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Objective: With the advent of a novel coronavirus in December 2019, several case studies have reported its adversity on cardiac cells. We conducted a systematic review that describes the symptomatology, prognosis, and clinical findings of patients with COVID-19-related myocarditis. Methods: Search engines including PubMed, Google Scholar, Cochrane Central, and Web of Science were queried for SARS-CoV-2 or COVID 19 and myocarditis. PRISMA guidelines were employed, and peer-reviewed journals in English related to COVID-19 were included. Results: This systematic review included 22 studies and 37 patients. Eight patients (36%) were confirmed myocarditis, while the rest were possible myocarditis. Most patients had elevated cardiac biomarkers, including troponin, CRP, CK, CK-MB, and NT-pro BNP. Electrocardiogram results noted tachycardia (47%), left ventricular hypertrophy (50%), ST-segment alterations (41%), and T wave inversion (18%). Echocardiography presented reduced LVEF (77%), left ventricle abnormalities (34%), right ventricle aberrations (12%), and pericardial effusion (71%). Further, CMR showed reduced myocardial edema (75%), non-ischemic patterns (50%), and hypokinesis (26%). The mortality was significant at 25%. Conclusions: Mortality associated with COVID-19 myocarditis appears significant but underestimated. Further studies are warranted to evaluate and quantify patients actual prognosis and outcomes with COVID-19 myocarditis.

Authors: Vikash Jaiswal, Shavy Nagpal, Christine Angela E.Labitag, Janelle Tayo, Abhinav Patel, Kevin Bryan Lo, Rupalakshmi Vijayan, Wanessa F Matos, Sadia Yaqoob, Priyanka Panday, Saloni Savani, Zeinab Alnahas, Arushee Bhatnagar, Yoandra Diaz, John R. Dylewski, Own Khraisat, Mohammed JM Ghanim. Objective: With the advent of a novel coronavirus in December 2019, several case studies have reported its adversity on cardiac cells. We conducted a systematic review that describes the symptomatology, prognosis, and clinical findings of patients with COVID-19-related myocarditis. Methods: Search engines including PubMed, Google Scholar, Cochrane Central, and Web of Science were queried for "SARS-CoV-2" or "COVID 19" and "myocarditis." PRISMA guidelines were employed, and peerreviewed journals in English related to COVID- 19 were included. Results: This systematic review included 22 studies and 37 patients. Eight patients (36%) were confirmed myocarditis, while the rest were possible myocarditis. Most patients had elevated cardiac biomarkers, including troponin, CRP, CK, CK-MB, and NT-pro BNP. Electrocardiogram results noted tachycardia (47%), left ventricular hypertrophy (50%), ST-segment alterations (41%), and T wave inversion (18%). Echocardiography presented reduced LVEF (77%), left ventricle abnormalities (34%), right ventricle aberrations (12%), and pericardial effusion (71%). Further, CMR showed reduced myocardial edema (75%), non-ischemic patterns (50%), and hypokinesis (26%). The mortality was significant at 25%. Conclusions: Mortality associated with COVID-19 myocarditis appears significant but underestimated. Further studies are warranted to evaluate and quantify patients’ actual prognosis and outcomes with COVID-19 myocarditis.

Introduction Gitelman syndrome, also known as familial hypokalemia-hypomagnesemia, is a rare autosomal recessive disorder that impairs the sodium chloride cotransporter (NCC) and magnesium channels in the renal distal convoluted tubule, causing salt-losing tubulopathy. It is characterized by hypokalemia, hypomagnesemia, hypocalciuria, and secondary hyperaldosteronism. Although hypocalciuria is a distinctive characteristic of Gitelman syndrome, it seldom can cause any change in the total plasma calcium level. Thus, the occurrence of hypercalcemia would need further investigation. Case presentation We reported a case of a 36-year-old normotensive man with a past medical history significant for bipolar depression disorder and a history of chronic atrial fibrillation secondary to chronic hypokalemia, hypomagnesemia, and mild hypercalcemia. He was diagnosed with Gitelman syndrome. However, he was noncompliant with spironolactone, potassium, and magnesium supplementation. He suffered a motor vehicle accident, and on presentation to the emergency room, he was found with a serum potassium of 2.5 mEq/L (reference value 3.5-5.1), serum magnesium of 0.8 mEq/L (reference value 1.6-2.6), total serum calcium of 11.3 mEq/L (reference value 8.4-10.2), and serum phosphorus of 2.7 (reference value 2.5-4.5 mg/dl). Random urine potassium was 122.1 mEq/L, and intact parathyroid hormone was 144 pg/mL (reference value 14-65). His CT neck scan showed a 1.5 cm nodule inferior to the right thyroid lobe pole consistent with an inferior parathyroid adenoma. However, a parathyroid radionuclide scan using technetium-99m MIBI showed no radiopharmaceutical localization for parathyroid adenoma. Conclusion Hypercalcemia is extremely rare in Gitelman syndrome, offset by the action of concomitant hypomagnesemia. Our case shows the importance of investigating other causes of hypercalcemia, such as primary hyperparathyroidism in patients with Gitelman syndrome. To our knowledge, Gitelman syndrome and primary hyperparathyroidism are an extremely rare association that is present in our case. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m., Monday, June 13, 2022 12:48 p.m. - 12:53 p.m.