scholarly journals Serum biomarkers of cardiovascular complications in COVID-19

2021 ◽  
Vol 26 (2S) ◽  
pp. 4456
Author(s):  
R. M. Gumerov ◽  
D. F. Gareeva ◽  
P. A. Davtyan ◽  
R. F. Rakhimova ◽  
T. I. Musin ◽  
...  

The coronavirus disease 2019 (COVID-19) affects not only the respiratory system, but also the cardiovascular system in 20-28% of cases, causing endothelial dysfunction, vasculitis, hyper- and hypocoagulation, myocarditis, endothelial dysfunction and other adverse effects. The presence of cardiovascular risk factors and diseases has been shown to worsen the disease severity and increase mortality from COVID-19. Recent studies have also found that elevations in some serum cardiovascular biomarkers can stratify the disease severity, in particular rates of hospitalizations to an internal medicine or intensive care unit, intubation, and mortality. They can be divided into markers of damage (TnT/I, creatine phosphokinase (CPK) and CPK-MB, myoglobin, NT-proBNP), coagulation (prothrombin time, fibrinogen and D-dimer), as well as prospective biomarkers for which the available evidence base is limited but there is a pathophysiological rationale (homocysteine and sST2). This review presents studies on the use of above serum biomarkers to stratify the risk of death in patients with COVID-19.

ESC CardioMed ◽  
2018 ◽  
pp. 2111-2116
Author(s):  
Darae Ko ◽  
Emelia Benjamin

Atrial fibrillation (AF) poses a substantial public health burden worldwide. About one in four adults over the age of 40 years are expected to develop AF during their lifetime. The risk for developing AF is higher in men compared to women. Globally, individuals of European ancestry appear to have a higher risk of AF onset than individuals from other racial/ethnic descents. Factors predisposing to AF include family history of AF, standard cardiovascular risk factors, and structural heart disease. Hypertension and obesity explain one-third of AF cases in high-income countries. AF can have devastating consequences including an increased risk of death; cardiovascular complications, such as stroke, systemic thromboembolism, heart failure, myocardial infarction, and sudden cardiac death; and non-cardiovascular complications, such as chronic kidney disease, cognitive impairment and dementia, and poor quality of life. There are major research opportunities to develop an evidence base to effectively prevent and manage AF and its outcomes.


2020 ◽  
Author(s):  
Feihong Yang ◽  
Jiaohong Gan ◽  
Hao Zou ◽  
Zhongxiang Zhang ◽  
Yan Zhao ◽  
...  

Abstract Background To investigate the clinical characteristics of 21 death cases and evaluate potential factors of disease severity and mortality risk in COVID-19. Methods Retrospective analysis was used to study the clinical data of 21 death cases with COVID-19. The assessment of disease severity and mortality risk were conducted by APACHE II, SOFA, MuLBSTA and PSI scores. Results The age was 66±14 years-old and 15 (71.4%) were men. 16 (76.2%) patients had chronic medical illnesses. 12 (57.1%) patients were overweight. Decreased lymphocytes were observed in 17 (81.0%) patients on admission. Elevated D-dimer levels were noticed in 11 (52.4%) patients and increased much more when pneumonia deteriorated. The initial APACHE II and SOFA scores demonstrated 18 (85.7%) and 13 (61.9%) patients in middle-risk levels, respectively. MuLBSTA and PSI scores after admission showed high-risk mortality in 13 (61.9%) patients. Most patients developed sequent organ failure and finally caused death. Conclusion Older, male, overweight patients, combined with chronic medical histories, continuous decreased lymphocyte proportion and increased D-dimer might have a higher risk of death. The combination of general scoring (SOFA) and pneumonia specific scoring (MuLBSTA and PSI) after admission might be more sensitive to assess the mortality risk for critical patients in COVID-19.


Author(s):  
Christian Mueller ◽  
Evangelos Giannitsis ◽  
Allan S Jaffe ◽  
Kurt Huber ◽  
Johannes Mair ◽  
...  

Abstract The coronavirus disease 2019 (COVID-19) pandemic has increased awareness that severe acute respiratory distress syndrome coronavirus-2 (SARS-CoV-2) may have profound effects on the cardiovascular system. COVID-19 often affects patients with pre-existing cardiac disease, and may trigger acute respiratory distress syndrome (ARDS), venous thromboembolism (VTE), acute myocardial infarction (AMI), and acute heart failure (AHF). However, as COVID-19 is primarily a respiratory infectious disease, there remain substantial uncertainty and controversy whether and how cardiovascular biomarkers should be used in patients with suspected COVID-19. To help clinicians understand the possible value as well as the most appropriate interpretation of cardiovascular biomarkers in COVID-19, it is important to highlight that recent findings regarding the prognostic role of cardiovascular biomarkers in patients hospitalized with COVID-19 are similar to those obtained in studies for pneumonia and ARDS in general. Cardiovascular biomarkers reflecting pathophysiological processes involved in COVID-19/pneumonia and its complications have a role evaluating disease severity, cardiac involvement, and risk of death in COVID-19 as well as in pneumonias caused by other pathogens. First, cardiomyocyte injury, as quantified by cardiac troponin concentrations, and haemodynamic cardiac stress, as quantified by natriuretic peptide concentrations, may occur in COVID-19 as in other pneumonias. The level of those biomarkers correlates with disease severity and mortality. Interpretation of cardiac troponin and natriuretic peptide concentrations as quantitative variables may aid in risk stratification in COVID-19/pneumonia and also will ensure that these biomarkers maintain high diagnostic accuracy for AMI and AHF. Second, activated coagulation as quantified by D-dimers seems more prominent in COVID-19 as in other pneumonias. Due to the central role of endothelitis and VTE in COVID-19, serial measurements of D-dimers may help physicians in the selection of patients for VTE imaging and the intensification of the level of anticoagulation from prophylactic to slightly higher or even therapeutic doses.


2020 ◽  
Vol 11 ◽  
Author(s):  
Jinpeng Li ◽  
Zeming Liu ◽  
Gaosong Wu ◽  
Meilin Yi ◽  
Yongfeng Chen ◽  
...  

Background: D-dimer is a small protein fragment and high levels of D-dimer have been associated with increased mortality in patients presenting to emergency departments with infection. Previous studies have reported increased levels of D-dimer in COVID-19; however, it is unclear whether an increased D-dimer level provides early warning of poor prognosis. Therefore, this study aimed to assess the usefulness of D-dimer as an early indicator of prognosis in patients with coronavirus disease (COVID-19).Methods: We conducted a retrospective study of patients with COVID-19 admitted to Leishenshan Hospital in Wuhan, China, from February 15 to March 30, 2020. The final date of follow-up was April 11, 2020.Results: Of the 1,643 patients with COVID-19, 691 had elevated D-dimer levels. Their median age was 65 years. Of the patients with elevated D-dimer levels, 45% had comorbidities, with cardiovascular disease (205 [29.7%]) being the most common. Patients with elevated D-dimer were more likely to require treatment with high-flow oxygen, anticoagulation, antibiotics, and admission to the intensive care unit They were also more likely to have increased interleukin-6, monocytes, and lymphocytes. Patients with elevated D-dimer levels had significantly higher mortality than those with normal or low D-dimer levels.Conclusion: In patients with COVID-19, elevated D-dimer was associated with abnormal immunity, underlying disease, increased disease severity, and increased mortality. Taken together, D-dimer may be a marker for the early warning of disease severity and increased risk of death. These findings provide insights into the potential risk of elevated D-dimer in patients with COVID-19.


2020 ◽  
Author(s):  
Rui Hu ◽  
Zhiyang Han ◽  
Chunling Zhang ◽  
Huajing Ren ◽  
Xiang Chen ◽  
...  

Abstract Background: Coronavirus disease 2019 (COVID-19) has rapidly spread throughout worldwide. Hypertension, diabetes, cardiovascular disease, and cerebrovascular disease were the most common coexisting illness among patients with severe SARS-CoV-2 infection. We aim to analyze the effect of them on the result of laboratory finding in patients with severe or critical SARS-CoV-2 infection.Methods: The date of a total of 49 patients who met the inclusion criteria from January 12 to March 20, 2020, from the first affiliated hospital of Harbin medical university were analyzed in our study.Results: Compared with patients without any coexisting illness, we found that PT levels were decreased in patients with cerebrovascular disease, hypertension or cardiovascular disease, and D-Dimer levels were decreased in patients with cerebrovascular disease, hypertension or diabetes. Similarly, LDH and ALT levels were lower in patients with cerebrovascular disease than that without any coexisting illness.Conclusions: Hypertension, diabetes, cardiovascular disease, and cerebrovascular disease are associated with an increased disease severity and risk of death in patients with COVID-19. Recently study also reported that the levels of PT, D-dimer, and LDH were increased and predicted the deterioration of disease in severe patients with SARS-CoV-2 infection. Interestingly, our results demonstrate that the levels of laboratory indicators such as PT, D-dimer, LDH and ALT were decreased in patients with coexisting illness than without any coexisting illness. It may give us the inaccurate result when we use those laboratory indicators to predict the deterioration of the patients and we need to pay more attention to it.


2021 ◽  
Vol 11 (12) ◽  
pp. 1264
Author(s):  
Lukas Hartl ◽  
Mathias Jachs ◽  
Benedikt Simbrunner ◽  
David J. M. Bauer ◽  
Georg Semmler ◽  
...  

(1) Background: Cirrhotic patients have an increased risk for severe COVID-19. We investigated the renin-angiotensin-aldosterone system (RAS), parameters of endothelial dysfunction, inflammation, and coagulation/fibrinolysis in cirrhotic patients and in COVID-19 patients. (2) Methods: 127 prospectively characterized cirrhotic patients (CIRR), along with nine patients with mild COVID-19 (mild-COVID), 11 patients with COVID-19 acute respiratory distress syndrome (ARDS; ARDS-COVID), and 10 healthy subjects (HS) were included in the study. Portal hypertension (PH) in cirrhotic patients was characterized by hepatic venous pressure gradient (HVPG). (3) Results: With increased liver disease severity (Child−Pugh stage A vs. B vs. C) and compared to HS, CIRR patients exhibited higher RAS activity (angiotensin-converting enzyme (ACE), renin, aldosterone), endothelial dysfunction (von Willebrand-factor (VWF) antigen), inflammation (C-reactive protein (CRP), interleukin-6 (IL-6)), and a disturbed coagulation/fibrinolysis profile (prothrombin fragment F1,2, D-dimer, plasminogen activity, antiplasmin activity). Increased RAS activity (renin), endothelial dysfunction (vWF), coagulation parameters (D-dimer, prothrombin fragment F1,2) and inflammation (CRP, IL-6) were significantly altered in COVID patients and followed similar trends from mild-COVID to ARDS-COVID. In CIRR patients, ACE activity was linked to IL-6 (ρ = 0.26; p = 0.003), independently correlated with VWF antigen (aB: 0.10; p = 0.001), and was inversely associated with prothrombin fragment F1,2 (aB: −0.03; p = 0.023) and antiplasmin activity (aB: −0.58; p = 0.006), after adjusting for liver disease severity. (4) Conclusions: The considerable upregulation of the RAS in Child−Pugh B/C cirrhosis is linked to systemic inflammation, endothelial dysfunction, and abnormal coagulation profile. The cirrhosis-associated abnormalities of ACE, IL-6, VWF antigen, and antiplasmin parallel those observed in severe COVID-19.


1994 ◽  
Vol 72 (02) ◽  
pp. 292-296 ◽  
Author(s):  
M Cortellaro ◽  
E Cofrancesco ◽  
C Boschetti ◽  
L Mussoni ◽  
M B Donati ◽  
...  

SummaryPatients with peripheral arterial disease have a high risk of death from cardiovascular events. As defective fibrinolysis associated with leg atherosclerosis has been suggested as a predisposing factor, we sought a relation among decreased fibrinolysis, the presence of leg atherosclerosis and the incidence of thrombotic events in a case control study nested in the PLAT.Fifty-eight patients with coronary and/or cerebral atherothrombotic disease, free of leg atherosclerosis at Doppler examination, were compared with 50 atherosclerotic patients with leg involvement. High D-dimer (153.0 vs 81.3 ng/ml, p <0.001) and tPA antigen before venous stasis (14.4 vs 11.8 ng/ml, p <0.03), and low tPA antigen (6.7 vs 15.6 ng/ml, p <0.01) and fibrinolytic activity released after venous stasis (fibrinolytic capacity: 113.2 vs 281.4 mm2, p <0.001) were found in patients with leg atherosclerosis. D-dimer and fibrinolytic capacity, in addition to age, were selected by stepwise discriminant analysis as characterizing patients with leg atherosclerosis. Moreover, higher D-dimer and tPA inhibitor characterized patients with leg atherosclerosis who subsequently experienced thrombotic events.These findings constitute evidence of high fibrin turnover and impaired fibrinolytic potential in patients with leg atherosclerosis. Thus impaired fibrinolysis may contribute to the prothrombotic state in these patients.


2020 ◽  
Author(s):  
Seshadri Reddy Varikasuvu ◽  
Naveen Dutt ◽  
Saurabh Varshney ◽  
Shahir Asfahan ◽  
Paresh P. Kulkarni ◽  
...  

2021 ◽  
Vol 10 (10) ◽  
pp. 2077
Author(s):  
Yi-Min Huang ◽  
Chiao Lo ◽  
Chiao-Feng Cheng ◽  
Cheng-Hsun Lu ◽  
Song-Chou Hsieh ◽  
...  

Idiopathic granulomatous mastitis (IGM) is a rare inflammatory breast disease mimicking breast cancer. Limited research has been conducted on the application of serum biomarkers. This study aims to investigate the association of serum biomarkers with disease severity in patients with IGM. From November 2011 to March 2020, medical records of patients with IGM were reviewed. Serum cytokine levels were measured in patients and healthy controls between July 2018 and March 2020. A total of 41 patients with histologically proven IGM were found. Serum interleukin (IL)-6 level was significantly higher in patients with IGM (n = 11) than healthy controls (n = 7). Serum IL-6 and C-reactive protein (CRP) levels were significantly higher in patients with severe disease than mild and moderate disease. Serum IL-6 (Spearman’s ρ = 0.855; p < 0.001) and CRP (Spearman’s ρ = 0.838; p = 0.001) levels were associated with time to resolution. A higher serum CRP level was associated with a longer time to resolution (B = 0.322; p < 0.001) in multiple linear regression analysis. Serum IL-6 and CRP levels can be used as biomarkers for the evaluation of disease severity in IGM. IL-6 may play a crucial role in the immunopathology of IGM.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Rapezzi ◽  
A.V Kristen ◽  
B Gundapaneni ◽  
M.B Sultan ◽  
M Hanna

Abstract Background In the Tafamidis in Transthyretin Cardiomyopathy Clinical Trial (ATTR-ACT), tafamidis was shown to be an effective treatment for patients with transthyretin amyloid cardiomyopathy (ATTR-CM). Further assessment of the efficacy of tafamidis in patients with more advanced ATTR-CM would aid treatment decisions. Purpose To characterize the benefits of tafamidis in patients with advanced ATTR-CM. Methods In ATTR-ACT, ATTR-CM patients were randomized to tafamidis (n=264) or placebo (n=177) for 30 months. Efficacy outcomes included all-cause mortality and frequency of cardiovascular (CV)-related hospitalisations. Key secondary endpoints were change from baseline to Month 30 in 6MWT distance and KCCQ-OS score. Efficacy assessments in NYHA Class III patients at baseline (n=141) were a pre-specified analysis. In a post-hoc analysis, mortality and CV-related hospitalizations were assessed in all patients grouped into quartiles of increasing disease severity based on 6MWT distance at baseline. Longer-term all-cause mortality (as of 1 Aug 2019) was assessed in NYHA Class III patients utilizing data from ATTR-ACT patients who enrolled in a long-term, extension study (LTE) and continued treatment with higher dose tafamidis (n=55; median treatment duration 51.6 months); or, if previously treated with placebo, started tafamidis treatment (placebo/tafamidis; n=63 [50.1 months]). Results In advanced ATTR-CM patients (NYHA Class III), tafamidis reduced the risk of death (HR [95% CI] 0.837, [0.541, 1.295], P=0.4253), and the decline in 6MWT distance (LS mean [SE], 31.6 (22.1) m; P=0.1526) and KCCQ-OS score (LS mean [SE], 13.1 (5.0); P=0.0090), vs placebo. Paradoxically, there was a higher frequency of CV-related hospitalizations with tafamidis (RR [95% CI] vs placebo, 1.411 [1.048, 1.900]). In all patients by 6MWT quartile, CV-related hospitalizations/year with tafamidis and placebo increased with disease severity, with the exception that placebo-treated patients in the highest severity quartile had fewer CV-related hospitalisations (0.73) than those in the third quartile (0.92). Mortality with tafamidis and placebo increased, and was greater with placebo, in every quartile (Figure). Survival (NYHA Class III patients in ATTR-ACT and LTE) was improved with high dose tafamidis with longer term follow-up (HR vs placebo/tafamidis [95% CI], 0.6569 [0.4175, 1.0336]; P=0.0692). Conclusions These analyses, including longer-term follow-up, demonstrate that patients with advanced ATTR-CM benefit from tafamidis. The decrease in CV-related hospitalisations in more severe patients treated with placebo suggests that the comparatively greater hospitalisation frequency in NYHA Class III patients treated with tafamidis is a consequence of their lower mortality rate. Figure 1 Funding Acknowledgement Type of funding source: Private company. Main funding source(s): This study was sponsored by Pfizer


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