scholarly journals Impact of Congestive Heart Failure and Role of Cardiac Biomarkers in COVID-19 patients: A Systematic Review and Meta-Analysis

Author(s):  
Tarun Dalia ◽  
Shubham Lahan ◽  
Sagar Ranka ◽  
Prakash Acharya ◽  
Archana Gautam ◽  
...  

Background: Coronavirus disease 2019 (COVID-19) has been reported to cause worse outcomes in patients with underlying cardiovascular disease, especially in patients with acute cardiac injury, which is determined by elevated levels of high-sensitivity troponin. There is a paucity of data on the impact of congestive heart failure (CHF) on outcomes in COVID-19 patients. Methods: We conducted a literature search of PubMed/Medline, EMBASE, and Google Scholar databases from 11/1/2019 till 06/07/2020, and identified all relevant studies reporting cardiovascular comorbidities, cardiac biomarkers, disease severity, and survival. Pooled data from the selected studies were used for metanalysis to identify the impact of risk factors and cardiac biomarker elevation on disease severity and/or mortality. Results: We collected pooled data on 5,967 COVID-19 patients from 20 individual studies. We found that both non-survivors and those with severe disease had an increased risk of acute cardiac injury and cardiac arrhythmias, our pooled relative risk (RR) was - 8.52 (95% CI 3.63-19.98) (p<0.001); and 3.61 (95% CI 2.03-6.43) (p=0.001), respectively. Mean difference in the levels of Troponin-I, CK-MB, and NT-proBNP was higher in deceased and severely infected patients. The RR of in-hospital mortality was 2.35 (95% CI 1.18-4.70) (p=0.022) and 1.52 (95% CI 1.12-2.05) (p=0.008) among patients who had pre-existing CHF and hypertension, respectively. Conclusion: Cardiac involvement in COVID-19 infection appears to significantly adversely impact patient prognosis and survival. Pre-existence of CHF and high cardiac biomarkers like NT-pro BNP and CK-MB levels in COVID-19 patients correlates with worse outcomes. Keywords: Acute cardiac injury; cardiac arrhythmia; mortality risk; cardiac biomarkers, COVID-19.

2021 ◽  
Vol 8 ◽  
Author(s):  
Chaoqun Ma ◽  
Dingyuan Tu ◽  
Jiawei Gu ◽  
Qiang Xu ◽  
Pan Hou ◽  
...  

Objective: Cardiac injury is detected in numerous patients with coronavirus disease 2019 (COVID-19) and has been demonstrated to be closely related to poor outcomes. However, an optimal cardiac biomarker for predicting COVID-19 prognosis has not been identified.Methods: The PubMed, Web of Science, and Embase databases were searched for published articles between December 1, 2019 and September 8, 2021. Eligible studies that examined the anomalies of different cardiac biomarkers in patients with COVID-19 were included. The prevalence and odds ratios (ORs) were extracted. Summary estimates and the corresponding 95% confidence intervals (95% CIs) were obtained through meta-analyses.Results: A total of 63 studies, with 64,319 patients with COVID-19, were enrolled in this meta-analysis. The prevalence of elevated cardiac troponin I (cTnI) and myoglobin (Mb) in the general population with COVID-19 was 22.9 (19–27%) and 13.5% (10.6–16.4%), respectively. However, the presence of elevated Mb was more common than elevated cTnI in patients with severe COVID-19 [37.7 (23.3–52.1%) vs.30.7% (24.7–37.1%)]. Moreover, compared with cTnI, the elevation of Mb also demonstrated tendency of higher correlation with case-severity rate (Mb, r = 13.9 vs. cTnI, r = 3.93) and case-fatality rate (Mb, r = 15.42 vs. cTnI, r = 3.04). Notably, elevated Mb level was also associated with higher odds of severe illness [Mb, OR = 13.75 (10.2–18.54) vs. cTnI, OR = 7.06 (3.94–12.65)] and mortality [Mb, OR = 13.49 (9.3–19.58) vs. cTnI, OR = 7.75 (4.4–13.66)] than cTnI.Conclusions: Patients with COVID-19 and elevated Mb levels are at significantly higher risk of severe disease and mortality. Elevation of Mb may serve as a marker for predicting COVID-19-related adverse outcomes.Prospero Registration Number:https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42020175133, CRD42020175133.


Hypertension ◽  
2020 ◽  
Vol 76 (4) ◽  
pp. 1104-1112 ◽  
Author(s):  
Juan-Juan Qin ◽  
Xu Cheng ◽  
Feng Zhou ◽  
Fang Lei ◽  
Gauri Akolkar ◽  
...  

The prognostic power of circulating cardiac biomarkers, their utility, and pattern of release in coronavirus disease 2019 (COVID-19) patients have not been clearly defined. In this multicentered retrospective study, we enrolled 3219 patients with diagnosed COVID-19 admitted to 9 hospitals from December 31, 2019 to March 4, 2020, to estimate the associations and prognostic power of circulating cardiac injury markers with the poor outcomes of COVID-19. In the mixed-effects Cox model, after adjusting for age, sex, and comorbidities, the adjusted hazard ratio of 28-day mortality for hs-cTnI (high-sensitivity cardiac troponin I) was 7.12 ([95% CI, 4.60–11.03] P <0.001), (NT-pro)BNP (N-terminal pro-B-type natriuretic peptide or brain natriuretic peptide) was 5.11 ([95% CI, 3.50–7.47] P <0.001), CK (creatine phosphokinase)-MB was 4.86 ([95% CI, 3.33–7.09] P <0.001), MYO (myoglobin) was 4.50 ([95% CI, 3.18–6.36] P <0.001), and CK was 3.56 ([95% CI, 2.53–5.02] P <0.001). The cutoffs of those cardiac biomarkers for effective prognosis of 28-day mortality of COVID-19 were found to be much lower than for regular heart disease at about 19%–50% of the currently recommended thresholds. Patients with elevated cardiac injury markers above the newly established cutoffs were associated with significantly increased risk of COVID-19 death. In conclusion, cardiac biomarker elevations are significantly associated with 28-day death in patients with COVID-19. The prognostic cutoff values of these biomarkers might be much lower than the current reference standards. These findings can assist in better management of COVID-19 patients to improve outcomes. Importantly, the newly established cutoff levels of COVID-19–associated cardiac biomarkers may serve as useful criteria for the future prospective studies and clinical trials.


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Bin Yan ◽  
Ruohan Li ◽  
Xuting Jin ◽  
Ya Gao ◽  
Jingjing Zhang ◽  
...  

Introduction: Previous studies have suggested that sleep habits were associated with cardiovascular risk factors. However, there is no evidence about the relationship between sleep timing and congestive heart failure (CHF). Hypothesis: We assessed the hypothesis that the bedtime and wake-up time on weekday and weekend may be associated with incident CHF. Methods: From the Sleep Heart Health Study (registration number, NCT00005275), participants without previous heart failure were enrolled in the present prospective study. Sleep timing including bedtime and wake-up time on weekday and weekend was acquired from a self-reported Sleep Habits Questionnaire. Bedtime on weekdays and weekend was divided into >24:00, 23:01 to 24:00, 22:01 to 23:00 and ≤22:00. Wake-up time on weekdays and weekend was classified as >8:00, 7:01 to 8:00, 6:01 to 7:00 and ≤6:00. Further subgroup analysis was conducted according to sleep duration of <6h, 6-8h and >8h. Participants were followed up until the first CHF diagnosed between the date of the completed questionnaire and the final censoring date. Cox regression analysis was used to investigate the association between sleep timing and CHF. Results: A total of 4765 participants including 2207 males and 2558 females with a mean age of 63.6±11.0 years were recruited in the study. During the mean follow-up period of 11 years, 519 participants were diagnosed with CHF. The incidence of CHF in participants with weekday bedtime at >24:00 was 15.6% (69 of 441), which is higher than those with bedtime at 23:01 to 24:00 [12.7% (166 of 1306)], 22:01 to 23:00 [7.0% (128 of 1837)], and ≤22:00 [13.2% (156 of 1181)]. Participants with wake-up time on weekday at > 8:00 also had the highest incidence of CHF [19.7% (45 of 229)] than those with wake-up time at 7:01 to 8:00 [14.2% (89 of 627)], 6:01 to 7:00 [11.5% (171 of 1485)], and ≤6:00 [8.8% (214 of 2424)]. After multivariate Cox regression analyses, individuals with bedtime at >24:00 on weekdays was associated with a higher incidence of CHF (HR 1.559, 95% CI 1.151-2.113, P = 0.004) than those with bedtime at 22:01 to 23:00. And compared with participants with wake-up time at ≤6:00, those with wake-up time at > 8:00 also had an increased risk of incident CHF (HR 1.525, 95% CI 1.074-2.166, P =0.018). After further subgroup analysis, the association between bedtime at >24:00 on weekdays and incident CHF were strengthened in the participants with 6-8 hours’ sleep duration (HR 2.087, 95% CI 1.446-3.013, P <0.001). Conclusion: In conclusion, late bedtime (>24:00) and late wake-up time (>8:00) on weekdays may correlate with an increased risk of CHF. The impact of sleep timing on incident cardiovascular diseases may be worth further prospective study.


2021 ◽  
Vol 8 ◽  
Author(s):  
Valérie Chetboul ◽  
Pierre Foulex ◽  
Kahina Kartout ◽  
Anne Marie Klein ◽  
Corinne Sailleau ◽  
...  

This report provides the first clinical, radiographic, echocardiographic, and biological description of SARS-CoV-2-associated myocarditis with a 6-month follow-up in a 5-year-old obese male domestic shorthair cat (Cat-1) presented for refractory congestive heart failure, with high cardiac troponin-I level (5.24 ng/ml), and a large lingual ulcer. The animal was SARS-CoV-2 positive on serology. The other cat living in the same household (Cat-2) never showed any clinical sign but was also confirmed SARS-CoV-2 positive on serology. Both cats were SARS-CoV-2 PCR negative. Cat-1 had closer contact than Cat-2 with their owner, who had been in close contact with a coworker tested PCR positive for COVID-19 (Alpha (B.1.1.7) variant) 4 weeks before Cat-1's first episode of congestive heart failure. A focused point-of-care echocardiography at presentation revealed for Cat-1 numerous B-lines, pleural effusion, severe left atrial dilation and dysfunction, and hypertrophic cardiomyopathy phenotype associated with focal pulmonary consolidations. Both myocarditis and pneumonia were suspected, leading to the prescription of cardiac medications and antibiotics. One month later, Cat-1 recovered, with normalization of left atrial size and function, and radiographic and echocardiography disappearance of heart failure signs and pulmonary lesions. An extensive literature review of SARS-CoV-2-related cardiac injury in pets in comparison with human pathology is discussed.


Author(s):  
Jingrui Sui ◽  
Denis F. Noubouossie ◽  
Sheetal Gandotra ◽  
Liyun Cao

BackgroundThe coronavirus disease-19 (COVID-19) is characterized with intense inflammatory response, cardiac involvement, and coagulopathy. Fibrinogen, as a biomarker for inflammation, cardiovascular disease, and coagulation, has not been fully investigated yet. The aim of this study was to assess the clinical application of fibrinogen in COVID-19 patients.MethodsWe retrospectively analyzed the demographic and laboratory characteristics of 119 COVID-19 patients in the University of Alabama of Birmingham Medical Center. Correlations of fibrinogen on admission with intensive care unit (ICU) admission, disease severity, and laboratory parameters were analyzed.ResultsAmong the 119 COVID-19 patients, 77.3% (92/119) had severe disease, and 59.5% (71/119) patients were admitted to the ICU. Elevated fibrinogen was detected in 67.2% (80/119) of the patients. Fibrinogen levels were significantly associated with inflammatory markers and disease severity, but not with cardiac injury biomarker high sensitivity troponin I. Patients with severe disease had increased fibrinogen levels upon admission compared to patients with non-severe disease (P = 0.001). Fibrinogen level at 528.0 mg/dl was the optimal cutoff to predict disease severity, with a sensitivity and specificity of 66.7% and 70.3% (area undty -60er the curve [AUC] 0.72, P = 0.0006).ConclusionsFibrinogen is commonly elevated in COVID-19 patients, especially in those with severe disease. Elevated fibrinogen correlates with excessive inflammation, disease severity, and ICU admission in COVID-19 patients.


2018 ◽  
Vol 69 (7) ◽  
pp. 1687-1691
Author(s):  
Razan Al Namat ◽  
Mihai Constantin ◽  
Ionela Larisa Miftode ◽  
Andrei Manta ◽  
Antoniu Petris ◽  
...  

Repetitive or recurrent hospitalizations are a general major health issue in patients with chronic disease. Congestive heart failure, is associated with a high incidence and presence of early rehospitalization, but variables in order to identify patients at increased risk and also an analysis of potentially remediable factors contributing to readmission have not been previously reported and it remains still a difficult problem. We retrospectively assessed 100 patients aged between 48-85 years old, of which 75% were men, who had been hospitalized with documentation of congestive heart failure in St. Spiridon County Emergency Hospital. They were hospitalized between 2010-2017. Even if recurrent heart failure was the most common cause for readmission or rehospitalization, other cardiac disorders and noncardiac illnesses were also accounted for readmission. Predictive factors of an increased probability of readmission included prior patient�s medical heart failure history, heart failure decompensation precipitated or accelerated by an ischaemic episode, atrial fibrillation or uncontrolled hypertension. Factors contributing to preventable readmissions included noncompliance with medications or diet, inadequate discharge planning or follow-up, failure of both social support system and the seek of a promp medical attention when symptoms reappeared. We also identified an inappropriate colaboration with family doctors especially for the patients from rural areas. Patients were more likely to cite side effects of prescribed medications rather than nonadherence as a precipitating factor for readmission. Thus, we can appreciate that early rehospitalization in patients with congestive heart failure may be avoidable in up to 50% of cases. Identification of high risk patients is possible and also necessary shortly after admission in order to identify nonpharmacological interventions designed to decrease readmission frequency.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Dilip Jayasimhan ◽  
Simon Foster ◽  
Catherina L. Chang ◽  
Robert J. Hancox

Abstract Background Acute respiratory distress syndrome (ARDS) is a leading cause of morbidity and mortality in the intensive care unit. Biochemical markers of cardiac dysfunction are associated with high mortality in many respiratory conditions. The aim of this systematic review is to examine the link between elevated biomarkers of cardiac dysfunction in ARDS and mortality. Methods A systematic review of MEDLINE, EMBASE, Web of Science and CENTRAL databases was performed. We included studies of adult intensive care patients with ARDS that reported the risk of death in relation to a measured biomarker of cardiac dysfunction. The primary outcome of interest was mortality up to 60 days. A random-effects model was used for pooled estimates. Funnel-plot inspection was done to evaluate publication bias; Cochrane chi-square tests and I2 tests were used to assess heterogeneity. Results Twenty-two studies were included in the systematic review and 18 in the meta-analysis. Biomarkers of cardiac stretch included NT-ProBNP (nine studies) and BNP (six studies). Biomarkers of cardiac injury included Troponin-T (two studies), Troponin-I (one study) and High-Sensitivity-Troponin-I (three studies). Three studies assessed multiple cardiac biomarkers. High levels of NT-proBNP and BNP were associated with a higher risk of death up to 60 days (unadjusted OR 8.98; CI 4.15-19.43; p<0.00001). This association persisted after adjustment for age and illness severity. Biomarkers of cardiac injury were also associated with higher mortality, but this association was not statistically significant (unadjusted OR 2.21; CI 0.94-5.16; p= 0.07). Conclusion Biomarkers of cardiac stretch are associated with increased mortality in ARDS.


Open Heart ◽  
2021 ◽  
Vol 8 (1) ◽  
pp. e001425
Author(s):  
Marc Meller Søndergaard ◽  
Johannes Riis ◽  
Karoline Willum Bodker ◽  
Steen Møller Hansen ◽  
Jesper Nielsen ◽  
...  

AimLeft bundle branch block (LBBB) is associated with an increased risk of heart failure (HF). We assessed the impact of common ECG parameters on this association using large-scale data.Methods and resultsUsing ECGs recorded in a large primary care population from 2001 to 2011, we identified HF-naive patients with a first-time LBBB ECG. We obtained information on sex, age, emigration, medication, diseases and death from Danish registries. We investigated the association between the PR interval, QRS duration, and heart rate and the risk of HF over a 2-year follow-up period using Cox regression analysis.Of 2471 included patients with LBBB, 464 (18.8%) developed HF during follow-up. A significant interaction was found between QRS duration and heart rate (p<0.01), and the analyses were stratified on these parameters. Using a QRS duration <150 ms and a heart rate <70 beats per minute (bpm) as the reference, all groups were statistically significantly associated with the development of HF. Patients with a QRS duration ≥150 ms and heart rate ≥70 bpm had the highest risk of developing HF (HR 3.17 (95% CI 2.41 to 4.18, p<0.001). There was no association between the PR interval and HF after adjustment.ConclusionProlonged QRS duration and higher heart rate were associated with increased risk of HF among primary care patients with LBBB, while no association was observed with PR interval. Patients with LBBB with both a prolonged QRS duration (≥150 ms) and higher heart rate (≥70 bpm) have the highest risk of developing HF.


2021 ◽  
Vol 26 (3) ◽  
pp. 5-5
Author(s):  
Alex Gough

Summary In this month's Small Animal Review, we summarise three recently published papers from other veterinary journals. The papers for this issue explore the impact of open registries on inbreeding, in the working Australian Kelpie population particularly, and the impact of vehicle trauma on the canine shock index, as well as the potential role for lung ultrasound in monitoring for cardiogenic pulmonary oedema in dogs being treated for left-sided congestive heart failure.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Peter D. Sly ◽  
Brittany A. Trottier ◽  
Catherine M. Bulka ◽  
Stephania A. Cormier ◽  
Julius Fobil ◽  
...  

Abstract Background An unusual feature of SARS-Cov-2 infection and the COVID-19 pandemic is that children are less severely affected than adults. This is especially paradoxical given the epidemiological links between poor air quality and increased COVID-19 severity in adults and that children are generally more vulnerable than adults to the adverse consequences of air pollution. Objectives To identify gaps in knowledge about the factors that protect children from severe SARS-Cov-2 infection even in the face of air pollution, and to develop a transdisciplinary research strategy to address these gaps. Methods An international group of researchers interested in children’s environmental health was invited to identify knowledge gaps and to develop research questions to close these gaps. Discussion Key research questions identified include: what are the effects of SAR-Cov-2 infection during pregnancy on the developing fetus and child; what is the impact of age at infection and genetic susceptibility on disease severity; why do some children with COVID-19 infection develop toxic shock and Kawasaki-like symptoms; what are the impacts of toxic environmental exposures including poor air quality, chemical and metal exposures on innate immunity, especially in the respiratory epithelium; what is the possible role of a “dirty” environment in conveying protection – an example of the “hygiene hypothesis”; and what are the long term health effects of SARS-Cov-2 infection in early life. Conclusion A concerted research effort by a multidisciplinary team of scientists is needed to understand the links between environmental exposures, especially air pollution and COVID-19. We call for specific research funding to encourage basic and clinical research to understand if/why exposure to environmental factors is associated with more severe disease, why children appear to be protected, and how innate immune responses may be involved. Lessons learned about SARS-Cov-2 infection in our children will help us to understand and reduce disease severity in adults, the opposite of the usual scenario.


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