Atrial Fibrillation
I. Epidemiology
II. Diagnosis
III. Causes and Research Implications
IV. Pathophysiology
V. Classification and Management VI. Anticoagulants VII. Electronic Pacing
GLOSSARY
arrhythmia general term for an irregularity or rapidity of the
heartbeat, an abnormal heart rhythm. cardiomyopathy heart muscle disease. heart failure failure of the heart to pump sufficient blood from
the chambers into the aorta; inadequate supply of blood
reaches organs and tissues. myocardial infarction death of an area of heart muscle due to
blockage of a coronary artery by blood and atheroma; medical
term for a heart attack or coronary thrombosis. tachycardia increase in heart rate exceeding 100 beats per
minute. torsades de pointes a very serious, life-threatening ventricular
arrhythmia. valvular disorders disease of heart valves, particularly mitral
stenosis, mitral regurgitation, aortic stenosis, and aortic
regurgitation. Wolff-Parkinson-White syndrome characterized by premature
excitation of the ventricles due to an anomalous conduction
bypass tract between the atria and ventricles; often leads to
rapid heart rates.
THE TERM ATRIAL FIBRILLATION IS USED TO describe an abnormal rhythm of the heartbeat; instead of beating regularly, the heart beats very erratically. The irregular heartbeats may speed up, and the heart rate may be as fast as 120–180 beats per minute. These fast and strong beats may be sensed as palpitations. Atrial fibrillation is the most common persistent heart rhythm abnormality observed in medical practice.
- I. EPIDEMIOLOGY
Atrial fibrillation is a common arrhythmia found in greater than 1% of persons older than 60 years. This rate rises to above 5% in people older than 69, and increases to more than 10% in people older than 79. Prevalence of this disorder increases dramatically with age, but it is also becoming more prevalent with time, even after adjustment for age and underlying structural heart disease. More than 85% of patients with atrial fibrillation are older than 65. In the elderly this disorder causes substantial morbidity including stroke, heart failure, and hospitalization. Patients require an anticoagulant to prevent stroke; this therapy occasionally causes cerebral hemorrhage and requires bothersome laboratory testing every 2 weeks. - II. DIAGNOSIS
Diagnosis of atrial fibrillation is based on history, clinical examination, and confirmation with an ECG. The patient may experience rapid and irregular heartbeats usually from one to several hours. Associated symptoms include mild shortness of breath that can become severe if serious underlying heart disease is present. During atrial fibrilla¬tion the atrium does not contract normally and blood is therefore not delivered rapidly into the left ventricle. Poor filling of the ventricle and the fast ventricular rate may cause a fall in blood pressure resulting in lightheadedness and dizziness. Because the atrium is fibrillating and notcontracting, there is stasis of blood in the atrial appendage. Stasis predisposes the patient to clot formation and these thrombi may be dislodged and fly into the circulation and travel to other organs (embolize). The embolus can block an artery in the brain and cause a stroke. - III. CAUSES AND RESEARCH IMPLICATIONS
Diseases or disorders that cause atrial fibrillation are shown in Fig. 2. Due to the vast number of both serious diseases and disorders that cause atrial fibrillation, it is not sur¬prising that a definitive cure is rarely possible. This has become most frustrating for cardiologists and technologists who strive to provide advances in technologic equipment and strategies for the management of atrial fibrillation.The prevention of atrial fibrillation is therefore of para¬mount importance. There has been little focus in the past 20 years on the prevention of this abnormality. - IV. PATHOPHYSIOLOGY
During the past 50 years different theories have been proposed to explain the mechanism underlying atrial fibrillation, but many controversies surrounded these mechanisms. In the past decade it seems well accepted that both focal and reentrant mechanisms are involved, playing a different role in the initiation and perpetuation of the arrhythmia. Several recent human multielectrode mapping systems and other studies indicate that in atrial fibrillation the dominant mechanism incorporates multiple meandering wavelets, both in the acute and chronic form of this condition. Multiple wavelengths of excitation propagate around the atrial myocardium and the arrhyth¬mia is perpetuated because of an abnormal atrial tissue substrate, particularly in patients with structural heart disease and permanent atrial fibrillation. Patients with paroxysmal atrial fibrillation with no evidence of structural heart disease appear to have a trigger-predominant mechanism, but the two basic mechanisms reflect a large overlap. After very long periods of permanent atrial fibrillation, if sinus rhythm is restored, reverse remodeling usually fails to occur. This may explain why in patients with persistent atrial fibrillation for more than 12 months it is difficult to maintain sinus rhythm following cardioversion. - V. CLASSIFICATION AND MANAGEMENT A. Acute Atrial Fibrillation
An episode of atrial fibrillation observed within 48 h of its onset is described as acute. If the ventricular rate is greater than 160 beats per minute and results in acute cardio¬vascular decompensation manifested by hypotension, shortness of breath, chest pain, confusion, or heart failure, the rhythm should be converted to normal sinus rhythm. DC cardioversion is usually the initial treatment of choice. - VI. ANTICOAGULANTS A. Warfarin
Patients with atrial fibrillation considered high risk for stroke require anticoagulation with warfarin to maintain an INR of 2–3 to prevent stroke. An INR of 1.4–1.9 has been shown to be associated with a stroke or mortality rate similar to that for an INR of less than 1.5. The loss of atrial contraction leads to stasis of blood in the atrium and is more marked in the left atrial appendage, the most common site for clot formation. Stasis is accompanied by hypercoagulability and there is increased concentrations of fibrinogen and fibrin D-dimer and increased concentra¬tions of von Willebrand factor. These derangements all contribute to the development of a prothrombotic state and embolization. Five randomized clinical trials indicate that warfarin anticoagulation reduces the risk of stroke by 68% and lowers mortality by 33%. The risk of hemorrhagic complications, particularly cerebral hemor¬rhage, rises greatly when the INR exceeds 3.9. Patients on oral anticoagulants should have blood tests every 2–3 weeks to maintain an INR of 2–3 in order to prevent serious hemorrhagic events. In patients over 80 years of age and in those with small risk of bleeding, the INR is maintained at 1.8–2.8. Patients at high risk for bleeding are not given anticoagulants. - VII. ELECTRONIC PACING
It is known that conversion of atrial fibrillation to sinus rhythm does not improve survival. The reason for trying to maintain sinus rhythm is mainly to control symptoms. Neither antiarrhythmic drugs nor atrial pacing alone have been successful in suppressing atrial fibrillation.