We describe a 46-year-old male with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection who presented as a Kawasaki-like syndrome with features including prolonged fever, bilateral conjunctivitis, oral mucosal swelling, diffuse erythematous rash, cervical and hilar lymphadenopathy, as well as cardiovascular complications and multi-organ failure. There are several reports of a similar clinical entity mimicking Kawasaki disease (KD) in the pediatric population, which has been termed Pediatric Inflammatory Multisystem Syndrome Temporally Associated with SARS-CoV-2 (PIMS-TS) by the Royal College of Pediatric and Child Health. To our knowledge, to date, there has been only one case report of COVID-19 presenting as KD in an adult patient.

There has been significant interest in research for the development of device-based therapy as a treatment option of heart failure (HF), whether it is with reduced or preserved ejection fraction. This is due to the high morbidity and mortality rate in patients with HF despite recent advances in pharmacologic treatment. Following the success of cardiac resynchronization therapy, baroreceptor activation therapy has emerged as another novel device-based treatment for HF. The Barostim neo was developed by CVRx Minneapolis, MN for the treatment of mild to severe HF. The device works by electrically activating the baroreceptor reflex with the goal to restore the maladaptive autonomic imbalance that is seen in patients with HF. Preliminary clinical investigations have given promising results with an encouraging safety profile. Baroreceptor activation therapy as a treatment option is still investigational at this time; however, several trials in different patient populations have already shown benefit with a very good safety profile. In this review, we will summarize the current state of technology and the available literature of the use of baroreceptor activation therapy in patients with different comorbidities, with a focus on this device-based therapy in patients with HF.

We describe a case of a 50-year-old man with alcohol cirrhosis status post transjugular intrahepatic portosystemic shunt (TIPS) who presented with dyspnea, refractory hepatic hydrothorax (HH), and no ascites who subsequently developed acute tension hydrothorax (TH). Urgent ultrasound-guided thoracentesis was performed with a significant improvement of symptoms. Further management consisted of a chest tube placement, subsequently removed with a plan for intermittent thoracentesis as needed, diuretic therapy, and salt restriction. HH occurs in 5%-10% of patients with cirrhosis, and TH in these patients is a rare entity that requires prompt recognition and drainage as it may be life-threatening.

Clinical Case: A 37-year-old transgender (TG) woman off gender-affirming hormonal therapy (GAHT) presented with substernal chest pain radiating to the left arm, worse with exertion and relieved with res. She was hypertensive and tachycardic on admission. Initial bloodwork revealed an elevated troponin I of 0.57 ng/mL, which peaked at 1.48 ng/mL. EKG on admission showed hyperacute T waves in the anterior leads without ST elevation (see Figure 1). She was diagnosed with non-ST elevation myocardial infarction (NSTEMI) and taken for left heart catheterization (LHC). Decision-Making: TTE showed preserved LVEF and basal inferior, basal inferolateral, basal anterolateral and mid-anterolateral hypokinesis. LHC showed proximal-to-mid right coronary artery (RCA) occlusion. After failed aspiration thrombectomy indicating calcified plaque, two overlapping drug-eluting stents (DES) were successfully deployed with restoration of flow. She was discharged home on aspirin, ticagrelor, atorvastatin, and carvedilol. Discussion: Despite a recent push to increase awareness, research and healthcare equality specific to lesbian, gay, bisexual, transgender, and queer (LGBTQ+) patients, a significant gap persists. Specifically, stress, inflammation, dyslipidemia, and thromboembolism predispose this understudied population to increased coronary artery disease (CAD) and myocardial infarction (MI). Accordingly, greater effort needs to be taken to mitigate preventable cardiac morbidity and mortality in this patient population. Conclusion: CAD in LGBTQ+ adults is well studied. However, there are few published studies on CAD specifically among TG men and women. National cross-sectional data highlights this disproportionate risk of CAD and MI among TG men and women relative to their cisgender female and male peers, a healthcare disparity recently emphasized by the AHA. Consequently, care must be taken to eliminate these aforementioned inequalities.

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