her peripheral eosinophilia resolved over the following days with increased corticosteroids and thereafter remained negligible. A repeat echocardiogram 3 weeks after initial initiation of immunosuppression demonstrated significant improvement in her LVEF to 53%, improvement of global strain, and reduction of left atrial dilatation. Discussion: Emerging data suggests that treatment with immunosuppression can improve outcomes in patients with GCM. Indeed, this patient did have a marked improvement in LV function within 3 weeks of initiating treatment. Additionally, the use of benralizumab to treat her peripheral eosinophilia demonstrates potential implications for use in other hypereosinophilic syndromes. However, given that her serum eosinophila recurred despite being on a multi-drug immunosuppression regimen, including benralizumab, identifies potential focus areas of future research including further examination of the exact mechanism of action, the relevance of expanded use in other hypereosinophilic syndromes, and delineation of appropriate end points for measuring response.

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studies included in the final analysis (n=125 patients) evaluated 30-day survival and adverse events such as cerebrovascular accident, limb ischemia, hemolysis, major bleeding, device malfunction, pump thrombosis, and infection. The mean age of patients across studies was 57 +/- 4.7 years, 83% were male, 43% were post-acute myocardial infarction. The mean length of support was 13.4 +/- 8.2 days. The 30-day survival was 64% (95% CI 51.7- 76.6 %). Percentages of patient experiencing adverse events are reported in Figure 1. Conclusions: This analysis demonstrates that axillary or subclavian Impella 5.0 has a relatively low adverse event rate and can be used for longer periods of time than is reported for other forms of temporary support.

170 Seismocardiography and Machine Learning Algorithms to Assess Clinical Status of Patients with Heart Failure in Cardiopulmonary Exercise Testing Mobashir Md Hasan Shandhi1, Joanna Fan2, J. Alex Heller3, Mozziyar Etemadi3, Omer T. Inan1, Liviu Klein2; 1Georgia Institute of Technology, Atlanta, GA; 2University of California San Francisco, San Francisco, CA; 3Northwestern University, Chicago, IL Introduction: Cardiopulmonary exercise testing (CPET) is an important risk stratification tool in patients (pts) with heart failure (HF); measures such as peak VO2, VE/ VCO2 slope have prognostic value in HF pts to determine whether a patient needs advanced heart therapy or not. In our previous studies, we have shown that wearable chest patch based seismocardiogram (SCG) signals can be used to estimate features from CPET and SCG can be used to differentiate between compensated (C) and decompensated (D) pts with HF following exercise (6 minute walk test). Hypothesis: We hypothesized that changes in SCG features from rest to peak exercise would be less in D pts compared to C pts, as D pts have less cardiovascular reserve to meet elevated cardiac demand during higher exercise intensity. Methods: We conducted CPET using ramp bicycle in 6 C pts (50% had HF, 100% men, ejection fraction [EF] 0.61 § 0.18) and 5 D pts (100% had HF, 40% men, EF 0.41 § 0.29). SCG and ECG signals were simultaneously recorded using our custom-built wearable chest patch (Fig. 1a). We have segmented these signals into heart beats and averaged the beats with a moving average window and extracted features (amplitude, frequency and time domain) from the SCG. We combined the SCG features (beat-by-beat) using dimension reduction techniques and compared the changes in SCG features from rest to different exercise intensity levels, by calculating the distance of a distribution for a particular intensity to rest distribution. We have compared the changes in SCG with exercise intensity between C and D pts (classified based on CPET results). Results: We found that normalized distance matrix (NDM) increased significantly (p<0.05) for C pts (Fig 1b & c) from anaerobic threshold (AT) to peak exercise and decreased significantly (p<0.05) into recovery (peak NDM of 1.91 § 0.53 for VO2-max of 17.41 § 5 mL/kg/min). Whereas for D pts it started a bit higher, increased in the first stage of exercise, and then showed little change (p>0.05) between AT and peak exercise and then decreased slightly (p>0.05) into recovery (peak NDM of 1.73 § 0.16

Meta-Analysis of Outcomes of Axillary and Subclavian Implanted Impella 5.0 for Cardiogenic Shock Jessica Schultz, Sue Duval, Andrew Shaffer, David Shisler, Cindy Martin, Ranjit John, Rebecca Cogswell; University of Minnesota, Minneapolis, MN Introduction: The purpose of this study was to summarize survival and adverse events in patients with cardiogenic shock supported by the 5.0 Impella (Abiomed Inc, Danvers, MA USA) via axillary or subclavian access. Methods: We performed a literature review of PUBMED and OVID databases for published, peer-reviewed manuscripts in English through March 31, 2019 for patients supported by Impella 5.0 devices. Only peer-reviewed studies with axillary or subclavian access, greater than or equal to 5 patients, and with clear reporting of survival and adverse events were included. A random effects meta-analysis was then performed. Results: The ten

Figure 1. (a) Image showing the wearable patch for measuring ECG and SCG signals from the chest simultaneously with CPET, corresponding wearable signals and data processing block diagram for wearable and CPET data. (b) Trend of VO2 and (c) SCG features at different levels of exercise intensity. Rest=baseline, UC=unloaded cycling, AT=anaerobic threshold, Max=peak exercise, R30=R30s into recovery, R60=60s into recovery, Comp = compensated pts, Decomp = decompensated pts. (*P<0.05 intragroup between exercise intensity for compensated subjects only, zP<0.01 intergroup at a particular exercise intensity).