D.BASEM ELSAID ENANYLECTURER OF CARDIOLOGY

AINSHAMS UNIVERSITY

Atrial fibrillation

--Most common cardiac arrhythmia.--Characteristics:•The RR intervals “irregularly irregular.”•There are no distinct P waves. Thus, even when P-P interval can be defined, it is not regular and often less than 200 milliseconds =atrial rate >300 beats/minute.--The prevalence of paroxysmal AF, which is more likely to be detected with ambulatory monitoring, is much higher--ATRIA study in USA (1.9 million):•The overall prevalence of AF was 1%; 70% were at least 65 years.•The prevalence of AF ranged from 0.1% among adults less than 55 years of age to 9% in those ≥80 years of age.•The prevalence was higher in men than women (1.1 versus 0.8 %)--Incidence increases with age, IHD

RISK FACTORS AND DISEASE ASSOCIATIONS

-Hypertensive heart disease and coronary heart disease (CHD) are the most common underlying disorders in developed countries-In AMI, AF develops in 6-10% due to atrial ischaemia or atrial stretching from HF-Rheumatic heart disease is associated with a much higher incidence of AF in developing countries-HF-HCM 10-28%, prognostic imp. unclear-Congenital heartASD (20%, inc with age)Ebstein's anomaly, PDAAfter surgical correction of some other abnormalities, including ventricular septal defect, tetralogy of Fallot, pulmonic stenosis, and transposition of the great vessels

-10-14% documented PE-COPD, peripartum cardiomyopathy, lupus myocarditis, and both idiopathic and uremic pericarditis-Possible causal relationship between obstructive sleep apnea (OSA) and AF -Obese individuals (BMI >30 kg/m2) are significantly more likely to develop AF-Metabolic syndrome-Hyperthyroidism:inc beta adrenergic tone, inc thyroid hormones (increased automaticity and enhanced triggered activity of pulmonary vein cardiomyocytes)-Subclinical hyperthyroidism (dec TSH)-Possible relationship between AF and hypothyroidism has been suggested but not proven

Surgery

--The incidence is greatest in patients undergoing coronary artery bypass graft (CABG) or cardiac valve surgery.

--Cardiac surgery :30 to 40% early post CABG37 to 50% after valve surgery60% valve replacement plus CABG 10 to 24% of patients with a denervated transplanted heart, often in the absence of significant rejection. Mostly within the first two weeks, while AF developing after two weeks may be associated with an increased risk of subsequent death--Noncardiac surgery:AF is less common after noncardiac compared to cardiac surgery.Most episodes occurred within the first three days after surgery. The risk was greatest with intrathoracic surgery (12%).

--Family history:The presence of AF in a first-degree relative, particularly a parent, has long been associated with an increase in risk--Genetics:-For the majority of patients, genetic susceptibility, if present, is probably a polygenic phenomenon=combined effects of a number of genes-Some families have been identified in which AF inheritance follows more typical Mendelian patterns, consistent with a single disease-causing gene-Mutations in SCN5A have also been identified in several other cardiac disorders, including the long QT syndrome, the Brugada syndrome, familial atrioventricular conduction block, and familial sick sinus syndrome

--Birth weight:A possible relationship between birth weight and the development of AF Incident AF increased significantly from the lowest to the highest birth weight--Inflammation and infection:Inflammation, as determined by CRP, is not likely to be causative of atrial fibrillation--Pericardial fat is visceral adipose tissue with inflammatory properties; both obesity and inflammation are risk factors for AF

--Autonomic dysfunction:The autonomic nervous system may be involved in the initiation and maintenance of AF as both heightened vagal and sympathetic tone can promote AF--Other supraventricular tachyarrhythmias:-Spontaneous transition between typical atrial flutter and AF has been observed. In addition, AF is, in some patients, associated with paroxysmal supraventricular tachycardia (PSVT)-Enhanced vagal tone, or atrial premature beat can cause stable PSVT to degenerate into AF or retrograde conduction via the accessory pathway of a premature beat, stimulating the atrial myocardium during its vulnerable period

--Alchol:AF occurs in up to 60% of binge drinkers with or without an underlying alcoholic cardiomyopathy ="the holiday heart syndrome.“ in most cases--Caffeine:Despite the theoretical relationship between caffeine and arrhythmogenesis, there is no evidence in humans that ingestion of caffeine in doses typically consumed can provoke AF or any other spontaneous arrhythmia--With regard to dietary fish intake and incident AF, three cohort studies (approximately 45,000, 48,000, and 5000 individuals) found no relationship, while one (approximately 5000 individuals) suggested a reduction in AF burden

--Medications:Certain medications can cause or contribute to the development of AF =theophylline, adenosine (with the WPW, due to conduction down the accessory pathway), drugs that enhance vagal tone, such as digitalis

Longterm outcome

1. Death : Death rate doubled (Only antithrombotic therapy has beenshown to reduce AF-related deaths).2. Stroke (includes haemorrhagic stroke and cerebral bleeds):Stroke risk increased; AF is associated with more severe stroke.3. Hospitalizations:Hospitalizations are frequent in AF patients and may contribute toreduced quality of life.4. Quality of life and exercise capacity:Wide variation, from no effect to major reduction.AF can cause marked distress through palpitations and other AF-related symptoms.5. Left ventricular function:Wide variation, from no change to tachycardiomyopathy with acuteheart failure.

PATHOGENESIS

--Sustained AF seems to require the development of multiple wavelets (rather than the single wavefront as seen in atrial flutter).--Majority of episodes of paroxysmal AF (PAF) are triggered by atrial premature beats, while a small number are preceded by typical atrial flutter or atrial tachycardia--Atrial premature beats appear to be most important as a trigger in patients with PAF who have normal or near-normal hearts, much less clear in patients with significant structural heart disease--Ectopic foci are most often located near the pulmonary veins, in patients with minimal or no structural heart disease--Ablation of sites with a high dominant frequency, mostly located at or close to the junction between the PVs and the left atrium, results in progressive prolongation of the AF cycle length and conversion to sinus rhythm in patients with paroxysmal AF, while in persistent AF, sites with a high dominant frequency are spread throughout the entire atria, and ablation or conversion to sinus rhythm is more difficult

--Other factors that may contribute to AF in near normal patients include increased vagal tone and possible subclinical myocarditis--As AF becomes established, the refractory period of the atrial muscle shortens (down-regulation of the L-type Ca2+ inward current, up-regulation of inward rectifier K+ currents) predisposes to further AF (ie, AF begets AF).--Conversely, when sinus rhythm is sustained, these electrophysiologic changes reverse (sinus rhythm begets sinus rhythm).--Echocardiographic risk factors: Left atrial enlargement, increased left ventricular wall thickness and reduced left ventricular fractional shortening.

Structural abnormalities associated with AF

Extracellular matrix alterationsInterstitial and replacement fibrosisInflammatory changesAmyloid depositMyocyte alterationsApoptosisNecrosisHypertrophyDedifferentiationGap junction redistributionIntracellular substrate accumulation (haemocromatosis, glycogen)Microvascular changesEndocardial remodelling (endomyocardial fibrosis)

Clinical correlates

1-Thrombo-embolism:-LAA is the dominant source of embolism(90%) in non-valvular AF.-‘Flow abnormalities’:stasis within the left atrium,reduced (LAA) flow velocitiesspontaneous echo-contrast on(TOE).-‘Endocardial abnormalities’:Progressive atrial dilatationendocardial denudationoedematous/fibroelastic infiltration of the extracellular matrix.-‘Abnormalities of blood constituents’:haemostatic and platelet activationInflammation and growth factor abnormalities

2-Haemodynamic changes:Loss of coordinated atrial contraction (5-15% of COP)High ventricular rates (dec filling as dec diastole)Irregularity of the ventricular responseDecrease in myocardial blood flowLong-term alterations such as atrial and ventricular cardiomyopathy.

CLASSIFICATION (ACC/AHA/ESC)applies to recurrent episodes of AF that last more than 30 seconds and that are unrelated to a reversible cause

•First detected or diagnosed, irrespective of the duration or the presence or absence of symptoms.•Paroxysmal (ie, self-terminating or intermittent) AF:Defined as recurrent AF (≥2 episodes) that terminate spontaneously in less than seven days, usually less than 24 hours. Progression to persistent and permanent AF occur in >50% beyond 10 years despite antiarrhythmic therapy.•Persistent AF:Fails to self-terminate within seven days. Episodes often require pharmacologic or electrical cardioversion to restore sinus rhythm. The ESC recognizes a category called “long-standing persistent AF,” which refers to AF that has lasted for one year or more when it has been decided to adopt a rhythm control strategy.•Permanent AF:More than one year and cardioversion either has not been attempted or has failed.

LONE AF

-Individuals with paroxysmal, persistent, or permanent AF who have no structural heart disease.-Less than 15 to 30% of cases of permanent AF and 25 to 45% of cases of paroxysmal AF-Younger than those with structural heart disease and are often male -Often symptomatic and associate certain triggers with episodes of AF: sleeping, exercise, alcohol, eating -Family history of AF is present in up to 38%

RECURRENT AF

Continuous monitoring studies have shown that approximately 90% of patients have recurrent episodes of AF. However, up to 90% of episodes are not recognized by the patient

History and physical examination

--Not all patients with AF are symptomatic.--Description of the symptoms: onset or date of discovery, the frequency and duration, severity, and qualitative characteristics.--Typical symptoms:palpitations, tachycardia, fatigue, weakness, dizziness, lightheadedness, reduced exercise capacity, increased urination, or mild dyspnea.More severe symptoms include dyspnea at rest, angina, presyncope, or infrequently, syncope.some patients present with an embolic event

--Precipitating causes: exercise, emotion, or alcohol. --Disease associations:cardiovascular or cerebrovascular disease, diabetes, hypertension, chronic obstructive pulmonary disease, or potentially reversible causes (eg, hyperthyroidism, excessive alcohol ingestion). --Examination: Abnormal findings may inform about either contributing factors for (eg, murmur of mitral stenosis) or the impact of (eg, evidence of heart failure) AF or complications (eg, CVS)

Electrocardiogram

Essential………….--The ECG should also be evaluated for the following information:

•Markers of nonelectrical cardiac disease, such as left ventricular hypertrophy (possible hypertension) or Q waves (possible coronary artery disease)•Markers of electrical heart disease, such as delta wave or short PR interval (preexcitation) or bundle branch block (conduction system disease) •The QT interval (to identify the potential risk of antiarrhythmic therapy).

Echocardiogram

--To evaluate the size of the right and left atria and the size and function of the right and left ventricles--To detect possible valvular heart disease, left ventricular hypertrophy, and pericardial disease--To assess peak right ventricular pressure.

--Transesophageal echocardiography is much more sensitive for identifying thrombi in the left atrium or left atrial appendage.

Additional testing

--Exercise testing :-For patients with signs or symptoms of ischemic heart disease (which is not a common cause of AF). -Help guide pharmacotherapy for AF as some antiarrhythmic medications are contraindicated in patients with coronary artery disease--Holter monitoring:-To identify the arrhythmia if it is intermittent and not captured on routine electrocardiography-To assess overall ventricular response rates, especially in individuals where a rate control strategy has been chosen--TSH should be obtained in all patients with AF--Complete blood count, a serum creatinine, an analysis for proteinuria, and a test for diabetes mellitus

EHRA score (for symptoms severity)

Classification of AF-related symptoms:EHRA I ‘No symptoms’EHRA II ‘Mild symptoms’; normal daily activity not affectedEHRA III ‘Severe symptoms’; normal daily activity affectedEHRA IV‘Disabling symptoms’; normal daily activitydiscontinued

CCS-SAF

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