Atrial Fibrillation¶
Chapter 258 | Harrison's 22e · Part 6 – Cardiovascular Disorders
Detailed clinical reference synthesised from Harrison's Principles of Internal Medicine, 22nd Edition
🔑 Key Clinical Points¶
- See source text for full details
📑 Table of Contents¶
📋 Figures in This Chapter¶
| # | Type | Description |
|---|---|---|
| 1 | 🖼 Figure | CHADS-VASc and HAS-BLED systems |
| 2 | 🖼 Figure | Pulsed-field electroporation |
| 3 | 🖼 Figure | Electrocardiogram of an irregularly irregular heart rhythm without for this patient |
| 4 | 🖼 Figure | A |
| 5 | 🖼 Figure | Figure / Illustration |
RAW CONTENT¶
[PAGE 1947] Atrial Fibrillation 1947 CHAPTER 258 ■ FURTHER READING embolism, pericarditis, and cardiac surgery, where AF occurs in up to Brugada J et al: 2019 ESC Guidelines for the management of patients 50% of patients postoperatively. with supraventricular tachycardia. The task force for the management AF is clinically most typically defined by the pattern of episodes. of patients with supraventricular tachycardia of the European Society Paroxysmal AF is defined as a pattern of AF episodes that occur and of Cardiology (ESC) developed in collaboration with the Association terminate with a relatively short duration either spontaneously or by for European Paediatric and Congenital Cardiology (AEPC). Eur pharmacologic or electrical cardioversion, most commonly defined as Heart J 41:655, 2020. 7 days or less. Persistent AF refers to AF that occurs continuously for Callans DJ: Josephson’s Clinical Cardiac Electrophysiology: Techniques >7 days but 1 year. These descriptors for AF correlate Jalife J, Stevenson W (eds): Zipes and Jalife’s Cardiac Electrophysiol- somewhat with the underlying pathophysiology of AF. AF tends to be ogy: From Cell to Bedside, 8th ed. Philadelphia, Elsevier, 2022. a progressive condition, with, at this point, no definitive “cure” that will Joglar JA et al: 2023 ACC/AHA/ACCP/HRS Guideline for the completely eliminate AF durably in a predictable fashion. The patho- Diagnosis and Management of Atrial Fibrillation: A report of the physiology of AF, however, remains incompletely understood. Most American College of Cardiology/American Heart Association Joint data support a multifactorial process that leads to the development of Committee on Clinical Practice Guidelines. J Am Coll Cardiol manifest AF. Clinical and epidemiologic studies have demonstrated 83:109, 2024. that, in addition to cardiovascular disease, age, alcohol use, obesity, hypertension, diabetes mellitus, and sleep-disordered breathing are associated with higher risk of developing AF. The proposed pathophys- iology suggests a “final common pathway” of these risk factors leading to electrophysiologic changes in atrial tissues. Alterations in regulation of membrane channels and other proteins result in abnormal electrical excitability. Atrial tissues, in particular pulmonary vein musculature, exhibit enhanced automaticity, resulting in ectopic beats (premature 258 Atrial Fibrillation atrial contractions), as shown in Fig. 258-2. Bouts of rapid atrial ectopy may then initiate either atrial tachycardia or frank AF. Additional cel- William H. Sauer, Jorge E. Romero, lular and, eventually, tissue remodeling results in abnormal conduction properties throughout the atria, including, in particular, shortening of Paul C. Zei atrial tissue refractory periods. This enables sustained AF through a combination of rapid automaticity-based “drivers” and areas of func- tional reentry. Further remodeling leads to the development of fibrosis PATHOPHYSIOLOGY AND EPIDEMIOLOGY and left atrial enlargement (Table 258-1). Atrial fibrillation (AF) is a cardiac arrhythmia characterized by seemingly These functional and anatomic changes in atrial tissues appear to disorganized, rapid, and irregular atrial electrical activation, resulting in correlate with the progression of clinical AF. AF tends to be a progres- loss of organized atrial mechanical contraction. These rapid and irregular sive disease in most, although exceptions occur. Typically, for a period electrical signals input into the atrioventricular (AV) node, which deter- of time, patients experience sporadic ectopic beats and short runs of mines ventricular activation and rate. The conducted ventricular rate is atrial tachycardia, likely originating from the pulmonary veins, preced- variable, resulting in an irregular, usually rapid ventricular rate, ranging ing the onset of frank AF. typically between 110 and 160 beats/min in most. In some patients, the Other regions of the atria have been demonstrated to produce ecto- sustained ventricular rate can exceed 200 beats/min, whereas in others pic depolarizations that may trigger AF; these include the posterior with either high vagal tone or AV nodal conduction disease, the ven- wall of the left atrium and muscular tissue sleeves within the superior tricular rate may be excessively slow (Fig. 258-1). vena cava, coronary sinus, or the remnant of the vein of Marshall. The disorganized atrial activation is best appreciated in lead V for When enough frequent bursts of ectopic beats/tachycardia and/or 1 this patient. AF is the most common sustained arrhythmia; as a result, changes in underlying substrate support the maintenance of AF for it is a major public health issue. Prevalence increases with age, with short periods, the patient develops episodes of paroxysmal AF. In the
95% of AF patients >60 years of age. The prevalence in humans over untreated patient, over time, as the electrical, contractile, and structural age 80 is ~20%. The lifetime risk of developing AF for men aged 40 years remodeling continues to progress, episodes of paroxysmal AF may be old is ~25%. AF is slightly more common in men than women and prolonged to the point of not terminating spontaneously, the hallmark more common in whites than blacks. Risk factors for developing AF in of persistent AF. After further remodeling, not only do patients con- addition to age and underlying cardiac disease include hypertension, tinue to long-standing persistent AF but also the efficacy of therapeutic diabetes mellitus, cardiac disease, family history of AF, obesity, thyroid interventions to restore sinus rhythm diminishes. disease, and sleep-disordered breathing. AF is not a benign condition, CLINICAL PRESENTATION AND with a 1.5- to 1.9-fold increased risk of mortality after controlling for underlying cardiac disease. Perhaps the most important consequence MANIFESTATIONS of AF is a significantly increased risk of stroke compared to the general The clinical manifestations of AF result from (1) symptoms related population, causing ~25% of all strokes. AF has been detected up to to the irregular, often rapid but sometimes slow ventricular rates that 8.9% of patients within 6 months following cryptogenic stroke using result; (2) the hemodynamic consequences of altered cardiac function; insertable cardiac monitors. (3) the consequences of cardioembolic phenomena; and/or (4) the The risk of dementia is increased in patients with AF, as is the risk impact of AF on cardiovascular function over time. AF is diagnosed of magnetic resonance imaging (MRI)-detected asymptomatic embolic by electrocardiogram (ECG), either by 12-lead standard ECG, limited infarct. AF, most often when ventricular rate remains uncontrolled for lead ambulatory monitor ECG and implantable loop recorders, with prolonged periods, increases the risk of developing congestive heart findings of lack of organized atrial activity (no P wave), with an irregu- failure and cardiomyopathy. Moreover, as a corollary, patients with lar ventricular response. The role of screening populations for AF is underlying heart disease, in particular cardiomyopathy and conges- evolving with the use of wearable monitors and home ECG capabilities. tive heart failure, are at higher risk for developing AF. AF is a marker With irregular, rapid ventricular rates, there is variable cardiac dis- for worsened morbidity and mortality in patients with existing heart placement and contraction, resulting in the sensation of palpitations disease, although the precise extent of the independent risk increase and awareness of the heartbeat, when of course, in a normal rhythm, associated with AF in heart disease is unclear. AF may, on occasion, be most humans do not sense each heartbeat. Interestingly, many patients associated with an identifiable precipitating fac
Figures & Illustrations¶
Reproduced from Harrison's 22nd Edition.
Figure 1¶
Caption: FIGURE 258-3 CHADS-VASc and HAS-BLED systems. The CHADS-VASc scoring system gives a poin 2 t fo 2 r each outlined stroke risk factor, where 2 as 2 the HAS-BLED scoring system gives a point for each bleeding risk factor, as outlined in the table. In the chart below the table, the corresponding risk of stroke (CHADS-VASC) or major 2 2 bleed event (HAS-BLED) is plotted as a percent risk per annum as a function of score. F, female; INR, international normalized ratio; TIA, transient ischemic attack.
Figure 2¶
Caption: FIGURE 258-5 Pulsed-field electroporation. (Top) Pulsed-field ablation has the structures or cells such as red blood cells, nerves, the esophagus, or arteries. (Bottom) pulse-field ablation; a combination of most of these parameters will eventually help in currently undergoing clinical evaluation for pulsed-field ablation (PFA). (Reproduced Review. Rev Cardiovasc Med 24:337, 2023 and Reproduced with permission from NA cease to concern us. J Cardiovasc Electrophysiol 33:1489, 2022.) (A) Farawave, from Medtronic; (C) Sphere-9, reproduced with permission from Medtronic; (D) Varipulse. ablation of atrial low-voltage myocardium in addition to pulmonary vein isolation significantly improved outcomes in patients with persistent AF in one study. Similarly, in patients with persistent AF,
Figure 3¶
Caption: FIGURE 258-1 Electrocardiogram of an irregularly irregular heart rhythm without for this patient.
Figure 4¶
Caption: FIGURE 258-4 A. (Left) Electroanatomic map superimposed on a cardiac computed this chamber. (Middle) Final radiofrequency lesion set around the pulmonary veins. (Right) vein (PV) ectopy initiating fibrillatory conduction contained within the isolated vein while
Figure 5¶
Caption: Figure 5
Generated from Harrison's Principles of Internal Medicine, 22nd Edition.