Pulmonary vein dilatation: another possible crosslink between left atrial enlargement and atrial fibrillation?

The interplay between left atrial (LA) dilatation and atrial fibrillation (AF) has been well established, but the underlying mechanisms of this vicious circle are not fully understood. Recent studies indicated that pulmonary vein (PV) dilatation is implicated in the development of AF. On the other hand, PV dilatation has been associated with LA dilatation. It is therefore reasonable to assume that PV dilatation represents a common pathophysiologic pathway between LA enlargement and AF.     

Atrial fibrillation in heart failure: the chicken or the egg?

Atrial fibrillation (AF) and heart failure (HF) are the emerging epidemics of cardiovascular disease in the new millennium. Both are responsible for considerable morbidity and mortality and health budget expenditure. The advent of catheter ablation for patients with AF has provided important new insights into the relative contribution of AF to left ventricular dysfunction. The aim of this review is to discuss the complex interplay in the pathophysiology of AF and HF to improve our understanding of the basis for current treatment strategies and guide future research direction.     

Atrial fibrillation: A progressive atrial myopathy or a distinct disease?

Atrial fibrillation is a complex arrhythmia with multiple possible mechanisms. A lot of experimental and clinical studies have shed light on the pathophysiological mechanisms of arrhythmia, especially on molecular basis. Electrical, contractile and structural remodeling, calcium handling abnormalities, autonomic imbalance and genetic factors seem to play a crucial role in atrial fibrillation initiation and maintenance. However, the exact pathophysiological mechanisms of atrial fibrillation are not completely understood and whether atrial fibrillation is an unclassified cardiomyopathy or a distinct disease still remains to be answered. This review highlights proarrhythmic and pathophysiological mechanisms of atrial fibrillation and approaches the molecular basis underlying atrial fibrillation susceptibility.     

Is left atrial appendage occlusion useful for prevention of stroke or embolism in atrial fibrillation?

Since in atrial fibrillation more than 90% of the thrombi are located in the left atrial appendage, an "elimination" of the left atrial appendage, either by resection or occlusion, seems an attractive alternative to oral anticoagulation. Although frequently regarded as an useless appendage, data from animal and human investigations show that the left atrial appendage may play an important role in the maintenance and regulation of the cardiac function, especially in arterial hypertension, atrial fibrillation, coronary heart disease, valvular heart disease and heart failure. Elimination of the left atrial appendage may impede thirst in hypovolemia, deteriorate hemodynamic responses to volume or pressure overload, decrease cardiac output and promote heart failure. Instead of preventing stroke, the consequences of left atrial appendage elimination may create new risk factors for stroke and thus might induce more harm than benefit to patients with atrial fibrillation. As long as the physiologic and pathophysiologic role of the left atrial appendage is not fully understood, left atrial appendage elimination should not be an alternative to oral anticoagulation.     

Atrial amyloidosis and atrial fibrillation: a gender-dependent "arrhythmogenic substrate"?

This editorial refers to "Amyloid deposition as a cause of atrialremodelling in persistent valvular atrial fibrillation"¹ byO. Leone et al. on page 1237 Atrial fibrillation (AF) is known to cause significant changesin atrial tissue architecture and electrophysiology.^1,2 It hasbecome clear over recent years that pre-existing alterations,such as autonomic dysbalance, degenerative tissue changes andfibrosis, can provide an electrophysiological and morphologicalsubstrate, which increases the likelihood of AF. In particular,alterations of the interstitial matrix in atrial tissue seemto be significant contributory factors.¹ Increased amounts offibrous tissue in fibrillating human atria were reported asearly as 30 years ago³ and it is known to impair cell-to-cell