Neurohormones and inflammatory mediators in patients with heart failure undergoing cardiac resynchronization therapy: Time courses and prediction of response

Boriani, Giuseppe; Regoli, François; Saporito, Davide; Martignani, Cristian; Toselli, Tiziano; Biffi, Mauro; Francolini, Gloria; Diemberger, Igor; Bacchi, Letizia; Rapezzi, Claudio; Ferrari, Roberto; Branzi, Angelo

doi:10.1016/j.peptides.2006.02.010

Cited by 47 publications

(33 citation statements)

References 50 publications

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“…33,34 Whether NE level is affected by CRT is controversial from limited studies; it was observed decrease, no change, or selected decrease in patients with a baseline NE > 800 ng/mL. [35][36][37][38][39] We observed a consistent improvement in HRV and MIBG, but not in NE level. One possible explanation for this discrepancy is that the uptake and release of NE in the sympathetic neuron level may not coincide with circular NE level.…”

Section: Crt Rebalances Cardiac Autonomic Function In Parallel To Impmentioning

confidence: 96%

Cardiac resynchronization therapy upregulates cardiac autonomic control

Cha¹,

Oh²,

Miyazaki³

et al. 2008

Autonomic Neuroscience

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Section: Crt Rebalances Cardiac Autonomic Function In Parallel To Impmentioning

confidence: 96%

Cardiac resynchronization therapy upregulates cardiac autonomic control

Cha¹,

Oh²,

Miyazaki³

et al. 2008

Autonomic Neuroscience

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“…The effect of CRT on arterial distensibility, compliance and inflammation alterations associated with CHF is not well understood [7][8][9]. Accordingly, the present study aims to assess the acute effects of ventricular resynchronization therapy with biventricular stimulation on arterial distensibility, echocardiographic parameters and serum norepinephrine (NE) levels in patients with symptomatic systolic HF and prolonged QRS duration.…”

Section: Introductionmentioning

confidence: 99%

Acute effects of cardiac resynchronization therapy on arterial distensibility and serum norepinephrine levels in advanced heart failure

Yıldız¹,

Hasdemir²,

Türkkan³

et al. 2013

Cardiol J

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“…On the basis of biochemical methodology and references available, 8,13,14 we had aimed at detecting a difference in TNF-α concentration of 10 pg/mL between any 2 groups and assumed a SD of 12 pg/mL. A sample size of 40 patients per group would then provide ≈90% power with a type I error rate of 0.0167 (to adjust for multiple comparisons).…”

Section: Sample Size Calculationmentioning

confidence: 99%

Heart Failure With Anemia

O’Meara

Rouleau

White

et al. 2014

Circ: Heart Failure

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Background— Anemia is a highly prevalent and strong independent prognostic marker in heart failure (HF), yet this association is not completely understood. Whether anemia is simply a marker of disease severity and concomitant chronic kidney disease or represents the activation of other detrimental pathways remains uncertain. We sought to determine which pathophysiological pathways are exacerbated in patients with HF, reduced ejection fraction (HFrEF) and anemia in comparison with those without anemia. Methods and Results— In a prospective study involving 151 patients, selected biomarkers were analyzed, each representing proposed contributive mechanisms in the pathophysiology of anemia in HF. We compared clinical, echocardiographic, and circulating biomarkers profiles among patients with HFrEF and anemia (group 1), HFrEF without anemia (group 2), and chronic kidney disease with preserved EF, without established HF (chronic kidney disease control group 3). We demonstrate here that many processes other than those related to chronic kidney disease are involved in the anemia–HF relationship. These are linked to the pathophysiological mechanisms pertaining to left ventricular systolic dysfunction and remodeling, systemic inflammation and volume overload. We found that levels of interleukin-6 and interleukin-10, specific markers of cardiac remodeling (procollagen type III N-terminal peptide, matrix metalloproteinase-2, tissue inhibitor of matrix metalloproteinase 1, left atrial volume), myocardial stretch (NT-proBNP [N-terminal probrain natriuretic peptide]), and myocyte death (troponin T) are related to anemia in HFrEF. Conclusions— Anemia is strongly associated not only with markers of more advanced and active heart disease but also with the level of renal dysfunction in HFrEF. Increased myocardial remodeling, inflammation, and volume overload are the hallmarks of patients with anemia and HF. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00834691.

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Neurohormones and inflammatory mediators in patients with heart failure undergoing cardiac resynchronization therapy: Time courses and prediction of response

Cited by 47 publications

References 50 publications

Cardiac resynchronization therapy upregulates cardiac autonomic control

Cardiac resynchronization therapy upregulates cardiac autonomic control

Acute effects of cardiac resynchronization therapy on arterial distensibility and serum norepinephrine levels in advanced heart failure

Heart Failure With Anemia

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