QJM Advance Access originally published online on September 6, 2006
QJM 2006 99(10):717-718; doi:10.1093/qjmed/hcl099
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Heart failure: be aware of reversible causes
Sir,Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. There is wide recognition that AF is an important risk factor for thromboembolic events, particularly stroke. A less well-recognized (but nonetheless important) consequence of prolonged and usually unrecognized AF is left ventricular dysfunction, which resolves with treatment of the atrial fibrillation.
A 50-year-old man developed breathlessness on exertion, and a cough productive of streaky haemoptysis. He had just returned from a recent business trip to the Middle East. Admission to hospital was precipitated by acute severe breathlessness. On examination, he looked unwell, with jaundice, ascites and gross oedema. He was in fast atrial fibrillation at 150 bpm, with a blood pressure of 92/60 mmHg. There were no murmurs. Liver and renal function tests were abnormal: creatinine 163 µmol/l; bilirubin 71 µmol/l. He was treated with intravenous dobutamine, nitrate, diuretics and amiodarone. Echocardiography revealed dilated cardiac chambers (left ventricle 6.8 cm in diastole and 5.6 cm in systole) with globally and severely impaired left and right ventricular function. Left ventricular ejection fraction was 20%. A coronary angiogram showed normal coronary arteries. A cardiac MRI study was performed, which revealed no evidence of myocarditis or infarction. A myocardial biopsy was taken, which was reported as normal. Initially, he was thought to be a possible candidate for heart transplantation but after treatment with ACE inhibitors, beta blockers and diuretics, there was good clinical improvement with reduction in the patient's heart rate. After 10 days he reverted to sinus rhythm. On discharge from hospital he was asymptomatic. On follow-up, the patient remained in sinus rhythm and denied any limiting symptoms. A repeat echocardiogram, 7 months after presentation, demonstrated marked improvement in left ventricular function (ejection fraction 60%; left ventricular diastolic dimension 5.3 cm and systolic dimension 4.0 cm). In addition, there was a notable reduction in cardiac size on follow-up chest X-ray (Figures 1 and 2).
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Left ventricular dysfunction in the presence of AF is believed to be a consequence of the rapid ventricular response to the atrial arrhythmia causing a tachycardia-induced cardiomyopathy.1,2 This was clearly described in 1913 by Gossage and Braxton Hicks in one of the first monographs on atrial fibrillation.3
This case illustrates the importance of identifying patients in whom atrial fibrillation is the cause rather than the consequence of left ventricular dysfunction. Pointers include the presence of AF with a rapid ventricular rate, mild rather than severe left ventricular dilatation, the lack of any other apparent cause of the heart failure (normal coronary arteries, normal thyroid function, no history of drug or alcohol abuse). As has been demonstrated in the above case, treatment of the underlying tachycardia results in positive left ventricular remodelling with resolution of ventricular dilatation, normalization of systolic function and complete resolution of symptoms of heart failure. Tachycardia-induced cardiomyopathy is one of the few reversible causes of heart failure.2,4 Recovery of ventricular function can be variable and depends on the duration of the tachycardia, as well as co-existent heart disease. Ventricular improvement occurs most quickly in the first weeks after correction of the tachycardia, with a period of slow improvement for up to 6–8 months.5 Furthermore, recurrent tachycardia can cause rapid decline in left ventricular function and development of heart failure in patients with previously treated tachycardia-induced cardiomyopathy. Sudden death has also been reported in such cases.6 It is thus important not only to recognize and treat this condition, but also to prevent recurrence.
Department of Cardiology
Queen Elizabeth Hospital
Edgbaston
Birmingham
email: arif.sayqa{at}uhb.nhs.uk
References
1. Khasnis A, Jongharangsin K, Abela G, Veerareddy S, Reddy V, Thakur R. Tachycardia-Induced Cardiomyopathy: A Review of Literature. Pacing Clin Electrophysiol 2005; 28:710–21.[CrossRef][Medline]
2. Grogan M, Smith HC, Gersh BJ, et al. Left ventricular dysfunction due to atrial fibrillation in patients initially believed to have idiopathic dilated cardiomyopathy. Am J Cardiol 1992; 69:1570–3.[CrossRef][Web of Science][Medline]
3. Gossage AM and Braxton Hicks JA. On auricular fibrillation. Q J Med 1913; 6:435–40.
4. Packer DL, Bardy GH, Worley SJ, et al. Tachycardia-induced cardiomyopathy: a reversible form of left ventricular dysfunction. Am J Cardiol 1986; 57:563–70.[CrossRef][Web of Science][Medline]
5. Maisel WH and Stevenson LW. Atrial fibrillation in Heart Failure: Epidemiology, Pathophysiology and Rationale for Therapy. Am J Cardiol 2003; 91:Suppl., 2–8D.
6. Nerheim P, Birger-Botkin S, Piracha L, Olshanky B. Heart Failure and Sudden Death in Patients with Tachycardia-Induced Cardiomyopathy and Recurrent Tachycardia. Circulation 2004; 110:247–52.
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