Presentazione sul tema: "Reflusso e Aritmie Dr. Paolo Pieragnoli SOD Aritmologia Firenze."— Transcript della presentazione:
Reflusso e Aritmie Dr. Paolo Pieragnoli SOD Aritmologia Firenze
Incidenza e prevalenza della fibrillazione atriale (FA) aumentano con l’aumentare dell’età Epidemiologia Incidenza (n 10 3 /2 anni) Benjamin EJ, et al. JAMA 1994 Uomini Donne Età (anni) 0 20 40 80 60 55-64 75-84 65-74 85-94 Framingham study
Prevalenza di fibrillazione atriale per et à e sesso nello Studio ATRIA <5555-6460-6470-7465-6980-8475-79>85 Gruppi di età (anni) Prevalenza (%) 0 2 4 6 8 10 12 Uomini Donne Go AS et al, JAMA 2001 17,974 soggetti con FA (0.95%) in una popolazione USA (California) di 1.89 milioni di persone Rif. 1.7.1996-31.12.1997
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)
Stima dei soggetti con FA (N, milioni) 0 4 8 12 16 2000201020202030 Anno 2040 Stima conservativa – Nessun ulteriore aumento di incidenza Miyasaka Y. Circulation, 2006 2050 Stima NON conservativa – Continuo aumento di incidenza
Fibrillazione atriale: cause Cardiaca Non cardiaca “Lone” atrial fibrillation
“Lone” Atrial Fibrillation The 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
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.
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
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 :
Reflux esophagitis in the pathogenesis of paroxysmal atrial fibrillation: results of a pilot study N° of patientsMethodology Results Conclusion Weilg et al, 2003
Thirty-two patients (13 women and 19 men, age 20-69 years) with a combination of dysrhytmias and GERD, and 9 patients (5 women and 4 men, age 43-58 years) with GERD only underwent simultaneous 24-hours pH and ECG monitoring Power spectrum analysis of heart rate variability was obtained woth both low-frequency (LF) (symptathetic modulation) and high-frequency (HF) (vagal modulation) components. Hourly mean esophageal pH and LF/HF ratio (esophagus-heart) were correlated. A 3-month regimen of esomeprazole 40 mg/day was prescrived. In 18 patients with dysrhythmias and in none with GERD only, a significant correlation between esophageal pH and LF/HF ratio was observed. A significatn reduction of cardiac symptoms after PPI therapy was observed only in these patients (13/16 vs 4/11, p<0.01)
The study concluded that there could be a subgroup of patients with heart dysrhythmias in whom esophageal acid stimulus elicited cardiac autonomic reflexes, and acid suppression in this subgroup may improve both GERD and cardiac symptoms. Although this study demonstrated a reduction or disappearance of the dysrhythmias in patients with a cardiac response to esophageal acid exposure, it had some limitations.
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
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