A Rare Presentation of Levetiracetam-Induced Torsades De Pointes.

Torsades de pointes occurs in the presence of a prolonged QTc interval, which has many congenital and acquired causes. Levetiracetam is a widely used anti-epileptic medication secondary to its favorable safety profile. We present a rare case of a 59-year-old male who developed torsades de pointes and cardiac arrest after levetiracetam administration. To our knowledge, there is only one other case report documenting torsades de pointes after levetiracetam administration, and our case report will be the first documenting cardiac arrest after levetiracetam administration.

Case Report of Acute Pancreatitis Associated With Combination Treatment of Dulaglutide and Glipizide.

The objective of this report is to discuss a case of drug-induced acute pancreatitis in a patient on a combination of dulaglutide and glipizide. The patient was a 61-year-old African American male with a past medical history of diabetes mellitus type 2 and essential hypertension, who was admitted for acute pancreatitis after presenting with upper abdominal pain. He was initially on glipizide but dulaglutide was added to improve control. The patient was a social drinker and an ex-cigarette smoker. He had serum lipase greater than 900 U/L, serum alcohol was negative, and abdominal computed tomography reported significant pancreatic edema consistent with acute pancreatitis but without features of necrotizing pancreatitis and no evidence of cholelithiasis or choledocholithiasis. His clinical state deteriorated after being complicated by paralytic ileus. He was managed conservatively, improved clinically, and was discharged home. Seeing that the incidence of pancreatitis is higher in patients with diabetes when compared to non-diabetics, it is important to counsel and monitor patients for risk factors of pancreatitis including medications. In the absence of other common causes in this case and considering the temporal relationship between presentation and the addition of dulaglutide to ongoing glipizide regimen, the combination of both drugs may have induced acute pancreatitis.

Why Pulmonary Vasodilation May Be Part of a Key Strategy to Improve Survival in COVID-19.

Oxygenation is a function of both ventilation and perfusion. While approaches to the treatment of COVID-19 have focused largely on ventilation strategies and antiviral therapies, attention towards the improvement of vascular perfusion defects has been neglected. This article examines clinical findings that indicate perfusion defects are a critical component of COVID-19 pathophysiology. They also support the notion that medications that promote perfusion with pulmonary vasodilatation can yield significantly improved outcomes that include overall survival. Calcium channel blocker usage has been associated with improved survival and outcomes in several retrospective reviews of patient populations with COVID-19 from across the world. This includes studies conducted in Paris, France; Wuhan, China; Daegu, South Korea; Brooklyn, New York; Brussels, Belgium; and a national sample from across the United States. These medications are generally prescribed to treat hypertension. Yet, they are also utilized in various pulmonary conditions to effectuate pulmonary vasodilatation. Thus, a concomitant benefit appears to have been revealed as patients that were taking these medications had significantly improved overall survival. Sildenafil is another medication that induces pulmonary vasodilatation. It was found to decrease the need for mechanical ventilation and reduce hospital length of stay in COVID-19 in a triple-blinded randomized control trial. The importance of pulmonary vasodilation in COVID-19 has been evaluated further. In a study of over 100 high-resolution CT scans, patients with COVID-19 showed a significant reduction in pulmonary blood volume contained in small blood vessels of <5 mm2 compared to healthy volunteers. Moreover, this was found to clinically correlate with a need for more oxygen supplementation. In radiologic perfusion studies, hypoperfusion was observed to occur in the healthy lung while hyperperfusion was present in non-healthy COVID-inflicted lung. It appears that perfusion of oxygen-carrying capacity, in the form of hemoglobin-carrying red blood cells, is being misappropriated towards unhealthy lung tissue. This was observed concurrently while the healthy lung had a paucity of perfusion. This can be a key aspect of hypoxic development in COVID-19. Mathematical modeling of perfusion abnormalities in COVID-19 has also implicated extensive perfusion defects, with ventilation-perfusion mismatching in the non-injured lung and hyperperfusion of up to threefold increases to afflicted regions. Vasodilation in the form of systemic intravascular medications may help improve outcomes by resetting this imbalance and by promoting perfusion of the alveolar-capillary unit where gas exchange and oxygenation occurs particularly in the non-injured lung. Furthermore, endothelialitis and microthrombosis have been observed on pathology specimens as many patients develop micro-thrombi following prolonged perfusion deficits. Vasodilatory agents can curb vasoconstriction and drive more perfusion towards healthy tissue. The temporal matching of consistent systemic intravascular vasodilation therapy throughout the gradual and progressive course of the illness may be integral to achieving improved outcomes. Improving perfusion to healthy tissue can help improve oxygenation and overall outcomes in COVID-19. These findings support further utilization and investigation of vasodilatory agents in the treatment of COVID-19.

Heterogeneous Perfusion in COVID-19 and High Altitude Pulmonary Edema: A Review of Two Cases Followed by Implications for Hypoxic Pulmonary Vasoconstriction, Thrombosis Development, Ventilation Perfusion Mismatch and Emergence of Treatment Approaches.

Coronavirus disease 2019 (COVID-19) has been compared to high altitude pulmonary edema (HAPE). Multiple similarities between the two conditions were drawn in the past. This article seeks to further clarify potential underlying mechanisms related to hypoxia and pulmonary vascular responses. It does so by looking at perfusion imaging of patients with COVID-19 and comparing them with patterns observed in HAPE and hypoxic exposure. Two separate clinical cases are reviewed. The salient aspect of each case that is emphasized is the perfusion scintigraphy results that revealed heterogeneous perfusion patterns in both patients. Heterogeneous or non-homogeneous perfusion is also observed in HAPE. A detailed clinical course of each patient is described. Medications utilized to treat the conditions are outlined as well as laboratory parameters and clinical findings. Interestingly, both of these patients were treated with calcium channel blockers and this class of medications is utilized to prevent HAPE as well. Discussion following the case presentations attempts to contextualize possible implications of this and other studies on the broader pathophysiology of COVID-19 disease. Findings related to pathophysiologic patterns and treatment strategies are also described. Micro-thrombi formation has been reported in both COVID-19 and HAPE as well and may be an accessory complication of perfusion compromise. In a separate study, vasodilatation with calcium channel blocker (CCB) therapy has been associated with improved mortality in COVID-19 and potential pathophysiologic mechanisms were previously presented. This case report provides further clinical findings that support the notion that perfusion deficits are an integral component of hypoxia in COVID-19. It also advances the basis for use of vasodilator therapy as part of treatment regimens in COVID-19. Vasodilators may improve micro-perfusion. In this way, oxygenation may be promoted by decreasing impedance and improving flow via the alveolar-capillary unit.

Nifedipine and Amlodipine Are Associated With Improved Mortality and Decreased Risk for Intubation and Mechanical Ventilation in Elderly Patients Hospitalized for COVID-19.

Dihydropyridine calcium channel blockers (CCB) are typically used agents in the clinical management of hypertension. Yet, they have also been utilized in the treatment of various pulmonary disorders with vasoconstriction. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been implicated in the development of vasoconstrictive, proinflammatory, and pro-oxidative effects. A retrospective review was conducted on CCB use in hospitalized patients in search of any difference in outcomes related to specific endpoints: survival to discharge and progression of disease leading to intubation and mechanical ventilation. The electronic medical records for all patients that tested positive for SARS-CoV-2 that were at or above the age of 65 and that expired or survived to discharge from a community hospital in Brooklyn, NY, between the start of the public health crisis due to the viral disease up until April 13, 2020, were included. Of the 77 patients that were identified, 18 survived until discharge and 59 expired. Seven patients from the expired group were excluded since they died within one day of presentation to the hospital. Five patients were excluded from the expired group since their age was above that of the eldest patient in the survival group (89 years old). With 65 patients left, 24 were found to have been administered either amlodipine or nifedipine (CCB group) and 41 were not (No-CCB group). Patients treated with a CCB were significantly more likely to survive than those not treated with a CCB: 12 (50%) survived and 12 expired in the CCB group vs. six (14.6%) that survived and 35 (85.4%) that expired in the No-CCB treatment group (P<.01; p=0.0036). CCB patients were also significantly less likely to undergo intubation and mechanical ventilation. Only one patient (4.2%) was intubated in the CCB group whereas 16 (39.0%) were intubated in the No-CCB treatment group (P<.01; p=0.0026). Nifedipine and amlodipine were found to be associated with significantly improved mortality and a decreased risk for intubation and mechanical ventilation in elderly patients hospitalized with COVID-19. Further clinical studies are warranted. Including either nifedipine or amlodipine in medication regimens for elderly patients with hypertension hospitalized for COVID-19 may be considered.

Acetazolamide, Nifedipine and Phosphodiesterase Inhibitors: Rationale for Their Utilization as Adjunctive Countermeasures in the Treatment of Coronavirus Disease 2019 (COVID-19).

Effective treatments for Coronavirus Disease 2019 (COVID-19) outbreak are urgently needed. While anti-viral approaches and vaccines are being considered immediate countermeasures are unavailable. The aim of this article is to outline a perspective on the pathophysiology of COVID-19 in the context of the currently available clinical data published in the literature. This article appreciates clinical data published on COVID-19 in the context of another respiratory illness - high altitude pulmonary edema (HAPE). Both conditions have significant similarities that portend pathophysiologic trajectories. Following this potential treatment options emerge. Both COVID-19 and HAPE exhibit a decreased ratio of arterial oxygen partial pressure to fractional inspired oxygen with concomitant hypoxia and tachypnea. There also appears to be a tendency for low carbon dioxide levels in both as well. Radiologic findings of ground glass opacities are present in up to 86% of patients with COVID-19 in addition to patchy infiltrates. Patients with HAPE also exhibit patchy infiltrates throughout the pulmonary fields, often in an asymmetric pattern and CT findings reveal increased lung markings and ground glass-like changes as well. Widespread ground-glass opacities are most commonly a manifestation of hydrostatic pulmonary edema. Similarly, elevated fibrinogen levels in both conditions are likely an epiphenomenon of edema formation rather than coagulation activation. Autopsy results of a COVID-19 fatality revealed bilateral diffuse alveolar damage associated with pulmonary edema, pro-inflammatory concentrates, and indications of early-phase acute respiratory distress syndrome (ARDS). HAPE itself is initially caused by an increase in pulmonary capillary pressure and induces altered alveolar-capillary permeability via high pulmonary artery hydrostatic pressures that lead to a protein-rich and mildly hemorrhagic edema. It appears that COVID-19 and HAPE both discretely converge on ARDS. In light of this, a countermeasure that has been shown to be effective in the analogous condition of HAPE is Acetazolamide. Acetazolamide has a myriad of effects on different organ systems, potently reduces hypoxic pulmonary vasoconstriction, improves minute ventilation and expired vital capacity. Other therapeutics to consider that are also directed towards decreased pulmonary pressure include Nifedipine and Phosphodiesterase inhibitors. This review describes COVID-19 in parallel to HAPE. Deranged respiratory parameters that are present in both conditions are highlighted. The utilization of medications found to be effective in HAPE, for the treatment of COVID-19, is proposed. Given the medical emergency of a growing contagion and the thousands of lives at stake, expedient attempts to improve survival are needed. Acetazolamide, Nifedipine and Phosphodiesterase inhibitors may be potential countermeasures.

Ecstasy induced acute systolic heart failure and Non-Ischemic Cardiomyopathy in a young female: a rare case report and literature review.

Ecstasy or 3,4-methylenedioxymethamphetamine (MDMA) is an illicit recreational drug. Effects include euphoria, increased sensory awareness, and central stimulation. Although various arrhythmias, as well as dilated cardiomyopathy, have been previously noted to occur with chronic use, cardiac toxicities are seldom reported in an acute setting. Herein, we present a 28-year-old female patient with no prior medical condition that presented to the Emergency Department with chest pain following intake of MDMA. Electrocardiographic findings, as well as laboratories, were suggestive of possible Acute Non-ST elevation myocardial infarction. Upon admission, cardiac catheterization revealed patent coronary arteries. Stark regional wall motion abnormalities were observed along with reduced ejection fraction. Acute systolic heart failure was treated with standard medical management. Subsequent reassessment of ventricular function with Echocardiography revealed marked improvement. This article describes a case of MDMA induced heart failure, including details of evaluation, management, and monitoring of patient progress. It brings further attention to potential acute harmful effects of MDMA on cardiac function and viability.

ALTERNATING THYROID STATUS BETWEEN THYROTOXICOSIS AND HYPOTHYROIDISM IN A PATIENT WITH VARYING ANTITHYROID ANTIBODIES.

OBJECTIVE: Autoimmune pathologies are a growing aspect of medicine. Knowledge about atypical cases is essential. This report will describe a case of unusual, alternating fluctuations in thyroid function. METHODS: We report a case of thyrotoxicosis alternating with hypothyroidism in a 44-year-old, African-American woman and detail the clinical course and management. RESULTS: The patient presented in a mildly thyrotoxic state with features of thyroiditis that resolved soon thereafter. Subsequently, the course shifted toward a hypothyroid state with a thyroid-stimulating hormone (TSH) level of 24.53 µIU/ml (normal range is 0.45 to 4.5 µIU/ml; measured September 5, 2013) and free thyroxine (FT4) of 0.35 ng/dL (normal range is 0.5 to 1.40 ng/dL; measured September 5, 2013). It ensued with alternating hypothyroid and hyperthyroid trajectories for several cycles. Clinical management was adjusted to negotiate each progression. During certain intervals, levothyroxine was increased. At other visits, it was decreased. Periods without medication were observed as well. Furthermore, methimazole and metoprolol were utilized when required. Reversal of the condition occurred repeatedly. The entire course is tracked with over 30 instances of thyroid function measures that included hypothyroid, euthyroid (TSH at 1.54 µIU/mL, FT4 at 1.16 ng/dL) and thyrotoxic states (TSH at <0.005 µIU/mL, FT4 at 2.67 ng/dL). Various antibody titers were elevated including thyroid-stimulating immunoglobulin, thyroid peroxidase antibody, and TSH receptor antibody. Close monitoring of TSH and FT4 allowed for appropriate medication dose adjustment. CONCLUSION: This case highlights the unusual phenomenon of fluctuating thyroid function with autoimmune involvement of thyroid-stimulating immunoglobulin and TSH receptor antibodies. Close follow up aided responsive clinical management throughout the fluctuating clinical course.

Embolization of an Aberrant Right Subclavian Artery Aneurysm with Amplatzer Vascular Plug without Bypass.

Aberrant right subclavian artery (ARSA) aneurysms are rare, but the risk of rupture and thromboembolism is high, with a postrupture mortality rate of 50%. Open surgical repair of ARSA aneurysms usually requires thoracotomy and aortic grafting, which can be contraindicated in high-risk patients with multiple comorbidities. Endovascular repair of ARSA aneurysms has been reported, with or without adjunctive surgical bypass. We report a case of an 80-year-old woman resenting with an asymptomatic 4 cm ARSA aneurysm who underwent a completely endovascular treatment of the aneurysm using an Amplatzer vascular plug II (St. Jude Medical Inc., St. Paul, MN).