scholarly journals Promising Therapy for Heart Failure in Patients with Severe COVID-19: Calming the Cytokine Storm

Author(s):  
Xiang Peng ◽  
Yani Wang ◽  
Xiangwen Xi ◽  
Ying Jia ◽  
Jiangtian Tian ◽  
...  

AbstractThe coronavirus disease 19 (COVID-19) pandemic poses a serious global threat to human health and the economy. Based on accumulating evidence, its continuous progression involves not only pulmonary injury but also damage to the cardiovascular system due to intertwined pathophysiological risks. As a point of convergence in the pathophysiologic process between COVID-19 and heart failure (HF), cytokine storm induces the progression of COVID-19 in patients presenting pre-existing or new onset myocardial damage and even HF. Cytokine storm, as a trigger of the progression of HF in patients with COVID-19, has become a novel focus to explore therapies for target populations. In this review, we briefly introduce the basis of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and illuminate the mechanism and links among COVID-19, cytokine storm, and HF. Furthermore, we discuss drugs and therapeutic targets for patients with COVID-19 and HF.

2021 ◽  
Vol 3 (3) ◽  
pp. 01-05
Author(s):  
Rima Chaddad ◽  
Matina Hamadeh ◽  
Amena Khatoun ◽  
Zouheir Kreidly ◽  
Claudette Najjar ◽  
...  

Coronavirus disease 2019 (COVID-19) is defined as illness caused by a novel coronavirus now called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; formerly called 2019-nCoV), which was first identified as an outbreak in Wuhan City, Hubei Province, China [1]. Cases of multisystem inflammatory syndrome after Covid – 19 infection have been extensively documented in children. CDC reported 27 cases of multisystem inflammatory syndrome in adults (MIS-A) in direct reports through October 2020, as well as various case series and published case reports [2]. Cytokine storm, as a trigger of the progression of HF in patients with COVID-19, has become a novel focus to explore therapies for target populations [3]. In this article, we briefly present a case of a Covid-19 infection associated myocarditis complicated by acute heart failure successfully treated with IVIG.


Life ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 165
Author(s):  
Filiberto Mottola ◽  
Nicoletta Verde ◽  
Riccardo Ricciolino ◽  
Marco Di Mauro ◽  
Marco Migliaccio ◽  
...  

As of January 2020, a new pandemic has spread from Wuhan and caused thousands of deaths worldwide. Several studies have observed a relationship between coronavirus disease (COVID-19) infection and the cardiovascular system with the appearance of myocardial damage, myocarditis, pericarditis, heart failure and various arrhythmic manifestations, as well as an increase in thromboembolic risk. Cardiovascular manifestations have been highlighted especially in older and more fragile patients and in those with multiple cardiovascular risk factors such as cancer, diabetes, obesity and hypertension. In this review, we will examine the cardiac involvement associated with SARS-CoV-2 infection, focusing on the pathophysiological mechanism underlying manifestations and their clinical implication, taking into account the main scientific papers published to date.


2021 ◽  
pp. 6-11
Author(s):  
Oleksii Korzh

COVID-19 affects not only the respiratory system, but also the cardiovascular system. The damage to the cardiovascular system in COVID-19 is multifactorial and several mechanisms are involved, including direct invasion, inflammation, thrombosis, autoantibody synthesis, and oxygen imbalance. The inflammation causes the release of cytokines, especially interleukin-6, and damage to cardiomyocytes. The overproduction of cytokines leads to an abnormal inflammatory response called a cytokine storm, which is believed to be the culprit in cardiovascular events in COVID-19 patients. Cardiovascular disease is common in patients with COVID-19, and these patients are at increased risk of morbidity and mortality. There is still no data on cardiac dysfunction due to myocardial damage in patients recovering from COVID-19. Most often, this is normal heart function after complete recovery. But often there are myocardial damage and an increased level of troponin as a marker of the severity of the disease associated with a cytokine storm, hypoxia, vasopressors and blood clotting disorders. It is important for every physician to make a differential diagnosis between decompensated heart failure complicated by pulmonary infection and COVID-19 infection. Monitoring and influencing myocardial injury is extremely important in critically ill patients. Treatment of COVID-19 patients with cardiovascular complications is mostly supportive. The role of pharmacological blocking of the reninangiotensin-aldosterone system in patients with cardiovascular disease and COVID-19 infection requires further research as the relationship appears to be very complex. To date, professional cardiological societies do not recommend canceling ACE inhibitors or agiotensin II receptor antagonists for patients taking these drugs for other indications. Special care should be taken about the potential cardiovascular side effects of the various therapies used to treat viral infections. When using them, daily monitoring of the QT interval on the ECG is proposed.


2020 ◽  
Vol 5 (5) ◽  
pp. 158-163
Author(s):  
V. I. Lysenko ◽  
◽  
E. A. Karpenko ◽  
Ya. V. Morozova

The study of intraoperative fluid therapy tactics has been of great interest over the past few years, especially in people with concomitant coronary heart disease, as they make up a significant proportion of all surgical patients. The purpose of our study was to assess the risk of intraoperative myocardial damage in patients with concomitant coronary heart disease depending on the fluid regimen used based on monitoring of hemodynamic parameters, electrocardiogram and biomarkers of myocardial damage. Material and methods. The study involved 89 patients, who were divided into two groups depending on the tactics of intraoperative fluid therapy – restrictive and liberal. In order to detect cardiac complications at different stages, we assessed biomarkers of myocardial damage Troponin I, NT-proBNP by solid-phase enzyme-linked immunosorbent assay (ELISA). Results and discussion. Analysis of the obtained data showed that MINS (myocardial injury in noncardiac surgery) incidents were diagnosed in 5 patients (11.1%) in the first group and in 6 patients (13.6%) in the second. In patients of both groups there was an increase in NT-proBNP in the dynamics at all stages, and in the 2nd group, with a liberal regimen of intraoperative fluid therapy, it was more pronounced. It should be noted that the obtained values of NT-proBNP in all patients did not differ significantly from those allowed for this age group; such dynamics of NT-proBNP may indicate a relative risk of complications of liberal fluid therapy in patients with baseline heart failure. One of the important points when choosing the mode of fluid therapy in patients with high cardiac risk is the assessment of the initial volemic status and careful monitoring of water balance in the perioperative period with the desire for "zero" balance. The obtained dynamics of laboratory markers of myocardial damage indicates that in patients with a significant reduction in cardiac reserves compensated for heart failure, a restrictive fluid regimen is preferable, which is also confirmed by slight changes in the concentration of biomarkers. Conclusion. Thus, the study demonstrated the relative safety of selected fluid regimens in patients with concomitant coronary heart disease without signs of congestive heart failure


1987 ◽  
Vol 9 (1) ◽  
pp. 57-61
Author(s):  
Toshiro Sato ◽  
Akihiro Takeuchi ◽  
Jun Yamagami ◽  
Hareaki Yamamoto ◽  
Shigeaki Akiyama ◽  
...  

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
B Zareini ◽  
P.B Blanche ◽  
A.H Holt ◽  
M.M Malik ◽  
D.P Rajan ◽  
...  

Abstract Background Development of type 2 diabetes (T2D) is common in patients with heart failure (HF), but knowledge of future cardiovascular events is lacking. Purpose We compared risk of heart failure hospitalization (HFH) or death versus ischemic events in real-life HF patients with new-onset T2D, prevalent T2D and no T2D. Methods Using the Danish nationwide registers, we identified all patients with HF between 1998–2016. The patients were separated in two different HF cohorts based on the status of T2D. One cohort consisted of HF patients with either prevalent or absent T2D at the time of HF diagnosis. The other cohort consisted of HF patients, who developed new-onset T2D, included at time of diagnosis. The two HF cohorts were analyzed separately. Outcomes for both cohorts were analyzed as time-to-first event as either an ischemic event (i.e. composite outcome of fatal and non-fatal myocardial infarction, stroke, and peripheral artery disease), HFH, or event-free death (not related to HFH or the ischemic event). For each cohort, we estimated the five-year absolute risk of ischemic event, HFH and event-free death, along with five-year risk ratio of HFH or event-free death versus ischemic events. Effects among subgroups were investigated by stratifying both cohorts based on age, gender and comorbidities present at inclusion. Results A total of 139,264 HF patients were included between 1998 and 2016, of which 29,078 (21%) patients had prevalent T2D at baseline. A total of 11,819 (8%) developed new-onset T2D and were included in the second cohort. The median duration of time between HF diagnosis and new-onset T2D diagnosis was: 4.1 years (IQR:1.5; 5.8). The absolute five-year risk of an ischemic event in patients with new-onset T2D, prevalent T2D and no T2D was: 17.9% (95% confidence interval (CI): 17.2; 18.6), 26.1% (95% CI: 25.6; 26.7), and 18.8% (95% CI:18.6; 19.0). Corresponding estimates for HFH were: 31.5% (95% CI: 30.6; 32.3), 33.6% (95% CI: 33.0; 34.2), and 30,7% (95% CI: 30.5; 31.0). The absolute five-year risk of event-free death among patients with new-onset T2D, prevalent T2D and no T2D was: 20.9% (95% CI: 20.2; 21.7), 18.9% (95% CI:18.4; 19.3), and 18.6% (95% CI: 18.4; 18.8) (see Figure). The five-year risk ratio of experiencing HFH or event-free death versus an ischemic event was: 2.9 (95% CI: 2.8; 3.1), 2.0 (95% CI:2.0; 2.1), and 2.6 (95% CI: 2.6; 2.7) for patients with new-onset T2D, prevalent T2D and no T2D, respectively. Similar results of absolute and relative risk were present across all subgroups. Conclusion In our population of HF patients, 8% developed new-onset diabetes. Development of T2D in patients with HF increases the risk of HFH and mortality three-fold. The increased risk of new-onset T2D is higher than the importance of prevalent T2D in patients with HF. Funding Acknowledgement Type of funding source: None


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