Covid-19 is known to cause both lung and endovascular dysfunction. Calcium channel blockers (CCBs) have been proposed as a potential treatment for COVID-19. The use of calcium channel blockers such as amlodipine, diltiazem, and nifedipine are among first-line therapy for treating systemic and pulmonary hypertension. CCBs have also been used in high altitude pulmonary edema. The utilization of the ACE2 receptor by SARS-CoV-2 can cause diffuse pulmonary vasoconstriction. In this study, we seek to investigate whether the use of CCBs has a beneficial influence on mortality and the rate of intubation among hospitalized COVID-19 patients.METHODS: This is a retrospective review of electronic medical records for 865 patients admitted from 3/1/2020 to 4/30/2020 who tested positive for SARS-CoV-2. Patients were divided into two groups based on whether they were prescribed CCBs or not. We examined baseline characteristics including comorbidities. The two primary outcomes measured were all-cause mortality and intubation. We used t-test for analysis of age. Pearson's chi-squared test was used for primary outcome as well as comorbidities.RESULTS: In this study, We identified 298 patients on CCBs and 568 not on CCBs. Mean age, sex, comorbidities, and prescribed hypertension medications were compared between patients on CCBs and those not on CCBs. The data shows patients on CCBs had a mean age of 70.4 AE 13.8 compared to the non-CCB group had a mean age of 65.27 AE 18.22 (p<0.001). Male patients comprised 61% of the CCB group compared to the 56% of males in the non-CCB group (p<0.162). Patients in the CCB group were seen to have a higher incidence of underlying comorbidities compared to the non-CCB group (p<0.003). Patients in the CCB group were seen to have higher rates of being on other antihypertensive medications compared to the non-CCB group (p<0.035). Patients treated with CCBs had a higher incidence of intubation (37% vs 26%) with an odds ratio of 1.72 (CI¼1.269 -2.32, P<0.001). There was no significant difference in terms of mortality between the two groups (34% vs 39%) with an odds ratio of 0.791 (CI¼0.590-1.061, p¼0.118) CONCLUSIONS: In this analysis of COVID-19 patients treated with either CCBs or non-CCBs, it was found that CCBs demonstrated a significantly elevated rate of intubation compared to the non-CCB group. We also found that the use of CCBs did not demonstrate a significant improvement to mortality, potentially due to the CCB group being older in age, having a higher number of comorbidities, and using a relatively small sample size.CLINICAL IMPLICATIONS: CCBs should be used with caution due to its association with increased intubation. There is no demonstrated benefit of using CCBs at this time as there was no difference in mortality between patients treated with and without CCBs. Further research using clinical trials and studies with a larger group of patients is needed.

Background and Aim There is limited research on the use of histamine‐H2 receptor antagonists and proton pump inhibitors for treating COVID‐19. We compare clinical outcomes between patients hospitalized with COVID‐19 receiving famotidine or pantoprazole. Methods This retrospective study included 2184 patients (famotidine: n = 638, pantoprazole: n = 727, nonuse: n = 819) aged 18 years or older treated for COVID‐19 from March 2020 to March 2021. Patients who received both famotidine and pantoprazole treatments were excluded. Multivariate logistic regression was used for the primary outcome, namely all‐cause mortality, and the secondary outcomes, namely mechanical ventilation, vasopressor use, acute kidney injury, and gastrointestinal bleeding. The main predictor variable was the use of famotidine or pantoprazole. Covariates were demographics, chronic diseases, and symptoms. Results As compared to nonuse, famotidine (OR: 0.30, 95% CI: 0.20–0.44, P < 0.001) and pantoprazole (OR: 0.47, 95% CI: 0.33–0.66, P < 0.001) were significantly associated with lower odds for all‐cause mortality. Comparison of famotidine and pantoprazole showed that the former had lower odds for all‐cause mortality (OR: 0.65, 95% CI:0.45–0.95, P < 0.05), mechanical ventilation (OR: 0.38, 95% CI: 0.25–0.58, P < 0.001), vasopressor use (OR: 0.33, 95% CI: 0.22–0.48, P < 0.001), acute kidney injury (OR: 0.40, 95% CI: 0.30–0.54, P < 0.001), and gastrointestinal bleeding (OR: 0.15, 95% CI: 0.08, 0.29, P < 0.001). Conclusions Famotidine is associated with lower odds for all‐cause mortality, mechanical ventilation, vasopressor use, acute kidney injury, and gastrointestinal bleeding as compared to pantoprazole in patients hospitalized with COVID‐19. We recommend that clinicians consider the use of famotidine over pantoprazole for hospitalized COVID‐19 patients. Future research with a clinical trial would be beneficial to further support such use of famotidine.

No abstract

No abstract

INTRODUCTION: Hypereosinophilic Syndrome (HES) is defined by the presence of peripheral eosinophilia of 1.5 x 10*9 /L for at least one month resulting in end organ damage in the absence of secondary causes of eosinophilia [1]. The most common organs involved at presentation are skin and lungs. Early cardiovascular and cerebrovascular involvement is rare [2]. CASE PRESENTATION:A 59 year old female with Diabetes Mellitus and hypertension presented with non-ST segment elevation myocardial infarction of the inferior wall. A few days later the patient developed acute right cerebral and cerebellar infarction confirmed by MRI of the brain.She had leukocytosis with an eosinophil count 79 x 10*3/mcL. Tests for parasitic infection, drug allergy, mast cell dyscrasias, and autoimmune process were negative. Bone marrow biopsy showed hypercellular bone marrow with dysplastic eosinophils suggestive of HES. In the absence of skin disease, negative PDGFRA 2 translocation, and normal vitamin B12 levels, a diagnosis of Idiopathic HES was made. She was treated with high dose steroids, hydroxyurea, and leukapheresis followed by imatinib, with no benefit.Over the next week MRI revealed multiple new bilateral infarcts in the cerebellum and cerebrum. Concomitantly she developed STEMI of the inferior wall. Echocardiogram on day three was normal. On days 6, 11, and 23, echocardiogram revealed worsening restrictive cardiomyopathy with infiltrative disease in both ventricles extending from apex to lateral wall and obliterating the left ventricular cavity resulting in cardiogenic shock and pulmonary edema. Rapidly progressing neurologic, as well as cardiac complications, were attributed to HES. Interleukin-5 receptor antibody, Benralizumab, was started without benefit and the patient died.DISCUSSION: In primary HES, eosinophilic expansion occurs due to underlying stem cell, myeloid, or eosinophilic neoplasm. In secondary HES, polyclonal eosinophilic expansion is driven by eosinophilopoietic cytokines. Neurological and cardiovascular involvement is well described but rare and presents usually in the form of parenchymal involvement and not vascular occlusive disease as in our patient [2].CONCLUSIONS: HES syndrome typically presents with features of gastrointestinal, pulmonary, and skin involvement [1]. Neurological involvement, when seen, is in the form of parenchymal involvement and later in disease course. Our patient instead had arterial occlusive disease involving coronary, cerebral, and vertebral basilar system as the primary manifestation of the disease, which is unique. Similarly, cardiac involvement occurs as a restrictive/infiltrative cardiomyopathy not as coronary artery occlusion. A striking feature was the rapid progression of infiltrative disease of the left ventricle leading to near occlusion of the LV cavity resulting in cardiogenic shock and death within 2 weeks.