13: Atrial/Flutter Fibrillation

Atrial/Flutter Fibrillation


Atrial fibrillation (AFib) is one of the most common types of cardiac arrhythmias, i.e., irregular heartbeats, which increases the risk of stroke, heart failure, and other cardiovascular‐related complications. During AFib, the heart’s two upper chambers (the atria) beat irregularly and out of coordination with the heart’s two lower chambers (the ventricles). In AFib, the electrical impulses are so fast and chaotic that the atria cannot contract and squeeze blood effectively into the ventricles (Pellman & Sheikh, 2015).

Episodes of AFib may be paroxysmal/transient in which the patient’s heart rhythm returns to normal automatically, or permanent, which require pharmacotherapy or other medical interventions to restore a normal heart rhythm. In some cases, AFib is caused by an underlying medical condition, such as myocardial infarction, pericarditis, pneumonia, pulmonary embolism, intravaginal thrombosis, and Wolff‐Parkinson‐White syndrome; however, in some patients there is no apparent reversible cause (absence of heart disease in clinical and laboratory evaluation) and AFib is considered idiopathic (Staerk, Sherer, Ko, Benjamin, & Helm, 2017). The definition and classification of AFib are presented in detail in Table 13.1.


The epidemiology of AFib is summarized in Figure 13.1. As with most heart‐related diseases, the incidence and prevalence of AFib are increasing globally. According to the available epidemiological data, between 1990 and 2010, there was a modest increase in the prevalence and a major increase in the incidence of AFib. In 2010, the prevalence rates per 100,000 population were 596.2 (95% uncertainty intervals [UI]: 558.4 to 636.7) in men (5% increase since 1990) and 373.1 (95% UI: 347.9 to 402.2) in women (4% increase since 1990), while AFib incidence per 100,000 population was 77.5 (95% UI: 65.2 to 95.4) in men (28% increase from 1990) and 59.5 (95% UI: 49.9 to 74.9) in women (35% increase from 1990). The estimated number of individuals with AFib globally in 2010 was 33.5 million (20.9 million men [95% UI: 19.5–22.2 million] and 12.6 million women [95% UI: 12.0–13.7 million]). Burden associated with AFib, measured as disability‐adjusted life‐years, increased by 18.8% (95% UI: 15.8–19.3) in men and 18.9% (95% UI: 15.8–23.5) in women from 1990 to 2010. For both men and women, the prevalence and incidence of AFib are disproportionately higher in high‐income nations compared with low‐income nations (Chugh et al., 2014).

Table 13.1 Definition and classification of atrial fibrillation.

Source: (Adapted from Hindricks et al., 2020).

Term Definition
AFib A supraventricular tachyarrhythmia with uncoordinated atrial electrical activation and consequently ineffective atrial contraction. Electrocardiographic characteristics of AFib include:

  • irregular R‐R intervals (when atrioventricular conduction is not impaired),
  • absence of distinct repeating P waves, and
  • irregular atrial activations.
Clinical AFib Symptomatic or asymptomatic AFib documented by surface ECG. The minimum duration of an ECG strip required to establish the diagnosis of clinical AF is ≥30 seconds, or an entire 12‐lead ECG.
AHRE, subclinical AFib Refers to individuals without symptoms attributable to AFib, in whom clinical AFib is not previously detected (that is, there is no surface ECG tracing of AFib).
AHRE ‐ events fulfilling programmed or specified criteria for AHRE that are detected by CIEDs with an atrial lead allowing automated continuous monitoring of atrial rhythm and tracings storage. CIED‐recorded AHRE need to be visually inspected because some AHRE may be electrical artifacts/false positives. Subclinical AFib includes AHRE confirmed to be AFib, AFL, or an AT, or AFib episodes detected by insertable cardiac monitor or wearable monitor and confirmed by visually reviewed intracardiac electrograms or ECG‐recorded rhythm.
First diagnosed AFib not diagnosed before, irrespective of its duration or the presence/severity of AFib‐related symptoms.
Paroxysmal AFib that terminates spontaneously or with intervention within 7 days of onset.
Persistent AFib that is continuously sustained beyond 7 days, including episodes terminated by cardioversion (drugs or electrical cardioversion) after ≥7 days.
Long‐standing persistent Continuous AFib of >12 months’ duration when decided to adopt a rhythm control strategy.
Permanent AFib that is accepted by the patient and physician, and no further attempts to restore/maintain sinus rhythm will be undertaken.
Permanent AF represents a therapeutic attitude of the patient and physician rather than an inherent pathophysiological attribute of AFib, and the term should not be used in the context of a rhythm control strategy with antiarrhythmic drug therapy or AFib ablation. Should a rhythm control strategy be adopted, the arrhythmia would be re‐classified as ‘long‐standing persistent AFib’.

Device‐programmed rate criterion for AHRE is ≥175 bpm, whereas there is no specific rate limit for subclinical AF. The criterion for AHRE duration is usually set at ≥5 min (mainly to reduce the inclusion of artifacts), whereas a wide range of subclinical AF duration cutoffs (from 10 to 20 seconds to >24 hours) is reported in studies of the association of subclinical AFib with thromboembolism. The reported duration refers to either the longest single episode or, more commonly, total duration of AHRE/subclinical AF during the specified monitoring period. Although not completely identical, the terms AHRE and subclinical AFib are often used interchangeably. Whereas a large body of high‐quality evidence from RCTs informing the management of AF patients pertains exclusively to ‘clinical’ AF (that is, the ECG documentation of AF was a mandatory inclusion criterion in those RCTs), data on the optimal management of AHRE and subclinical AFib are lacking. For this reason, AFib is currently described as either ‘clinical’ or ‘AHRE/subclinical’, until the results of several ongoing RCTs expected to inform the management of AHRE and ‘subclinical’ AF are available.

AHRE = atrial high‐rate episode; AFib = atrial fibrillation; ECG = electrocardiogram; AFL = atrial flutter; AT = atrial tachycardia; bpm = beats per minute; CIED = cardiac implantable electronic device; ECG = electrocardiogram; RCT = randomized controlled trial.

In the European Union, it is estimated that ~7.5 million people over 65 years old had AFib in 2016, and this number is expected to increase by 90%, i.e., to ~14.5 million, by 2060 (Di Carlo et al., 2019). Based on data from the Framingham heart study, the prevalence of AFib increased 3‐fold over the last 50 years in the USA. The lifetime risk of AFib was estimated at about 1 in 4 in white men and women older than 40 years in 2004, while a decade later, lifetime risk estimates reached about 1 in 3 for white individuals and 1 in 5 for black individuals. In the USA, at least 3 to 6 million people have AFib, and the numbers are projected to reach 6 to 16 million by 2050 (Kornej, Borschel, Benjamin, & Schnabel, 2020). In addition, there are more than 450,000 hospitalizations with AFib as the primary diagnosis each year in the USA, which leads to approximately 158,000 deaths (Benjamin et al., 2019). Based on Centers for Disease Control and Prevention data, white people are more likely to have AFib than African Americans. With regards to gender, AFib incidence is generally lower in women than men, however, women have a higher prevalence of AFib at older ages, a fact that can be attributed to women’s’ higher life expectancy and a more severe disease clinical presentation and symptomatology compared to men (Mohanty, Trivedi, Gianni, & Natale, 2018). Figure 13.2 presents important gender‐specific considerations in AFib epidemiology and treatment.


AFib is a multifactorial condition. Risk factors for AFib include increased age, hypertension, coronary artery disease, congenital heart diseases, mitral valve disease, cardiomyopathy, pericarditis, heart surgery, hyperthyroidism, obstructive sleep apnea, alcohol abuse, smoking, excessive caffeine consumption, atrial murmur, and several types of pulmonary diseases (Table 13.2) (Dilaveris & Kennedy, 2017; Ling, Kistler, Kalman, Schilling, & Hunter, 2016; Staerk et al., 2017).

In each patient, there may be a major mechanism that causes or maintains AFib, but often more than one mechanism coexists. In general, three mechanisms are considered predominant for the initiation and progression of AFib in most patients (Al‐Kaisey, Parameswaran, & Kalman, 2020; Bosch, Cimini, & Walkey, 2018; Iwasaki, Nishida, Kato, & Nattel, 2011):

Schematic illustration of epidemiology of atrial fibrillation: prevalence (upper panel); and lifetime risk and projected rise in the incidence and prevalence (lower panel).

FIGURE 13.1 Epidemiology of atrial fibrillation: prevalence (upper panel); and lifetime risk and projected rise in the incidence and prevalence (lower panel). AF = atrial fibrillation; AFL = atrial flutter; BP = blood pressure; CI = confidence interval; EU = European Union. a Smoking, alcohol consumption, body‐mass index, BP, diabetes mellitus (type 1 or 2), and history of myocardial infarction or heart failure. b Risk profile: optimal ‐ all risk factors are negative or within the normal range; borderline ‐ no elevated risk factors but >1 borderline risk factor; elevated ‐ >1 elevated risk factor.

Source: (Hindricks et al., 2020 / with permission of European Heart Journal).

Schematic illustration of gender-specific considerations in atrial fibrillation.

FIGURE 13.2 Gender‐specific considerations in atrial fibrillation. AF = atrial fibrillation; NPV = non‐PV; NOAC = novel oral anticoagulants; IV = intravenous; CAD = coronary artery disease; COPD = chronic obstructive pulmonary disease; QOL = quality of life.

Source: (Mohanty et al., 2018 / with permission of Taylor & Francis).

  • Autonomous nervous system. Autonomic nervous system activation can induce significant and heterogeneous changes in atrial electrophysiology and induce atrial tachyarrhythmias, including atrial tachycardia and AFib. In this context, neuromodulation may be helpful in controlling AFib. Potential therapeutic applications include ganglionated plexus ablation, renal sympathetic denervation, cervical vagal nerve stimulation, baroreflex stimulation, and cutaneous stimulation.
  • Electrophysiology of the pulmonary veins. Rapidly spreading foci, usually located in the smooth muscle that extends into the initial part of the pulmonary veins, are responsible for AFib in a subset of patients. Ablation of these foci and electrical isolation of the pulmonary veins from the myocardium of the left atrium can effectively treat atrial fibrillation in patients whose arrhythmia is due to this mechanism. This mechanism is of high importance in young individuals without organic heart disease.
  • Substrate abnormalities, i.e., pathological changes of the atrial myocardium. Beyond the impact of AFib itself on structural remodeling, several diseases, such as heart failure, valvular disease, hypertensive heart disease, and coronary heart disease contribute to the development of abnormal atrial substrate and create heterogeneity in the electrophysiological properties of the atrial myocardium. Promising emerging work suggests an important role for atrial substrate imaging in guiding substrate‐based ablation strategies and for risk factor management in reversing atrial remodeling.


Patients with AFib may have various symptoms, such as palpitations, dyspnea, fatigue, chest pain, poor effort tolerance, dizziness, syncope, and disordered sleep, but ~50–90% are initially asymptomatic with possibly a less favorable prognosis (Hindricks et al., 2020). Although many patients with AFib can live for years without significant complications, AFib is a wellestablished risk factor for cardiovascular diseases, including stroke, systolic embolism, left ventricular dysfunction, and heart failure and is associated with significant declines in quality of life and functional status as well as increased risk of hospitalization, cognitive impairment/dementia, and mortality (Figure 13.3) (Hindricks et al., 2020).

Table 13.2 Risk factors for atrial fibrillation.

Sources: (Dilaveris & Kennedy, 2017; Ling et al., 2016; Staerk et al., 2017).

  1. Increased age. AFib is closely related to age and is extremely rare in young individuals without underlying heart disease.

  1. Hypertension, i.e., increased blood pressure.

  1. Coronary artery disease, also known as coronary heart disease. In coronary artery disease, plaques form inside the coronary arteries, which supply the myocardium with oxygen‐enriched blood.

  1. Congenital heart diseases, i.e., problems with the structure of the heart that exist from birth. This includes malformations of the inner walls of the heart, valves or blood vessels that carry blood to and from the heart. Congenital abnormalities alter the normal flow of blood to the heart.

  1. Mitral valve disease, i.e., abnormal blood flow from the mitral valve, from the left ventricle to the left atrium of the heart.

  1. Cardiomyopathy, i.e., a serious disease in which the myocardium is inflamed or does not work as well as it should.

  1. Pericarditis, i.e., inflammation of the pericardium, the protective cover that surrounds the heart.

  1. Heart surgery, a significantly higher number of patients who have undergone heart surgery have AFib compared to the general population.

  1. Hyperthyroidism, i.e., the disease in which the thyroid gland is overactive.

  1. Obstructive sleep apnea, is a common disease in which the patient experiences breathing pauses during sleep due to obstructions of the upper airways. Obstructive sleep apnea often causes high blood pressure (hypertension), which increases the risk of cardiovascular diseases.

  1. Alcohol abuse. Systematic, excessive, long‐term alcohol consumption is closely associated with an increased risk of AFib. Studies have shown that the risk of atrial fibrillation is up to 45% higher in heavy drinkers compared to those who abstain from alcohol consumption.

  1. Smoking. It is a well‐established risk factor for AFib and other heart diseases.

  1. Excessive caffeine consumption. This includes overconsumption of coffee, energy drinks, and/or soft drinks containing caffeine.

  1. Atrial murmur. This is like AFib, but abnormal heart rhythms are less chaotic and better organized.

  1. Chest infections and pulmonary diseases, such as pneumonia, lung cancer, emphysema, pulmonary embolism, and carbon‐monoxide poisoning.

AFib = atrial fibrillation.

Stroke is probably the most well‐documented cardiovascular complication of AFib. In AFib, the chaotic heart rhythm may cause blood to pool in the heart’s upper chambers and form clots. Once a blood clot forms, it can dislodge from the heart and travel to the brain, causing an ischemic stroke. Patients with AFib are 5 to 7 times more likely to experience a stroke compared to the general population, and AFib is estimated as the cause of 15% to 20% of total ischemic strokes (Castellano, Chinitz, Willner, & Fuster, 2014; Kamel, Okin, Elkind, & Iadecola, 2016). Cardioembolic strokes associated with AFib are usually severe, highly recurrent, and often fatal, or with permanent disability (Hindricks et al., 2020). Clots from the heart can also travel to other parts or organs of the body, such as the kidneys, the lungs, and the gastrointestinal tract and cause significant damage (Jaakkola, Kiviniemi, & Airaksinen, 2018). AFib combined with a fast heart rate for a long period of time can also lead to heart failure, a pathophysiological state in which cardiac output is insufficient to meet the needs of the body and lungs, as described in Chapter 12 (Anter, Jessup, & Callans, 2009; Lee Park & Anter, 2013). Sharing common risk factors, AFib and heart failure often coexist, or may precipitate/exacerbate each other, which results in significantly greater mortality than either condition alone (Hindricks et al., 2020).


The complexity of AFib requires a multifaceted, holistic, and multidisciplinary management approach, with patients and clinicians in an active partnership. Streamlining the care of patients with AFib in daily clinical practice is a challenging but essential requirement for the effective management of AFib. In recent years, substantial progress has been made in the detection of AFib and its management.

The proper management of AFib starts with an accurate diagnosis through an in‐depth examination from the physician. In most patients, AFib can be easily recognized from the surface electrocardiogram with the presence of rapid, irregular fibrillatory waves, and irregular ventricular response (G. Y. Lip & Tse, 2007). After diagnosis, the atrial fibrillation better care (ABC) pathway can be used as an integrated approach for AFib management across all healthcare levels and among different specialties (G. Y. H. Lip, 2017). In the ABC pathway, A stands for “anticoagulation/avoid stroke”, B for “better symptom management” and C for “comorbidity optimization”. Compared with usual care, implementation of the ABC pathway has been associated with a lower risk of all‐cause mortality, lower risk of a composite outcome of stroke/major bleeding/cardiovascular death and hospitalization, lower rates of cardiovascular events, and lower health‐related costs (Hindricks et al., 2020).

The first step, “anticoagulation/avoid stroke”, aims to identify low‐risk patients who do not need antithrombotic therapy. Step 2 is to offer stroke prevention, i.e., oral anticoagulants, to those with ≥1 non‐sex stroke risk factors. Step 3 is the choice of an oral anticoagulant—a non‐vitamin K antagonist oral anticoagulant (given their relative effectiveness, safety, and convenience these drugs are generally the first choice as oral anticoagulant for stroke prevention in AFib) or vitamin K antagonist (Freedman, Potpara, & Lip, 2016; G. Y. Lip & Lane, 2015). The “better symptom control” step of the ABC pathway mainly focuses on heart rate control, which is an integral part of AFib management and is often sufficient to improve AFib‐related symptoms. Drug choices for heart rate control include beta‐blockers, calcium‐channel blockers, and digitalis as first‐line agents, with consideration of other sympatholytic in resistant cases (Hindricks et al., 2020

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Oct 25, 2023 | Posted by in CARDIOLOGY | Comments Off on 13: Atrial/Flutter Fibrillation

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