Elevated serum lipoprotein(a) is a risk factor for left atrial thrombus in patients with chronic atrial fibrillation: A transesophageal echocardiographic study

Igarashi, Yutaka; Yamaura, Masayuki; Ito, Masahiro; Inuzuka, Hiroshi; Ojima, Kenji; Aizawa, Yoshifusa

doi:10.1016/s0002-8703(98)70151-6

Cited by 37 publications

(31 citation statements)

References 36 publications

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“…An aliquot of the plasma was immediately frozen at -80°C. The plasma ANP and BNP concentrations were measured with a specific immunoradiometric assay for human alpha-ANP (Shionoria ANP Kit, Osaka, Japan) 10 and for human BNP (Shionoria BNP Kit, Osaka, Japan). 12 Venous blood samples for D-dimer and TAT analysis were anticoagulated with trisodium citrate.…”

Section: Blood Sampling and Assaysmentioning

confidence: 99%

Left Atrial Appendage Dysfunction in Chronic Nonvalvular Atrial Fibrillation is Significantly Associated With an Elevated Level of Brain Natriuretic Peptide and a Prothrombotic State.

et al. 2001

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trial fibrillation (AF) is associated with serious complications such as arterial thromboembolism, 1 and in patients with nonvalvular AF (NVAF) left atrial appendage (LAA) thrombi are believed to be the source of embolism. 2 In sinus rhythm, the LAA vigorously contracts with a peak emptying flow velocity greater than 50 cm/s, 3 but this is reduced in patients with chronic NVAF. 4,5 Although LAA dysfunction is a significant predictor of thrombus formation, the pathophysiologic mechanisms responsible have not been fully defined. Patients with AF are in a prothrombotic state compared with individuals in sinus rhythm. 6,7 Elevated plasma concentrations of D-dimer and thrombin -antithrombin III complex (TAT), which are markers of the intravascular activation of the coagulation system, have been found in patients with AF, 6,7 but the predictors of a hypercoagulable state in patients with NVAF have not been identified.We hypothesized that LAA dysfunction is associated with the development of a prothrombotic state and that left ventricular dysfunction leads to LAA dysfunction. The present study tested the hypothesis that LAA dysfunction would correlate with elevated levels of natriuretic peptides, which are biochemical markers of left ventricular dysfunction, 8 and with a prothrombotic state. Methods Study PopulationSixty-seven patients with a median age of 70 years (25th and 75th percentile, 65 and 74 years) with chronic NVAF between July 1999 and July 2000 were evaluated and those with a history of AF of more than 6 months duration were enrolled in the study. Patients with NVAF who had been treated with warfarin prior to transesophageal echocardiography (TEE) were excluded. Baseline clinical characteristics included age, sex, details of previous embolic events, the presence or absence of systemic hypertension, the use of aspirin, and the duration of AF. Because there were a substantial number of patients who did not have any symptoms at the onset of AF, the duration of AF was defined as the duration from the first confirmation of AF on electrocardiogram. EchocardiographyAll patients underwent transthoracic and transesophageal echocardiography. The institutional review board approved the research protocol and informed consent was obtained from all patients before undergoing TEE. The left atrial and ventricular dimensions were measured from the M-mode echocardiogram according to the recommendations of the

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Section: Blood Sampling and Assaysmentioning

confidence: 99%

Left Atrial Appendage Dysfunction in Chronic Nonvalvular Atrial Fibrillation is Significantly Associated With an Elevated Level of Brain Natriuretic Peptide and a Prothrombotic State.

et al. 2001

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“…Existing data strongly support its connection with ishemic heart disease, arterial hypertension, heart failure, obesity and metabolic syndrome [3-7]. In past years few studies tried to elucidate the association between AF and lipoprotein(a), particularly in connection with thrombembolic complications [8,9]. Major component of lipoprotein(a), or Lp(a) is large glycoprotein molecule named apoprotein(a), which is produced in hepatocytes.…”

Section: Introductionmentioning

confidence: 99%

Lipoprotein(a) and inflammation in patients with atrial fibrillation after electrical cardioversion

Naji

Šabovič

2011

J Negat Results BioMed

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BackgroundRecently few studies tried to confirm the association between AF and lipoprotein(a) (Lp(a)), however the results remained conflicted. In present study we evaluated the possible interaction between Lp(a), inflammatory state and echocardiographic characteristics in patients after successful electrical cardioversion (EC) of persistent AF. We also tried to investigate the role of Lp(a) as a possible prognostic factor for AF recurrence after successful EC.ResultsData of 79 patients admitted due to planned EC was analyzed. After successful procedure patients were monitored for 2 years. For analytical purposes patients were divided in two groups according to AF recurrence. There was no significant difference between Lp(a) levels in both groups. We also didn't find any positive correlation between Lp(a) and CRP levels, as well as between Lp(a) levels and left atrium diameter. For logistic and survival analysis optimal cut-off value of Lp(a) ≥ 0.32 (upper quartile) was used. In logistic regression model with AF recurrence as dependent variable Lp(a) didn't show any statistically significant association with AF recurrence. Survival analysis showed slightly higher AF recurrence rate in group with higher Lp(a) levels but not to the level of statistical significance (log rank test, p = 0.62).ConclusionsWe weren't able to confirm the association between Lp(a) levels and AF recurrence, inflammation and left atrium diameter in patients after successful EC of persistent AF. Further studies are needed to elucidate the role of Lp(a) in this clinical setting.

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“…It was reported that the Lp(a) level was significantly higher in patients with left atrial thrombus than in patients without left atrial thrombus in chronic atrial fibrillation. 36) But, Lippi, et al 37) found that no statistically significant differences were observed in the median Lp(a) concentration between patients with deep venous thrombosis and without deep venous thrombosis. Our study also found no relationship between plasma Lp(a) levels and LV thrombus formation.…”

Section: Discussionmentioning

confidence: 97%

Serum Lipoprotein(a) and Its Relation to Left Ventricular Thrombus in Patients with Acute Myocardial Infarction.

Çelık¹,

Baykan²,

Örem³

et al. 2001

Jpn Heart J

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SUMMARYIt is well known that the incidence of left ventricular (LV) thrombosis is high in patients with acute myocardial infarction (AMI). Due to the high degree of structural homology with plasminogen, lipoprotein(a) may produce thrombogenic effects by modulating the fibrinolytic system. However, the role of Lp(a) level in the formation of LV thrombus has not been studied. This study sought to determine whether Lp(a) is a risk factor for LV thrombus in patients with AMI.We have analyzed clinical, echocardiographic and biochemical data in 102 consecutive patients (aged 58 ± 12 years; 92 men / 10 women) with first anterior AMI. Twodimensional examination was performed on days 1, 3, 7, 15, and 30. Blood samples were obtained within 12 h after the onset of symptoms and before beginning the therapy. Plasma levels of fibrinogen and Lp(a) were measured using enzyme-linked immunosorbent assay and immunonephelometric methods, respectively. LV thrombus was detected in 20 (20.3 %) patients. No significant difference was found for admission Lp(a) levels between patients with or without thrombus (30.5 ± 17.2 vs 32.3 ± 22.4 mg / dl, p = 0.7).Univariate analysis showed that patients with LV thrombus had a higher wall motion score index (1.8 ± 0.3 vs 1.4 ± 0.3, p = 0.002), a higher peak creatine kinase level (2945 ± 898 vs 1805 ± 1336, I / U p = 0.004), a larger end-diastolic volume (139.7 ± 38.6 vs 114.1 ± 41.8 ml, p = 0.04), a larger end-systolic volume (83.1 ± 34.3 vs 59.2 ± 30.6 ml, p = 0.02 ), and a lower ejection fraction (38 ± 12 vs 47 ± 11, p = 0.04). In multivariate analyses, only peak creatine kinase level (p = 0.04) and LV wall motion score index (p = 0.002) were independent predictors of left ventricular thrombus formation.These results suggest that Lp (a) is not a risk factor for LV thrombus in patients with AMI. Our data demonstrate that the best predictors of LV thrombus formation after AMI are a high peak creatine kinase level and a high LV wall motion score index. (Jpn Heart J 2001; 42: 5-14)

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Elevated serum lipoprotein(a) is a risk factor for left atrial thrombus in patients with chronic atrial fibrillation: A transesophageal echocardiographic study

Cited by 37 publications

References 36 publications

Left Atrial Appendage Dysfunction in Chronic Nonvalvular Atrial Fibrillation is Significantly Associated With an Elevated Level of Brain Natriuretic Peptide and a Prothrombotic State.

Left Atrial Appendage Dysfunction in Chronic Nonvalvular Atrial Fibrillation is Significantly Associated With an Elevated Level of Brain Natriuretic Peptide and a Prothrombotic State.

Lipoprotein(a) and inflammation in patients with atrial fibrillation after electrical cardioversion

Serum Lipoprotein(a) and Its Relation to Left Ventricular Thrombus in Patients with Acute Myocardial Infarction.

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