reflusso e aritmie dr. paolo pieragnoli sod aritmologia firenze
DESCRIPTION
Lo sport come mezzo di prevenzione 14 Settembre 2013. Reflusso e Aritmie Dr. Paolo Pieragnoli SOD Aritmologia Firenze. 80. Framingham study. 60. Uomini. 40. Donne. 20. Incidenza (n • 10 3 /2 anni). 0. 55-64. 65-74. 75-84. 85-94. Età (anni). Benjamin EJ, et al. JAMA 1994. - PowerPoint PPT PresentationTRANSCRIPT
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Reflusso e Aritmie
Dr. Paolo Pieragnoli
SOD AritmologiaFirenze
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•Incidenza e prevalenza della fibrillazione atriale (FA) aumentano con l’aumentare dell’età
Epidemiologia
Inci
denz
a (n
• 1
03 /2
anni
)
Benjamin EJ, et al. JAMA 1994
Uomini
Donne
Età (anni)
0
20
40
80
60
55-64 75-8465-74 85-94
Framingham study
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Prevalenza di fibrillazione atriale per età e sesso nello Studio ATRIA
0,10,4
11,7
3,4
5
7,2
9,1
0,20,9
1,7
3
5
11,1
10,3
7,3
<55 55-64 60-64 70-7465-69 80-8475-79 >85
Gruppi di età (anni)
Prev
alen
za (%
)
0
2
4
6
8
10
12
Uomini
Donne
Go AS et al, JAMA 2001
17,974 soggetti con FA (0.95%) inuna popolazione USA (California)di 1.89 milioni di personeRif. 1.7.1996-31.12.1997
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AF in the general population
• 1.6% prevalence of AF in general population (Framingham study, AHJ 1983)
• 3.2% people aged 30-62 yrs develop AF during the subsequent 24 years (Framingham study, AHJ 1983)
• 5.5% people >65 yrs have AF (Furberg, AJC 1994)
• 41% paroxysmal, 59% chronic (Framingham study, AHJ 1983)
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Stim
a de
i sog
getti
con
FA
(N, m
ilion
i)
0
4
8
12
16
2000 2010 2020 2030Anno
2040
Stima conservativa – Nessun ulteriore aumento di incidenza
Miyasaka Y. Circulation, 2006
2050
Stima NON conservativa – Continuo aumento di incidenza
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Fibrillazione atriale: cause
• Cardiaca
• Non cardiaca
• “Lone” atrial fibrillation
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“Lone” Atrial FibrillationThe Olmsted County Study.
N Engl J Med 1987; 317: 669-674
• Absence of identifiable cardiovascular, pulmonary, or precipitating illness, age <60 yrs
• 2.7% of patients with atrial fibrillation
• Mean 15 yrs follow-up
• 1.3% incidence of stroke
• 94% survival
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Fibrillazione atriale: cause cardiache• Malattia cardiaca ipertensiva• Malattia cardiaca ischemica• Malattia cardiaca valvolare
– Reumatica: stenosi della mitrale– Non reumatica: stenosi dell’aorta, rigurgito mitrale
• Pericardite• Tumori cardiaci• Sick sinus syndrome• Cardiomiopatia
– Ipertrofica– Idiopatica dilatativa
• Chirurgia post bypass coronarico
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Fibrillazione atriale: cause non cardiache
• Polmonare
• Metabolica
– Ipertiroidismo
– Disordine elettrolitico
• Tossica: alcol (‘holiday heart’ syndrome)
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• Ageing
•Hypertension
•Symptomatic heart failure
•Tachycardiomyopathy
•Valvular heart disease
•Cardiomyopathies
•Atrial septal defect
•Other congenital heart disease
•Thyroid dysfunction
• Obesity
•Diabetes mellitus
•Chronic obstructive pulmonary disease (COPD)
•Sleep apnea
•Chronic renal disease
•Alcohol abuse
•Exercise
•Local or systemic inflammation
• ACID REFLUX DISEASE
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Gastroesophageal reflux disease or acid reflux disease is the most common gastrointestinal diagnosis recorded during visits to outpatien clinics
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The potential mechanism of
GERD-induced AF
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REFLUX DISEASE
INFLAMMATION AUTOIMMUNE
Afferent-efferent reflux mechanism
with cerebral representation of
cardiac rhythm
Local pericarditis myocarditis
Vagal nerves, peripheral
nerves
Inflammatory mediators-
cytokines and interleukins
Autoantibodies against myosin
chains
ATRIAL FIBRILLATION
Sympatho-vagal imbalance
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Relationship between the esophagus and the left atrium. A: posterior-anterior aspect of the left atrium.B: Right anterior oblique view
Circulation 112(4), 459–464 (2005)
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Recurrent acid secretion induces mucosal inflammation and secretion of interleukin IL-1b and IL-6
These inflammatory cytokines play a pivotal role in the pathogenesis of AF.
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INFLAMMATION AND ATRIAL FIBRILLATION
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• The human esophagus produces IL-6 and other inflammatory citokines
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Acid reflux causes a local inflammatory process that may alter the autonomic innervations of the esophageal mucosa, and may also penetrate the esophageal wall and affect the adjacent vagal nerves due to the close juxtaposition of the esophagus and atria, especially the left atrium, where most triggers associated with atrial fibrillation have been described, affecting myelination and thus propagation of stimuli.
Inflammation of the esophagegal mucosa affects local receptors that may induce afferent-efferent reflex mechanisms of the cardiac rhythm which can lead to secondary stimulation of the vagal nerves inducing AF.
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AUTONOMIC SYSTEM AND ATRIAL FIBRILLATION
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GERD Autoantibodies
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Hiatal hernia is a condition in which parts of the abdominal contents, mainly the GEJ and the stomach, are proximally displaced above the diaphram through the esophageal hiatus into the mediastinum.
Hiatal hernia (10% in patients younger than 40 years to 70% in patients older than 70 years) may predispose to GERD or worsen existing GERD in a few individuals
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• Atrial arrhythmias may be induced by a mechanical effect on the left atrial wall that is related to the passage of food
• A large hiatal hernia may also cause compression of the left atrium and may result in an area of relative ischemia and anatomical block resulting in reentry and arrhythmias
Possible mechanisms are :
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Reflux esophagitis in the pathogenesis of paroxysmal atrial fibrillation: results of a pilot study
N° of patients Methodology
Results
Conclusion
Weilg et al, 2003
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N° of patients
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N° of patients Methodology
Results Conclusion
Relationship between atrial fibrillation and gastroesophageal reflux disease:
multicenter questionnaire survey
Shimazu et al, 2011
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Pulmonary veins isolation: pathophysiology
M. Gulizia et al “Diagnosi e terapia del Flutter e della Fibrillazione atriale” 2009
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European Heart Journal (2010) 31, 2369–2429
Choice between ablation and antiarrhythmic drug therapy for patients with and without structural heart disease
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40% 37% 29%
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87% 81% 63%
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Major Complications of Catheter Ablation for Atrial Fibrillation
Circ J 2010; 74: 1972 – 1977
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The association between AF and GERD is still debated, predominantly because of shared confounding factors such as obesity, diabetes and sleep apnea.
However, there is a mounting body of evidence that suggests an association between the two; therefore, a large randomized clinical trial is warranted.
Currently, the most likely potential mechanism for GERD-induced AF is local release of cytokines secondary to esophageal injury, which creates a proarrhythmogenic environment. Perhaps the most compelling evidence that supports this association is that proton pump inhibitors seem to reduce the incidence and the duration of AF.
CONCLUSION 1
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At present, few clinicians outside the field of cardiac electrophysiology and gastroenterology are aware of the possible association of GERD, hiatal hernia and AF. As more patients with these disorders are treated and studied, our insights into the pathogenesis will be elucidated. It will be interesting to see whether AF causes GERD reciprocally, thus creating a cycle.
Increasing awareness that GERD and/or hiatal hernia may be independent risk factors for AF may result in physicians being more aggressive in treating patients with proton pump inhibitors and hiatal hernia repair, since both of these therapies have shown a reduction in the incidence and duration of AF.
CONCLUSION 2