Dynamics in Insulin Resistance and Plasma Levels of Adipokines in Patients With Acute Decompensated and Chronic Stable Heart Failure

Schulze, P. Christian; Biolo, Andréia; Gopal, Daksha; Shahzad, Khurram; Balog, Joshua; Fish, Mark; Siwik, Deborah A.; Colucci, Wilson S.

doi:10.1016/j.cardfail.2011.08.010

Cited by 39 publications

(23 citation statements)

References 35 publications

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“…Our study provides further support of the relationship between elevated resistin and HF events in this multi-ethnic population, as has been described in other populations 21,28,29 . However, the strength of this relationship was attenuated after adjusting for traditional cardiovascular risk factors, a concept also appreciated by other groups 30 .…”

Section: Discussionsupporting

confidence: 89%

The association of resistin with cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis

Muse¹,

Feldman²,

Blaha³

et al. 2015

Atherosclerosis

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Objective To describe the relationship between circulating resistin levels and cardiovascular diseases (CVD) and all-cause death in a multi-ethnic cohort. Methods and Results We studied 1,913 participants from the Multi-Ethnic Study of Atherosclerosis with measurements of plasma resistin levels. Absolute proportions experiencing new-onset atrial fibrillation (AF), atherosclerotic CVD (myocardial infarction, angina, resuscitated cardiac arrest, stroke), heart failure (HF), and all-cause death were calculated for each quartile of resistin. We used adjusted Cox proportional regression modeling resistin as a continuous variable per standard deviation of log-transformed resistin and secondarily as a categorical variable using resistin quartiles. Results were stratified by sex and race/ethnicity. The mean age of the population was 64.5 ± 10 years with half being female and a median resistin concentration of 15.1 ng/mL (11.9–19.1). Mean follow-up time was 7.2 ± 1.8 years. There was a graded increase in the occurrence of all outcomes across increasing quartiles of resistin. Modeled as a continuous variable, after adjustment for anthropomorphic measures, traditional risk factors, markers of inflammation, and other adipokines, significant associations were noted for HF (HR 1.4, CI 1.0–2.0), hard and all CVD (HR 1.3, 1.1–1.7 and 1.3, 1.1–1.6, respectively), and CHD (HR 1.31, 1.0–1.6), but not for AF or death. Significant interaction terms were noted between resistin and race, with Hispanic race/ethnicity showing the strongest relationship between resistin and outcomes. Conclusions In an ethnically diverse population without known CVD at baseline, there was a strong, independent association between higher resistin levels and incident CVD, CHD and HF.

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Section: Discussionsupporting

confidence: 89%

The association of resistin with cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis

Muse¹,

Feldman²,

Blaha³

et al. 2015

Atherosclerosis

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show abstract

“…In humans, circulating leptin levels are increased after myocardial infarction [94]. Similarly, leptin levels are also increased in heart failure patients independent of body mass [95], and mechanical unloading reverses this increase [96]. Leptin-deficient mice display greater cardiac hypertrophy [97], increased mortality in a model of viral myocarditis [98], and greater cardiac remodeling in response to chronic ischemic injury [99].…”

Section: Role Of Leptin In Metabolic and Cardiovascular Diseasementioning

confidence: 99%

Adipokines: A link between obesity and cardiovascular disease

Nakamura

Fuster

Walsh

2014

Journal of Cardiology

435

348

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Obesity is a risk factor for various cardiovascular diseases including hypertension, atherosclerosis, and myocardial infarction. Recent studies aimed at understanding the microenvironment of adipose tissue and its impact on systemic metabolism have shed light on the pathogenesis of obesity-linked cardiovascular diseases. Adipose tissue functions as an endocrine organ by secreting multiple immune-modulatory proteins known as adipokines. Obesity leads to increased expression of pro-inflammatory adipokines and diminished expression of anti-inflammatory adipokines, resulting in the development of a chronic, low-grade inflammatory state. This adipokine imbalance is thought to be a key event in promoting both systemic metabolic dysfunction and cardiovascular disease. This review will focus on the adipose tissue microenvironment and the role of adipokines in modulating systemic inflammatory responses that contribute to cardiovascular disease.

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“…For reasons that are not completely understood, circulating leptin levels are elevated independent of body weight in patients with systolic heart failure (39). Furthermore, levels of leptin and other adipokines are elevated in patients with acute decompensated heart failure and decreased as patients became more compensated (40). These clinical observations, when taken into context with our findings and others such as McGaffin et al (29), suggest that augmented cardiac leptin signaling may help the heart maintain ATP formation and systolic function during myocardial stress.…”

Section: Discussionmentioning

confidence: 99%

Cardiomyocyte-specific deletion of leptin receptors causes lethal heart failure in Cre-recombinase-mediated cardiotoxicity

Hall

Smith

Hall

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Although disruption of leptin signaling is associated with obesity as well as cardiac lipid accumulation and dysfunction, it has been difficult to separate the direct effects of leptin on the heart from those associated with the effects of leptin on body weight and fat mass. Using Cre-loxP recombinase technology, we developed tamoxifen-inducible, cardiomyocyte-specific leptin receptor-deficient mice to assess the role of leptin in regulating cardiac function. Cre recombinase activation in the heart resulted in transient reduction in left ventricular systolic function which recovered to normal levels by day 10. However, when cardiomyocyte leptin receptors were deleted in the setting of Cre recombinase-induced left ventricular dysfunction, irreversible lethal heart failure was observed in less than 10 days in all mice. Heart failure after leptin receptor deletion was associated with marked decreases of cardiac mitochondrial ATP, phosphorylated mammalian target of rapamycin (mTOR), and AMP-activated kinase (pAMPK). Our results demonstrate that specific deletion of cardiomyocyte leptin receptors, in the presence of increased Cre recombinase expression, causes lethal heart failure associated with decreased cardiac energy production. These observations indicate that leptin plays an important role in regulating cardiac function in the setting of cardiac stress caused by Cre-recombinase expression, likely through actions on cardiomyocyte energy metabolism.

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Dynamics in Insulin Resistance and Plasma Levels of Adipokines in Patients With Acute Decompensated and Chronic Stable Heart Failure

Cited by 39 publications

References 35 publications

The association of resistin with cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis

The association of resistin with cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis

Adipokines: A link between obesity and cardiovascular disease

Cardiomyocyte-specific deletion of leptin receptors causes lethal heart failure in Cre-recombinase-mediated cardiotoxicity

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