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Difference between revisions of "Montaigne 2013 J Am Coll Cardiol"

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{{Publication
{{Publication
|title=Montaigne D, Marechal X, Lefebvre P, Modine T, Fayad G, Dehondt H, Hurt C, Coisne A, Koussa M, Remy-Jouet I, Zerimech F, Boulanger E, Lacroix D, Staels B, Neviere R (2013) Mitochondrial Dysfunction as an Arrhythmogenic Substrate. J Am Coll Cardiol 62:1466-1473.  
|title=Montaigne D, Marechal X, Lefebvre P, Modine T, Fayad G, Dehondt H, Hurt C, Coisne A, Koussa M, Remy-Jouet I, Zerimech F, Boulanger E, Lacroix D, Staels B, Neviere R (2013) Mitochondrial dysfunction as an arrhythmogenic substrate. J Am Coll Cardiol 62:1466-73.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23644086 PMID: 23644086]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23644086 PMID: 23644086]; [http://www.sciencedirect.com/science/article/pii/S0735109713017300 sciencedirect.com Open Access]
|authors=Montaigne D, Marechal X, Lefebvre P, Modine T, Fayad G, Dehondt H, Hurt C, Coisne A, Koussa M, Remy-Jouet I, Zerimech F, Boulanger E, Lacroix D, Staels B, Neviere R
|authors=Montaigne D, Marechal X, Lefebvre P, Modine T, Fayad G, Dehondt H, Hurt C, Coisne A, Koussa M, Remy-Jouet I, Zerimech F, Boulanger E, Lacroix D, Staels B, Neviere R
|year=2013
|year=2013
|journal=J Am Coll Cardiol
|journal=J Am Coll Cardiol
|abstract=OBJECTIVES:
|abstract=This study sought to provide bedside evidence of the potential link between cardiac mitochondrial dysfunction and arrhythmia as reported in bench studies.
 
This study sought to provide bedside evidence of the potential link between cardiac mitochondrial dysfunction and arrhythmia as reported in bench studies.
 
BACKGROUND:


Atrial fibrillation (AF) is a frequent complication of cardiac surgery. Underlying mechanisms of post-operative atrial fibrillation (POAF) remain largely unknown. Because cardiac mitochondrial dysfunction has been reported in clinical conditions with a high risk of POAF, we investigated whether a causal link exists between POAF onset and pre-operative function of cardiac mitochondria.
Atrial fibrillation (AF) is a frequent complication of cardiac surgery. Underlying mechanisms of post-operative atrial fibrillation (POAF) remain largely unknown. Because cardiac mitochondrial dysfunction has been reported in clinical conditions with a high risk of POAF, we investigated whether a causal link exists between POAF onset and pre-operative function of cardiac mitochondria.
METHODS:


Pre-operative mitochondrial respiration and calcium retention capacity, respiratory complex activity, and myocardial oxidative stress were quantified in right atrial tissue from 104 consecutive patients with metabolic syndrome, in sinus rhythm, and undergoing coronary artery bypass graft surgery.
Pre-operative mitochondrial respiration and calcium retention capacity, respiratory complex activity, and myocardial oxidative stress were quantified in right atrial tissue from 104 consecutive patients with metabolic syndrome, in sinus rhythm, and undergoing coronary artery bypass graft surgery.
RESULTS:


In this high-risk population, POAF occurred in 44% of patients. Decreased pre-operative mitochondrial respiration and increased sensitivity to calcium-induced mitochondrial permeability transition pore opening were significantly associated with POAF. Adenosine diphosphate-stimulated mitochondrial respiration supported by palmitoyl-l-carnitine was significantly lower in POAF patients and remained independently associated with AF onset after adjustment for age, body mass index, heart rate, beta-blocker use, and statin medication (multivariate logistic regression coefficient per unit = -0.314 ± 0.144; p = 0.028). Gene expression profile analysis identified a general downregulation of the mitochondria/oxidative phosphorylation gene cluster in pre-operative atrial tissue of patients in whom AF developed.
In this high-risk population, POAF occurred in 44% of patients. Decreased pre-operative mitochondrial respiration and increased sensitivity to calcium-induced mitochondrial permeability transition pore opening were significantly associated with POAF. Adenosine diphosphate-stimulated mitochondrial respiration supported by palmitoyl-l-carnitine was significantly lower in POAF patients and remained independently associated with AF onset after adjustment for age, body mass index, heart rate, beta-blocker use, and statin medication (multivariate logistic regression coefficient per unit = -0.314 ± 0.144; p = 0.028). Gene expression profile analysis identified a general downregulation of the mitochondria/oxidative phosphorylation gene cluster in pre-operative atrial tissue of patients in whom AF developed.
CONCLUSIONS:


Our prospective study identifies an association between pre-operative mitochondrial dysfunction of the atrial myocardium and AF occurrence after cardiac surgery in patients with metabolic disease, providing novel insights into the link between mitochondria and arrhythmias in patients.
Our prospective study identifies an association between pre-operative mitochondrial dysfunction of the atrial myocardium and AF occurrence after cardiac surgery in patients with metabolic disease, providing novel insights into the link between mitochondria and arrhythmias in patients.
|keywords=ADP, AF, ATP, BMI, CABG, MnSOD, OXPHOS, POAF, ROS, SR, V(Cox), V(palm+ADP), adenosine diphosphate, adenosine diphosphate–stimulated respiration supported by palmitoyl-l-carnitine, adenosine triphosphate, atrial fibrillation, body mass index, cardiac surgery, complex IV–related uncoupled maximum respiration, coronary artery bypass graft, diabetes, gene expression, mCRC, mPTP, manganese superoxide dismutase, mitochondria, mitochondrial calcium retention capacity, mitochondrial permeability transition pore, oxidative phosphorylation, post-operative atrial fibrillation, reactive oxygen species, sinus rhythm
|keywords=Atrial fibrillation; Cardiac surgery; Diabetes; Gene expression; Mitochondria
|mipnetlab=FR Lille Neviere R
|mipnetlab=FR Lille Neviere R
}}
}}
{{Labeling
{{Labeling
|area=Respiration, mt-Medicine
|diseases=Obesity, Other
|injuries=Permeability transition, Oxidative stress;RONS
|organism=Human
|tissues=Heart
|preparations=Permeabilized tissue
|couplingstates=LEAK, OXPHOS, ET
|pathways=N, S
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|additional=Labels
}}
}}

Latest revision as of 15:25, 13 November 2017

Publications in the MiPMap
Montaigne D, Marechal X, Lefebvre P, Modine T, Fayad G, Dehondt H, Hurt C, Coisne A, Koussa M, Remy-Jouet I, Zerimech F, Boulanger E, Lacroix D, Staels B, Neviere R (2013) Mitochondrial dysfunction as an arrhythmogenic substrate. J Am Coll Cardiol 62:1466-73.

» PMID: 23644086; sciencedirect.com Open Access

Montaigne D, Marechal X, Lefebvre P, Modine T, Fayad G, Dehondt H, Hurt C, Coisne A, Koussa M, Remy-Jouet I, Zerimech F, Boulanger E, Lacroix D, Staels B, Neviere R (2013) J Am Coll Cardiol

Abstract: This study sought to provide bedside evidence of the potential link between cardiac mitochondrial dysfunction and arrhythmia as reported in bench studies.

Atrial fibrillation (AF) is a frequent complication of cardiac surgery. Underlying mechanisms of post-operative atrial fibrillation (POAF) remain largely unknown. Because cardiac mitochondrial dysfunction has been reported in clinical conditions with a high risk of POAF, we investigated whether a causal link exists between POAF onset and pre-operative function of cardiac mitochondria.

Pre-operative mitochondrial respiration and calcium retention capacity, respiratory complex activity, and myocardial oxidative stress were quantified in right atrial tissue from 104 consecutive patients with metabolic syndrome, in sinus rhythm, and undergoing coronary artery bypass graft surgery.

In this high-risk population, POAF occurred in 44% of patients. Decreased pre-operative mitochondrial respiration and increased sensitivity to calcium-induced mitochondrial permeability transition pore opening were significantly associated with POAF. Adenosine diphosphate-stimulated mitochondrial respiration supported by palmitoyl-l-carnitine was significantly lower in POAF patients and remained independently associated with AF onset after adjustment for age, body mass index, heart rate, beta-blocker use, and statin medication (multivariate logistic regression coefficient per unit = -0.314 ± 0.144; p = 0.028). Gene expression profile analysis identified a general downregulation of the mitochondria/oxidative phosphorylation gene cluster in pre-operative atrial tissue of patients in whom AF developed.

Our prospective study identifies an association between pre-operative mitochondrial dysfunction of the atrial myocardium and AF occurrence after cardiac surgery in patients with metabolic disease, providing novel insights into the link between mitochondria and arrhythmias in patients. • Keywords: Atrial fibrillation; Cardiac surgery; Diabetes; Gene expression; Mitochondria

• O2k-Network Lab: FR Lille Neviere R


Labels: MiParea: Respiration, mt-Medicine  Pathology: Obesity, Other  Stress:Permeability transition, Oxidative stress;RONS  Organism: Human  Tissue;cell: Heart  Preparation: Permeabilized tissue 


Coupling state: LEAK, OXPHOS, ET  Pathway: N, S  HRR: Oxygraph-2k 


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