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Prognosis and Management of Atrial Fibrillation in Patients Without Structural Heart Disease

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Prognosis and Management of Atrial Fibrillation in Patients Without Structural Heart Disease Prognosis and Management of Atrial Fibrillation in Patients Without Structural Heart Disease M. DI BIASE,R.TROCCOLI Atrial fibrillation (AF), the most common sustained cardiac rhythm distur- bance, is increasing in prevalence as the population ages. Although it is often associated with heart disease, AF occurs in many patients with no detectable disease. AF may be related to acute, temporary causes, including alcohol intake (‘holiday heart syndrome’), surgery, electrocution, myocardial infarction, pericarditis, myocarditis, pulmonary embolism or other pulmonary diseases, and hyperthyroidism or other metabolic disorders. In such cases, successful treatment of the underlying condition may eliminate AF.AF may be associat- ed with another supraventricular tachycardia, the Wolff-Parkinson-White (WPW) syndrome, or atrioventricular (AV) nodal re-entrant tachycardias, and treatment of these primary arrhythmias reduces the incidence of recur- rent AF. AF is a common early postoperative complication of cardiac or tho- racic surgery. Specific cardiovascular conditions associated with AF include valvular heart disease (most often mitral valve disease), coronary artery dis- ease, and hypertension, particularly when left ventricular hypertrophy is present. In addition, AF may be associated with hypertrophic or dilated car- diomyopathy or with congenital heart disease, especially atrial septal defect in adults. The list of aetiologies also includes restrictive cardiomyopathies (such as amyloidosis, haemochromatosis, and endomyocardial fibrosis), car- diac tumours, and constrictive pericarditis. Other heart diseases, such as mitral valve prolapse even without mitral regurgitation, calcification of the mitral annulus, cor pulmonale, and idiopathic dilation of the right atrium, have been associated with a high incidence of AF. AF is commonly encoun- Institute of Cardiology, University of Foggia, Foggia, Italy 118 M.Di Biase,R.Troccoli tered in patients with the sleep apnoea syndrome, but whether the arrhyth- mia is provoked by hypoxia or another biochemical abnormality or mediated by changes in pulmonary dynamics or right atrium factors has not been determined. AF and Hyperthyroidism AF occurs in 10–25% of patients with hyperthyroidism, more commonly in men and the elderly than in women or patients less than 75 years old [1, 2]. Treatment is primarily directed toward restoring a euthyroid state, which is usually associated with a spontaneous reversion to sinus rhythm. Anti- arrhythmic drugs and electrical cardioversion are generally unsuccessful while the thyrotoxic condition persists [3, 4]. β-Blockers are somewhat effec- tive in controlling the ventricular rate in this situation, and aggressive treat- ment with intravenous β-blockers is particularly important in cases of thy- roid storm, for which high doses may be required. Calcium channel antago- nists may also be useful [4]. Although specific evidence is lacking in AF caused by hyperthyroidism, oral anticoagulation is recommended to prevent systemic embolism [5]. AF and Pulmonary Diseases Supraventricular arrhythmias, including AF, are common in patients with chronic obstructive lung disease [6, 7] and have adverse prognostic implica- tions in patients with acute exacerbations of chronic obstructive pulmonary disease [8]. Treatment of the underlying lung disease and correction of hypoxia and acid–base imbalance are of primary importance. AF and Wolff-Parkinson-White Syndrome AF may induce ventricular fibrillation and sudden death in patients with the WPW syndrome when atrial impulses are conducted antegrade across a bypass tract. This complication is feared but infrequent. The incidence of sudden death ranges from 0 to 0.6% per year in patients with WPW syn- drome. Radiofrequency ablation of the accessory pathway is usually the pre- ferred therapy for patients with pre-excitation syndromes and AF. Anti- arrhythmic drugs may be useful in selected cases. Digoxin should be avoided because of the risk of paradoxical acceleration of the ventricular rate during AF. β-Blockers do not decrease conduction over accessory pathways during Prognosis and Management of Atrial Fibrillation in Patients Without Structural Heart Disease 119 pre-excited periods of AF and could cause hypotension or other complica- tions in patients with tenuous haemodynamics. AF and Pregnancy AF is rare during pregnancy [9] and is usually associated with another underlying cause, such as mitral stenosis [10], congenital heart disease [11], or hyperthyroidism [12]. A rapid ventricular response to AF can have serious haemodynamic consequences for both the mother and the fetus. In a preg- nant woman who develops AF, diagnosis and treatment of the underlying condition causing the dysrhythmia is the first priority. The ventricular rate should be controlled with digoxin, a β-blocker, or a calcium channel antago- nist [13–15]. References 1. Davidson E, Weinberger I, Rotenberg Z et al (1989) Atrial fibrillation: cause and time of onset. Arch Intern Med 149:457–459 2. Agner T, Almdal T, Thorsteinsson B et al (1984) A reevaluation of atrial fibrillation in thyrotoxicosis. Dan Med Bull 31:157–159 3. Nakazawa HK, Sakurai K, Hamada N et al (1982) Management of atrial fibrillation in the post-thyrotoxic state. Am J Med 72:903–906 4. Clozel JP,Danchin N, Genton P et al (1984) Effects of propranolol and of verapamil on heart rate and blood pressure in hyperthyroidism. Clin Pharmacol Ther 36:649 5. Hirsh J (1991) Oral anticoagulant drugs. N Engl J Med 324:1865–1875 6. Shih HT, Webb CR, Conway WA et al (1988) Frequency and significance of cardiac arrhythmias in chronic obstructive lung disease. Chest 94:44–48 7. Hudson LD, Kurt TL, Petty TL et al (1973) Arrhythmias associated with acute respi- ratory failure in patients with chronic airway obstruction. Chest 63:661–665 8. Fuso L, Incalzi RA, Pistelli R et al (1995) Predicting mortality of patients hospitali- zed for acutely exacerbated chronic obstructive pulmonary disease. Am J Med 98:272–277 9. Bhanderi AK, Isher N (1998) Cardiac arrhythmias and pregnancies. In: Gleicher N, Galbraith RM, Gall SA, Buttino L, Sibai BM (eds) Principles and practice of medical therapy in pregnancy. Appleton & Lange, Stanford, pp 975–987 10. Bryg RJ, Gordon PR, Kudesia VS et al (1989) Effect of pregnancy on pressure gra- dient in mitral stenosis. Am J Cardiol 63:384–386 11. Whittemore R, Hobbins JC, Engle MA (1982) Pregnancy and its outcome in women with and without surgical treatment of congenital heart disease. Am J Cardiol 50:641–651 12. Forfar JC, Miller HC, Toft AD (1979) Occult thyrotoxicosis: a correctable cause of ‘idiopathic’ atrial fibrillation. Am J Cardiol 44:9–12 13. Page RL (1995) Treatment of arrhythmias during pregnancy. Am Heart J 130:871–876 14. Cox JL, Gardner MJ (1998) Cardiovascular drugs in pregnancy and lactation. In: 120 M.Di Biase,R.Troccoli Gleicher N, Galbraith RM, Gall SA, Buttino L, Sibai BM (eds) Principles and practi- ce of medical therapy in pregnancy. Appleton & Lange, Stanford, pp 911–926 15. Chow T, Galvin J, McGovern B (1998) Antiarrhythmic drug therapy in pregnancy and lactation. Am J Cardiol 82:58I–62I.
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