Ethical Considerations Surrounding Vaccine Development During A Public Health Crisis

Epidemics and Pandemics have been plaguing mankind since many centuries, and are a cause of major healthcare expense in modern times. The novel coronavirus pandemic of 2019-2020 spread worldwide faster than many previous pandemics, including EBOLA in 2017. Although personal protective equipment, and social distancing slowed the outbreak, a vaccine is needed to ensure global immunization and to stop this deadly outbreak. Developing a vaccine in times of a public health crisis comes with a lot of ethical considerations, including overlooking proper informed consent, the issue of using placebo in control arm of trials, extended timelines of development of vaccines, randomized placebo control trial of secondary vaccine once the first vaccine is approved, and utilizing vulnerable population for trials. These issues are often overlooked due to the urgency of the situation, and the need of developing a cure/vaccine can lead to potential oversight of many regulations. We discuss some of these issues related to vaccine development in a pandemic situation in this commentary paper. We also discuss some of the arguments supporting a secondary vaccine development such as logistical/economic issue, better efficacy, and the conditions of Equipoise

Ranolazine Induced Bradycardia, Renal Failure, and Hyperkalemia: A BRASH Syndrome Variant

Ranolazine is a well-known antianginal drug, that was first licensed for use in the United States in 2006. It was objectively shown to improve exercise capacity and to lengthen the time to symptom onset in patients with coronary artery disease. The most commonly reported side effects of ranolazine include dizziness, headache, constipation, and nausea. Here, we describe a case of bradycardia, hyperkalemia, and acute renal injury in the setting of ranolazine use. Our patient is an 88-year-old female who presented with abdominal pain, nausea, and vomiting. Her medical comorbidities included hypertension, diabetes, CAD, heart failure with preserved ejection fraction, paroxysmal atrial fibrillation, hypothyroidism, and a history of cerebrovascular accident without any residual deficits. Her prescription regimen included amlodipine, furosemide, isosorbide mononitrate, levothyroxine, metformin, omeprazole, and ranolazine. Physical examination was remarkable for bradycardia and decreased breath sounds in the left lower lung field. Laboratory studies were significant for a serum potassium level of 6.8 mEq/L and a serum creatinine level of 1.6 mg/dL. She was given insulin with dextrose, sodium polystyrene, and calcium gluconate in addition to fluids. Her bradycardia and renal function worsened over the next 24 hours. Ranolazine was discontinued. Metabolic derangements were treated appropriately. After 48 hours from presentation, potassium and renal function returned to baseline and her heart rate improved to a range of 60–100 bpm. She was discharged with an outpatient cardiology follow-up. Ranolazine treatment was not continued upon discharge. In summary, our case illustrates an association between ranolazine and renal failure induced hyperkalemia, leading to conduction delays in the myocardium. Though further studies are warranted, we suspect that this is a variant of the recently described BRASH syndrome. We propose that in cases such as ours, along with treatment of the hyperkalemia, medication review and removal of any offending agent should be considered