Plasmin-α2-antiplasmin Complex in Patients with Atrial Fibrillation

1999 ◽  
Vol 82 (07) ◽  
pp. 100-103 ◽  
Author(s):  
William Feinberg ◽  
Elizabeth Macy ◽  
Elaine Cornell ◽  
Sarah Nightingale ◽  
Lesly Pearce ◽  
...  

SummaryPlasmin-α2-antiplasmin complex (PAP) is an index of recent fibrinolytic activity. We examined PAP levels in patients with atrial fibrillation (AF) to determine whether these levels are correlated with clinical characteristics associated with stroke risk. We obtained blood for measurement of PAP in a non-random sample of 586 patients with AF on entering the Stroke Prevention in Atrial Fibrillation III Study. PAP levels were measured with an ELISA assay. PAP values were transformed with a natural logarithm (PAPln) prior to all analyses. Older age, female gender, recent congestive heart failure, decreasing fractional shortening, recent onset of AF, and coronary artery disease were each univariately associated with higher levels of PAP (all p <0.05, two-sample t-test, simple linear regression). Older age, recent congestive heart failure, decreasing fractional shortening, and recent onset of AF were independently associated with higher PAP levels by multivariate analysis (linear regression). Among patients receiving warfarin, PAP levels were not correlated with INR levels (linear regression, p = 0.60). Patients classified as high-risk for thromboembolism by our risk stratification criteria (systolic blood pressure >160 mm Hg, prior thromboembolism, recent congestive heart failure, poor left ventricular function, and women over age 75) had higher PAP levels than low-risk patients (antilog mean PAPln 5.6 vs 4.9, p <0.001, two-sample t-test). PAP levels in patients with AF are associated with clinical characteristics predictive of thromboembolism. Elevated PAP levels are particularly associated with poor left ventricular function and are not affected by anticoagulation. PAP levels may be a marker of stroke risk in patients with AF.Presented in part at the American Heart Association 22nd annual Joint Conference on Stroke and the Cerebral Circulation, Anaheim, CA, February, 1997.

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
J Molvin ◽  
M Pareek ◽  
O Melander ◽  
L Rastam ◽  
U Lindblad ◽  
...  

Abstract Background Although Azurocidin-1 (Azu-1), also known as heparin binding protein, has been associated with myocardial infarction, possible associations of Azu-1 with congestive heart failure (CHF) remains unknown. Here we tested the possible association of Azu-1 with prevalent diastolic dysfunction and/or incident CHF in a large Swedish prospective population based cohort. Methods Azu-1 was analyzed using the Proseek Multiplex CVD III panel in 1737 participants from a subsample of the population (mean age 67 years, 29% women) who underwent a complete echocardiographic examination. All biomarkers were logarithmized and standardized prior to statistical analysis. Logistic and linear regression were adjusted for age, sex, BMI, diabetes, systolic and diastolic blood, anti-hypertensive treatment and subjects with an ejection fraction below 50% were excluded for the analysis of prevalent diastolic dysfunction and Azu-1. For the linear regression model, we used E/é ratio as a key functional variable in assessing diastolic function according to ESC 2016 Guidelines for Acute and Chronic Heart Failure. Furthermore, we dichotomized the E/é ratio at >13 in another logistic regression model. Finally, in line with ESC Guidelines 2016, we combined the key functional (E/é >13) and key structural (left ventricular mass index (LVMI) ≥115 g/m2 for males and ≥95 g/m2 for females) alterations for diastolic dysfunction and used this variable in both logistic regression for association with Azu-1 and for Cox regression analysis of incident CHF. 1439 subjects (938 cases with some degree of diastolic dysfunction and 501 controls) remained for the analysis. For the analysis of incident CHF, Cox regression was used excluding subjects with ejection fraction below 50% and prevalent CHF and further adjusted for prevalent coronary disease on top of age, sex, BMI, diabetes, systolic and diastolic blood and anti-hypertensive treatment. 1,511 subjects (64 incident cases of CHF vs 1447 controls; median follow up time 8.9 years) remained. Results After adjustment for above mentioned risk factors, each 1 standard deviation (SD) of increase in Azu-1 was associated with any degree of prevalent diastolic dysfunction (odds ratio (OR) 1.13, p=0.048), E/é >13 OR 1.21, p=0.028 and for combined LVMI and E/é OR 1.17, p=0.015. In fully adjusted linear regression Azu-1 was associated with E/é with a β-coefficient of 0.056, p=0.018. In a fully adjusted Cox regression models Azu-1 was associated with incident CHF (hazard ratio (HR) 1.32, p=0.025). As expected and as proof of concept E/é >13 and combined LVMI with E/é were also associated with incident CHF; HR 2.84, p<0.001 and HR 2.12, p=0.006, respectively. Conclusion An inflammatory mediator, Azurocidin-1, is associated with prevalent diastolic dysfunction, E/é, E/é combined with LVMI as well as incident congestive heart failure in a population-based cohort.


2002 ◽  
Vol 283 (3) ◽  
pp. H1225-H1236 ◽  
Author(s):  
Ivar Sjaastad ◽  
Janny Bøkenes ◽  
Fredrik Swift ◽  
J. Andrew Wasserstrom ◽  
Ole M. Sejersted

Attenuated L-type Ca2+ current ( I Ca,L), or current-contraction gain have been proposed to explain impaired cardiac contractility in congestive heart failure (CHF). Six weeks after coronary artery ligation, which induced CHF, left ventricular myocytes from isoflurane-anesthetized rats were current or voltage clamped from −70 mV. In both cases, contraction and contractility were attenuated in CHF cells compared with cells from sham-operated rats when cells were only minimally dialyzed using high-resistance microelectrodes. With patch pipettes, cell dialysis caused attenuation of contractions in sham cells, but not CHF cells. Stepping from −50 mV, the following variables were not different between sham and CHF, respectively: peak I Ca,L (4.5 ± 0.3 vs. 3.8 ± 0.3 pApF−1 at 23°C and 9.4 ± 0.5 vs. 8.4 ± 0.5 pApF−1 at 37°C), the bell-shaped voltage-contraction relationship in Cs+ solutions (fractional shortening, 15.2 ± 1.0% vs. 14.3 ± 0.7%, respectively, at 23°C and 7.5 ± 0.4% vs. 6.7 ± 0.5% at 37°C) and the sigmoidal voltage-contraction relationship in K+ solutions. Caffeine-induced Ca2+ release and sarcoplasmic reticulum Ca2+-ATPase-to-phospholamban ratio were not different. Thus CHF contractions triggered by I Ca,L were normal, and the contractile deficit was only seen in undialyzed cardiomyocytes stimulated from −70 mV.


Author(s):  
Andreas Schäfer ◽  
Ulrike Flierl ◽  
Johann Bauersachs

AbstractImpaired left-ventricular ejection-fraction (LV-EF) is a known risk factor for ischemic stroke and systemic embolism in patients with heart failure (HF) even in the absence of atrial fibrillation. While stroke risk is inversely correlated with LV-EF in HF patients with sinus rhythm, strategies using anticoagulation with Vitamin-K antagonists (VKA) were futile as the increase in major bleedings outweighed the potential benefit in stroke reduction. Non-Vitamin K oral anticoagulants (NOACs) proved to be an effective and in general safer approach for stroke prevention in patients with atrial fibrillation and may also have a favourable risk–benefit profile in HF patients. In HF patients with sinus rhythm, the COMPASS trial suggested a potential benefit for rivaroxaban, whereas the more dedicated COMMANDER-HF trial remained neutral on overall ischemic benefit owed to a higher mortality which was not influenced by anticoagulation. More recent data from subgroups in the COMMANDER-HF trial, however, suggest that there might be a benefit of rivaroxaban regarding stroke prevention under certain circumstances. In this article, we review the existing evidence for NOACs in HF patients with atrial fibrillation, elaborate the rationale for stroke prevention in HF patients with sinus rhythm, summarise the available data from anticoagulation trials in HF with sinus rhythm, and describe the patient who might eventually profit from an individualised strategy aiming to reduce stroke risk. Graphic abstract


2017 ◽  
Vol 95 (7) ◽  
pp. 613-617
Author(s):  
V. I. Podzolkov ◽  
A. I. Tarzimanova ◽  
L. Mohammadi

An appreciable progress has recently been achieved in the study of the nature of atrial fibrillation (AF), from its early asymptomatic stages to irreversible arrhythmia. There are data on the risk factors of AF in the literature, but predictors of progressive arrhythmia remain to be elucidated. This study was aimed to identify predictors of AF progression in patients with congestive heart failure (CHF). Material and methods. The study involved 64 patients aged 59-82 (mean 69,4±3,9) followed up prospectively from September 2010 till June 2016 (observations of mean duration 60±3 mo included regular telephone interviews (each 3 mo) and annual general clinical examination with laboratory and instrumental studies. Continuous or persisting AF served as the criterion for progressive arrhythmia. Results. Cardiovascular complications and progressive arrhythmia were documented in 23 (36%) and 38 (59%) patients respectively during the 60±3 mo observation period. The multifactorial analysis revealed the significant influence of a decrease of left ventricular ejection function (EF) to below 40% and a rise in the plasma level of brain natriuretic peptide (Nt-proBNP) to more than 903 pg/ml on the risk of development of arrhythmia. Conclusion. Independent predictors of arrhythmia in patients with CHF and persistent AF are a decrease in left ventricular ejection function (EF) to below 40% (1,2, 95% CI 0,9-1,5) and a rise in the plasma Nt-proBNP level to more than 903 pg/ml (OR 1,3, 95% , CI+1,1-2,9). Such a rise predicts transition of arrhythmia into continuous form with sensitivity 92,1% and specificity 84,6%.


2021 ◽  
Vol 14 (7) ◽  
pp. e244027
Author(s):  
Sean Gaine ◽  
Patrick Devitt ◽  
John Joseph Coughlan ◽  
Ian Pearson

A 58-year-old man presented to the emergency department with recent-onset palpitations and progressive exertional dyspnoea. ECG demonstrated new-onset atrial fibrillation. Transthoracic echocardiogram showed global impairment in left ventricular systolic function with left ventricular ejection fraction of 20%. Cardiac MRI (CMRI) demonstrated generalised severe myocarditis. A SARS-CoV-2 PCR was positive for SARS-CoV-2 RNA. As such, we diagnosed our patient with COVID-19-associated myocarditis based on CMRI appearances and positive SARS-CoV-2 swab. This case highlights that COVID-19-associated myocarditis can present as new atrial fibrillation and heart failure without the classic COVID-19-associated symptoms.


Medicine ◽  
2018 ◽  
Vol 97 (45) ◽  
pp. e13074 ◽  
Author(s):  
Paweł Balsam ◽  
Monika Gawałko ◽  
Michał Peller ◽  
Agata Tymińska ◽  
Krzysztof Ozierański ◽  
...  

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