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Background: Acute eosinophilic myocarditis (EM) is a rare form of heart failure that is characterized by myocardial eosinophilic infiltration usually in association with peripheral eosinophilia. The underlying cause is variable and can include allergic reactions, parasitic infection, idiopathic hypereosinophilic syndrome, malignancy, Loeffler's syndrome, Churg-Strauss syndrome (CSS), early giant cell myocarditis and malignancy. The course is potentially fatal, and early diagnosis and treatment with steroids is essential. Conclusion: Here, we present an illustrative case of eosinophilic myocarditis secondary to CSS followed by a brief review of epidemiology, pathogenesis, diagnosis and treatment of both disease entities.

Background: Myxedema heart disease is an extremely rare disease entity and should be suspected in patients with unexplained heart failure refractory to conventional treatment. Myxedema coma with co- existent heart disease is not well known and very few cases have been reported. Conclusion: Here, we present an interesting case of myxedema coma with severe valvular cardiomyopathy followed by a concise review of the literature with special emphasis on epidemiology, pathophysiology, diagnosis and therapeutic modalities.

Heart failure (HF) has a large societal and economic burden and is expected to increase in magnitude and complexity over the ensuing years. A number of telemonitoring strategies exploring remote monitoring and management of clinical signs and symptoms of congestion in HF have had equivocal results. Early studies of remote haemodynamic monitoring showed promise, but issues with device integrity and implantation-associated adverse events hindered progress. Nonetheless, these early studies established that haemodynamic congestion precedes clinical congestion by several weeks and that remote monitoring of intracardiac pressures may be a viable and practical management strategy. Recently, the safety and efficacy of remote pulmonary artery pressure-guided HF management was established in a prospective, single-blind trial where randomisation to active pressure-guided HF management reduced future HF hospitalisations. Subsequent commercial use studies reinforced the utility of this technology and post hoc analyses suggest that tight haemodynamic management of patients with HF may be an additional pillar of therapy alongside established guideline-directed medical and device therapy. Currently, there is active exploration into utilisation of this technology and management paradigm for the timing of implantation of durable left ventricular assist devices (LVAD) and even optimisation of LVAD therapy. Several ongoing clinical trials will help clarify the extent and utility of this strategy along the spectrum of patient with HF from individuals with chronic, stable HF to those with more advanced disease requiring heart replacement therapy.

Background:We present a case of a young female with no pre-existent conditions, who presented to the hospital one month after a mild COVID-19 infection with severe myocarditis complicated by cardiogenic shock.Case:A 40-year-old female with no prior medical history and a regular, vigorous exercise program developed a mild COVID-19 infection with symptoms of mild fatigue, myalgias, chills, fever, and loss of taste, which resolved within a week. A month later, she presented to the hospital with exertional dyspnea, weakness, chest pressure, abdominal pain, and fatigue. A transthoracic echocardiogram revealed a left ventricular ejection fraction of 15% with a severely dilated left ventricle, global hypokinesis and severe mitral regurgitation. Right heart catheterization demonstrated cardiogenic shock with a cardiac index of 1.4 liters per minute by Fick equation, and she was admitted to the cardiac intensive care unit. Cardiac magnetic resonance revealed subepicardial delayed enhancement along the lateral and inferolateral walls and elevated T1 mapping consistent with myocarditis. A right ventricle biopsy revealed myocyte hypertrophy and patchy interstitial fibrosis without evidence of inflammatory tissue. She was diuresed, supported with inotropic therapy, and empirically treated with high doses of glucocorticoids. She clinically improved with weaning of inotropes and was discharged in stable condition on goal-directed medical therapy after 2.5 weeks.Conclusion:This patient represents a case of severe cardiogenic shock, after initial infection and in the absence of previously identified risk factors for development of COVID myocarditis. The absence of inflammatory tissue on pathology raises questions regarding the centrality of inflammatory processes in COVID-19-related myocardial injury leading to “long COVID” syndrome. These findings indicate the need for ongoing investigation of the long-term cardiovascular consequences of COVID-19.

To better understand how different histologic patterns of allograft inflammation found on biopsies of human cardiac allografts progress to high-grade rejection, we undertook a statistical analysis of our institutional database to detect statistical patterns among different types of myocardial allograft inflammations found on sequential biopsies.

The aim of this study was to assess sex differences in the efficacy and safety of baroreflex activation therapy (BAT) in the BeAT-HF (Baroreflex Activation Therapy for Heart Failure) trial.

The incidence of ramp test echocardiogram-associated embolic events in the setting of therapeutic anticoagulation is likely rare and has not been reported. We present such a case in a patient with a HeartMate II left ventricular assist device (LVAD) whose serial head computed tomography images, deteriorating clinical course, and the multiembolic nature of the event suggest causality. If the pretest probability of pump thrombosis in an individual LVAD patient is sufficiently high, the potential risks of performing a ramp study echocardiogram may not be warranted, even in the setting of adequate anticoagulation.