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Atrial fibrillation is target organ damage caused by an impaired haemodynamic state
  1. Kristian Wachtell
  1. Department of Cardiology, Section for Cardiology Intervention, Division of Cardiovascular and Pulmonary Diseases, Oslo University Hospital, Oslo, Norway
  1. Correspondence to Dr Kristian Wachtell, Division of Cardiovascular and Pulmonary Diseases, Department of Cardiology, Section for Cardiology Intervention, Oslo University Hospital, Oslo 0315, Norway; kristian{at}wachtell.net

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Although the phenotype presentation of atrial fibrillation may have many causes, the most common aetiology is pressure overload as hypertension and the consequent cardiac changes in left atrial and ventricular structure and function.

What is increasingly clear is that atrial fibrillation should not solely be regarded as a disease entity with electrical disturbances. Increasing evidence supports that atrial fibrillation is caused by an unfavourable haemodynamic state or frank hypertension. In fact, hypertensive heart disease and other pressure overload states (eg, aortic stenosis)1 are strong predictors of atrial fibrillation due to both structural and functional changes in the left atrium and left ventricle.

The changes in the haemodynamic state by increased blood pressure have many direct effects on left atrial and ventricular structure and function. Since the first report that angiotensin-converting enzyme inhibition (ACEI) reduced the incidence of atrial fibrillation in patients with acute myocardial infarction, there have been many reports that treatment with either ACEI or angiotensin receptor blockers reduces the risk of atrial fibrillation.2 These reports have led to further research into the pathophysiology of atrial fibrillation caused by pressure overload and hypertensive heart disease.

One of the central parts of the developing atrial fibrillation from hypertension is the increased afterload that in turn changes left ventricular geometry with increased left ventricular mass and relative wall thickness as a response to the increased end-systolic stress. These changes in left ventricular structure have a direct impact on enlarging left atrial size as well as stretching the pulmonary veins from where atrial fibrillation often originates. This stretching of cells in the left atrium and the pulmonary veins leads to cellular …

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