Evaluation of NT-proBNP to predict outcomes in advanced heart failure

MacGowan, Guy A.; Neely, Dermot; Peaston, R; Wrightson, Neil; Parry, Gareth

doi:10.1111/j.1742-1241.2010.02388.x

Cited by 20 publications

(10 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Elevated bilirubin levels have been shown to correlate with increased heart failure and death and corroborate the observations made with the previously mentioned biomarkers [30,25]. By contrast, other studies demonstrate that lower bilirubin levels correlate closely to coronary heart disease and metabolic syndrome components [31,32].…”

Section: Discussionsupporting

confidence: 80%

Omentin changes following bariatric surgery and predictive links with biomarkers for risk of cardiovascular disease

Lapointe

Poirier

Martin

et al. 2014

Cardiovasc Diabetol

View full text Add to dashboard Cite

BackgroundAlthough no receptor has yet been identified, changes in circulating levels of the adipokine designated as Omentin have been demonstrated in obesity and related comorbidities such as cardiovascular disease, insulin resistance, metabolic syndrome and chronic inflammation.MethodsChanges in Omentin levels at 1 and 5 days and 6 and 12 months in response to biliopancreatic diversion with duodenal switch bariatric surgery were evaluated, specifically to investigate if changes preceded gain of insulin sensitivity.ResultsPre-operative plasma Omentin was not different between men (n = 18) vs women (n = 48), or diabetic status but correlated with body mass index (BMI). Altogether, Omentin increased as early as 24-h post-surgery, with changes maintained up to 1-year. Fifty-nine percent of subjects increased Omentin >10% by 24-H following surgery (OmentinINC p < 0.0001), while 18% of subjects decreased (OmentinDEC p < 0.0001), with changes maintained throughout one-year. These two groups had comparable age, sex distribution, diabetes, BMI, waist circumference and fat mass, however OmentinDEC had elevated levels of cardiovascular risk markers; homocysteine (p = 0.019), NT-proBNP (p = 0.006) and total bilirubin (p = 0.0001) while red blood cell (RBC) count was lower (p = 0.0005) over the one-year period. Omentin levels at 1-DAY also correlated with immune parameters (white blood cell count, % neutrophil, % monocytes, % lymphocytes).ConclusionOmentinDEC at 1 day following surgery may be a marker of cardiovascular “at-risk” group before weight loss or insulin sensitivity restoration.

show abstract

Section: Discussionsupporting

confidence: 80%

Omentin changes following bariatric surgery and predictive links with biomarkers for risk of cardiovascular disease

Lapointe

Poirier

Martin

et al. 2014

Cardiovasc Diabetol

View full text Add to dashboard Cite

show abstract

“…Bilirubin is known to correlate closely with right atrial pressure in HF patients. 12 Hemoglobin was decreased as a result of some perioperative blood loss. Of note, the significantly lower bilirubin level indicated that this lower hemoglobin was not related to hemolysis.…”

Section: Resultsmentioning

confidence: 99%

“…There were also significant increases in serum sodium and reductions in bilirubin indicating reduced neurohumoral activation 11 and reduced hepatic congestion, respectively. Bilirubin is known to correlate closely with right atrial pressure in HF patients 12 . Hemoglobin was decreased as a result of some perioperative blood loss.…”

Section: Resultsmentioning

confidence: 99%

Hemodynamic, Echocardiographic, and Exercise‐Related Effects of the HeartWare Left Ventricular Assist Device in Advanced Heart Failure

McDiarmid¹,

Gordon²,

Wrightson

et al. 2012

Congestive Heart Failure

View full text Add to dashboard Cite

©2012 Wiley Periodicals, Inc. The aim of this study was to determine the effects of the HeartWare left ventricular assist device (HVAD) (HeartWare International, Inc, Framingham, MA) on hemodynamics, ventricular function, and exercise capacity. Between July 2009 and March 2011, 46 patients with advanced heart failure had implantation of the HVAD. Of these patients, 30 had subsequent assessments for transplantation and these patients formed the study cohort. Thirty patients had assessments at a mean of 201±86 days and 13 went on to have a second assessment at 351±86 days. There were marked improvements in hemodynamics and exercise capacity at both assessments, with significant decreases in right and left heart filling pressures; increases in cardiac index, New York Heart Association class, and peak exercise oxygen consumption; and reduction in pulmonary vascular resistance (all P<.05). Left ventricular end‐diastolic and end‐systolic dimensions were unchanged at the first assessment, although there was a significant reduction in end‐diastolic diameter at the second assessment (P<.01). There were no significant changes in a visual grade of right ventricular function. After up to 1 year of support, the HVAD system results in significant benefits in overall heart failure status, with improved hemodynamics and exercise capacity. This occurs in the absence of marked changes in left ventricular size or right ventricular function.

show abstract

“…In human subjects with DCM, the levels of β‐AR mRNA did not predict response to β‐blockers 31. In human heart failure, circulating NT‐proBNP correlates closely with cardiac index 32. Thus, the data on BNP mRNA from the myocardium of the mouse models seem to correlate well with clinical results, because the Sgcd null mice had the highest cardiac output and lowest levels of BNP mRNA at baseline, and overall emphasize the early stage of the cardiomyopathy in these mouse models.…”

Section: Discussionmentioning

confidence: 95%

Intolerance to β‐blockade in a mouse model of δ‐sarcoglycan‐deficient muscular dystrophy cardiomyopathy

Bauer

Blain

Greally

et al. 2010

European J of Heart Fail

View full text Add to dashboard Cite

AimsPatients with mutations predisposing to cardiomyopathy often have routine assessments of left ventricular function. It is unclear whether asymptomatic mild cardiomyopathy should be treated with standard heart failure therapies. Methods and resultsWe tested the effect of metoprolol on cardiac haemodynamics and pathology in two animal models for muscular dystrophy and cardiomyopathy. Treatment started at an early stage in the development of the cardiomyopathy. Metoprolol was given orally (2.5 mg/kg/day) over 8 weeks to mdx mice (model for Duchenne muscular dystrophy) and d-sarcoglycan-deficient (Sgcd null ) mice (model for Limb girdle muscular dystrophy type 2F). In vivo pressurevolume loops, fibrosis, in vivo myocyte sarcolemmal injury, and b-adrenergic receptor mRNA were assessed. In b-blocked mdx mice, there was a beneficial reduction in afterload and restored contractility resulting in an increased stroke volume. In contrast, in Sgcd null mice, there was marked deterioration in haemodynamics (prolonged relaxation, Tau, and reduced stroke volume). Furthermore, challenging the b-blocked Sgcd null mice with the b-adrenergic agonist dobutamine led to markedly increased mortality. Patterns of sarcolemmal injury or b-adrenergic receptor mRNA could not account for this, though the acute rise in markers of active relaxation suggested abnormally high levels of intracellular calcium. Conclusionb-Blockers may not necessarily be beneficial in all cardiomyopathies, even when given at an early stage of development. Clinical trials of b-blockers in muscular dystrophy-associated cardiomyopathy may need to stratify patients by genotype.--

show abstract

Evaluation of NT-proBNP to predict outcomes in advanced heart failure

Cited by 20 publications

References 24 publications

Omentin changes following bariatric surgery and predictive links with biomarkers for risk of cardiovascular disease

Omentin changes following bariatric surgery and predictive links with biomarkers for risk of cardiovascular disease

Hemodynamic, Echocardiographic, and Exercise‐Related Effects of the HeartWare Left Ventricular Assist Device in Advanced Heart Failure

Intolerance to β‐blockade in a mouse model of δ‐sarcoglycan‐deficient muscular dystrophy cardiomyopathy

Contact Info

Product

Resources

About