Hypertension as an Independent Risk Factor for In-Patient Mortality in Hospitalized COVID-19 Patients: A Multicenter Study.

Despite the lack of direct evidence that hypertension increases the likelihood of new infections, hypertension is known to be the most common comorbid condition in COVID-19 patients and also a major risk factor for severe COVID-19 infection. The literature review suggests that data is heterogeneous in terms of the association of hypertension with mortality. Hence, it remains a topic of interest whether hypertension is associated with COVID-19 disease severity and mortality. Herein, we perform a multicenter retrospective analysis to study hypertension as an independent risk for in-hospital mortality in hospitalized COVID-19 patients. This multicenter retrospective analysis included 515 COVID-19 patients hospitalized from March 1, 2020 to May 31, 2020. Patients were divided into two groups: hypertensive and normotensive. Demographic characteristics and laboratory data were collected, and in-hospital mortality was calculated in both groups. The overall mortality of the study population was 25.3% (130 of 514 patients) with 96 (73.8%) being hypertensive and 34 (26.2%) being normotensive (p-value of 0.01, statistically non-significant association). The mortality rate among the hypertensive was higher as compared to non-hypertensive; however, hypertensive patients were more likely to be old and have underlying comorbidities including obesity, diabetes mellitus, coronary artery disease, congestive heart failure, stroke, chronic kidney disease (CKD), chronic obstructive pulmonary disease (COPD), and cancer. Therefore, multivariable logistic regression failed to show any significant association between hypertension and COVID-19 mortality. To our knowledge, few studies have shown an association between hypertension and COVID-19 mortality after adjusting confounding variables. Our study provides further evidence that hypertension is not an independent risk factor for in-hospital mortality when adjusted for other comorbidities in hospitalized COVID-19 patients.

Reactivation of Tuberculosis in the Setting of COVID-19 Infection.

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV- 2) was declared a pandemic by WHO in March 2020. The causative organism has since undergone a series of mutations. COVID-19 primarily being a respiratory illness causes pre-existing pulmonary diseases to show worse clinical outcomes. About one-third of the world's population is thought to be infected with latent Mycobacterium tuberculosis (MTB). Both previous and newly developed tuberculosis (TB) infection are risk factors for COVID-19 and are associated with poor outcomes. T lymphocytes play a pivotal role in defense against MTB and with evidence suggesting depletion of T lymphocytes in COVID-19, it can be postulated that COVID-19 can increase the risk of reactivation of latent TB.  Given that a large population around the globe is infected with latent tuberculosis, it is interesting to study and note cases where the virus leads to the reactivation of latent tuberculosis infection. Herein, we present a 76-year-old Brazilian male recently treated for COVID-19 pneumonia, presenting with new-onset cough and weakness diagnosed with latent MTB reactivation.

Fever and Hyponatremia Unmasking Brugada Pattern Electrocardiogram in a Patient With SARS-CoV-2 Infection.

Brugada syndrome is an autosomal dominant genetic disorder that primarily affects myocardial sodium channels and has been associated with an increased risk of ventricular tachyarrhythmias and sudden cardiac death. Here, we report a case of a 58-year-old Hispanic male with a history significant for prior pulmonary tuberculosis infection who presented with pleuritic left-sided chest pain associated with body aches, productive cough, fevers, and chills and was found to be positive for SARS-CoV-2 by real-time reverse-transcription-polymerase chain reaction (rRT-PCR). Electrocardiogram (ECG, EKG) on presentation demonstrated a coved ST-segment elevation in V1-V2, suggesting Brugada pattern type 1 without evidence of ischemic changes. EKG changes normalized once fever and hyponatremia improved.

Does Baseline Diuretics Use Affect Prognosis in Patients With COVID-19?

The rapid emergence of coronavirus disease 2019 (COVID-19) has become the biggest healthcare crisis of the last century, resulting in thousands of deaths worldwide. There have been studies that evaluated the role of angiotensin-converting enzyme (ACE) inhibitors (ACEi) and angiotensin receptor blockers (ARBs) in treating patients with COVID-19. However, the prior use of diuretics and their effect on mortality in this setting remains unknown. The aim of the study was to evaluate the effect of diuretics in patients admitted with COVID-19. The current study was conducted between March 15, 2020, and April 30, 2020, during the COVID-19 pandemic in three different hospitals in Northern New Jersey, USA. The primary outcome was survival or in-hospital mortality from COVID-19 from the day of admission. The secondary outcome was severe or non-severe illness from COVID-19. This retrospective study included a total of 313 patients with a median age of 61.3 ± 14.6 years. There was a total of 68 patients taking diuretics at home and 245 patients who were not taking diuretics. There was a total of 39 (57.35%) deaths in patients taking diuretics as compared to 93 (37.96%) deaths in patients not taking diuretics (p-value 0.0042). Also, 54 (79.41%) patients who took diuretics had severe COVID-19 illness as compared to 116 (47.35%) who did not take diuretics (p-value <.0001). However, after adjusting for the confounding factors, there was no difference in mortality or severity of illness in COVID-19 patients taking diuretics at the time of admission. In conclusion, there was no effect of the baseline use of diuretics in the prognosis of COVID-19.

A Rare Complication of Myocardial Infarction: Ventricular Septal Defect.

Ventricular septal defect (VSD) is a rare but lethal complication of myocardial infarction. We present a case of a 65-year-old male who presented with a history of progressive shortness of breath associated with productive cough. Physical examination was significant for crepitation in both lower lung fields and bilateral lower extremity edema. Chest X-ray revealed bilateral reticular opacities with small bilateral pleural effusions. Polymerase chain reaction (PCR) for COVID was positive. Echo showed a left ventricular ejection fraction (LVEF) of 30-35%, ischemic cardiomyopathy, and muscular ventricular septal defects with left to right shunting and severely elevated pulmonary artery systolic pressure. Overtime during the hospital course, he developed respiratory and fulminant hepatic failure. Our patient had VSD due to an undiagnosed old myocardial infarction (MI). Initially heart failure was compensated and treated with medical management. Later on, he developed respiratory complications related to COVID-19 infection as well as hepatic failure in addition to a cardiomyopathy which made him a poor surgical candidate leading to death.

A Case Report of Polymerase Chain Reaction-Confirmed COVID-19 in a Patient With Right Ventricular Thrombus and Bilateral Deep Vein Thrombosis.

The new coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), that causes the highly contagious coronavirus disease 2019 (COVID-19) has led to an unprecedented global health crisis. Infected patients have been shown to trigger a heightened inflammatory response, increasing thrombotic risk. We report the case of a polymerase chain reaction (PCR)-confirmed COVID-19 in a Hispanic male with no past medical history who presented to the ED with upper respiratory tract symptoms including shortness of breath and cough, requiring continuous positive airway pressure (CPAP) therapy. He was found to have a right ventricular thrombus (RVT) and bilateral deep vein thrombosis (DVT) on the day of admission, which were detected on transthoracic echocardiogram and duplex venous ultrasound, respectively. The patient was started on therapeutic enoxaparin sodium, which led to an improvement in oxygenation, and he was eventually downgraded to the medical floors for further management.