Clevidipine and COVID 19: From Hypertension to Inflammatory Response.

Globally, more than 4 million have died from COVID-19, World Health Organization (WHO) to declare COVID-19 a pandemic. The COVID 19 pathology, produced by SARS-COV2, a virus from the coronavirus family, emerged at the end of 2019. The majority of cases usually have a mild or moderate form, characterized by fever, cough, intense asthenia and multiple symptoms derived from the initial replicative effect and subsequent hyperimmune effect. Severe cases present with Acute Respiratory Distress Syndrome (ARDS), due to pneumonia with bilateral involvement, which lead to hospital admission of patients and the need for admission to intensive care units (ICU) of approximately 10‒20%. According to the different series; the mortality of the condition once the patient is admitted to the ICU is close to 35‒45%. Currently, more than 4 million people have died in the world due to this pathology. The volume of infections generated the declaration by the World Health Organization (WHO) of the pandemic situation. Factors associated with a higher risk of progression into severe disease include age and comorbidities, especially systemic arterial hypertension due to its high incidence in the general population. Clevidipine can be rapidly and effectively adjusted to the clinical status of the patient, since it can be withdrawn and its effects reversed in just a few minutes, and contains high concentrations of lipids, and it could reduce the inflammatory response induced by SARS-COV2, which is key to progression into severe disease. However, its application in pro-inflammatory settings has not yet been explored, although it must play a key role in inflammation as a scavenger molecule.

Renal and Neurologic Benefit of Levosimendan vs Dobutamine in Patients With Low Cardiac Output Syndrome After Cardiac Surgery: Clinical Trial FIM-BGC-2014-01.

BACKGROUND: Low-cardiac output syndrome (LCOS) after cardiac surgery secondary to systemic hypoperfusion is associated with a higher incidence of renal and neurological damage. A range of effective therapies are available for LCOS. The beneficial systemic effects of levosimendan persist even after cardiac output is restored, which suggests an independent cardioprotective effect. METHODS: A double-blind clinical trial was conducted in patients with a confirmed diagnosis of LCOS randomized into two treatment groups (levosimendan vs. dobutamine). Monitoring of hemodynamic (cardiac index, systolic volume index, heart rate, mean arterial pressure, central venous pressure, central venous saturation); biochemical (e.g. creatinine, S100B protein, NT-proBNP, troponin I); and renal parameters was performed using acute kidney injury scale (AKI scale) and renal and brain ultrasound measurements [vascular resistance index (VRI)] at diagnosis and during the first 48 h. RESULTS: Significant differences were observed between groups in terms of cardiac index, systolic volume index, NT-proBNP, and kidney injury stage at diagnosis. In the levosimendan group, there were significant variations in AKI stage after 24 and 48 h. No significant differences were observed in the other parameters studied. CONCLUSION: Levosimendan showed a beneficial effect on renal function in LCOS patients after cardiac surgery that was independent from cardiac output and vascular tone. This effect is probably achieved by pharmacological postconditioning. CLINICAL TRIAL REGISTRATION: EUDRA CT, identifier 2014-001461-27. https://www.clinicaltrialsregister.eu/ctr-search/search?query=2014-001461-27.