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      Augmentation of Pulmonary Vein Backflow Velocity during Left Atrial Contraction: A Novel Phenomenon Responsible for Progression of Atrial Fibrillation in Hypertensive Patients

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          Background: Atrial fibrillation (AF) is a common arrhythmia showing disease progression. However, echocardiographic prediction of such progression remains incomplete. This study aimed to identify echocardiographic predictors of AF progression in hypertensive patients. Methods: Hypertensive patients with paroxysmal AF were divided into two groups: patients with AF which became permanent (group A; n = 13) and those with AF which remained paroxysmal (group B; n = 46) during the same follow-up period (8.0 ± 2.4 years). Clinical baselines showed no significant differences except for age. Transthoracic echocardiography was recorded 1–2 weeks after termination of the first-detected paroxysms of AF. Results: Echocardiography showed greater left atrial (LA) dimension (p = 0.023) and late diastolic pulmonary vein (PV) backflow velocity (p < 0.001), and a lower LA fractional shortening (p = 0.008) in group A than in group B. Multilogistic regression analysis demonstrated that augmented PV backflow (p = 0.007) and reduced LA fractional shortening (p = 0.032) were independent predictors of the progression of AF. The receiver-operating characteristic curve demonstrated that PV backflow augmentation is the best predictor of future AF perpetuation. Conclusion: PV backflow leading to cyclic stretching of PV musculature contributes to AF progression.

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          Most cited references 18

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          Electrical, contractile and structural remodeling during atrial fibrillation.

          The natural history of atrial fibrillation (AF) is characterized by a gradual worsening with time. The recent finding that AF itself produces changes in atrial function and structure has provided a possible explanation for the progressive nature of this arrhythmia. Electrical remodeling (shortening of atrial refractoriness) develops within the first days of AF and contributes to an increase in stability of AF. However, 'domestication of AF' must also depend on a 'second factor' since the persistence of AF continues to increase after electrical remodeling has been completed. Atrial contractile remodeling (loss of contractility) leads to a reduced atrial transport function after cardioversion of AF. An important clinical consequence is that during several days after restoration of sinus rhythm, the risk of atrial thrombus formation is still high. In addition, the reduction of atrial contractility during AF may enhance atrial dilatation which may add to the persistence of AF. Tachycardia-induced structural remodeling takes place in a different time domain (weeks to months). Myolysis probably contributes to the loss of atrial contractile force. Although it might explain the loss of efficacy of pharmacological cardioversion and the development of permanent AF, the role of structural remodeling in the progression of AF is still unclear. Atrial structural remodeling also occurs as a result of heart failure and other underlying cardiovascular diseases. The associated atrial fibrosis might explain intra-atrial conduction disturbances and the susceptibility for AF. Thus, both AF itself and the underlying heart disease are responsible for the development of the arrhythmogenic substrate. New strategies for prevention and termination of AF should be build on our knowledge of the mechanisms and time course of AF-induced atrial remodeling.
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            Structural correlate of atrial fibrillation in human patients.

            We tested the hypothesis that structural remodeling of cellular connections, alterations in the expression of connexins (Cx), and an increase in fibrosis represent anatomic substrates of atrial fibrillation (AF). In 31 patients with AF undergoing a Maze procedure and 22 patients in sinus rhythm (SR), biopsies were taken intraoperatively from the right atrial (RA) free wall and appendages and investigated with immunoconfocal and electron microscopy. All patients with AF exhibited a concomitant lateralization of gap junctional proteins Cx43 and Cx40, and N-cadherin (the major mechanical junction protein), instead of being confined to the intercalated discs, as observed in SR. These results were confirmed by quantitative immunoconfocal analysis and electron microscopy. Among diverse junctional proteins, in AF, Cx40 was markedly heterogeneous in distribution. As compared with the SR group, Cx43 was significantly decreased in AF by 57% in RA appendages and by 56% in RA free wall. Cx40 was reduced by 54% in appendages, but had a tendency to be increased in the RA free wall. Collagen I was significantly higher in AF than in SR by 48% in RA appendages and by 69% in the RA free wall tissues. The structural correlate of AF comprises extensive concomitant remodeling of mechanical and electrical junctions, reduction of Cx43, heterogeneous distribution of Cx40 in terms of different amounts of Cx40 in different RA tissues or in spatially adjacent regions of atrial myocardium. These changes, together with augmentation of fibrosis, may underlie localized conduction abnormalities and contribute to initiation and self-perpetuation of re-entry pathways and AF.
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              Impaired left atrial mechanical function after cardioversion: relation to the duration of atrial fibrillation.

              We hypothesized that the time course of the recovery of atrial systolic function may be related to the duration of atrial fibrillation before cardioversion and sought to study noninvasively the recovery of left atrial mechanical function utilizing serial transthoracic Doppler studies. Recovery of atrial mechanical function may be delayed for several weeks after successful cardioversion of atrial fibrillation to sinus rhythm. After successful cardioversion, 60 patients with atrial fibrillation of brief ( 2 to 6 weeks, 22 patients) or prolonged (> 6 weeks, 21 patients) duration were followed up with serial transmitral pulsed Doppler echocardiography immediately (60 patients) and at 24 h (45 patients), 1 week (41 patients), 1 month (31 patients) and > 3 months (30 patients) after cardioversion. Atrial mechanical function is greater immediately and at 24 h and 1 week after cardioversion in patients with "brief" compared with "prolonged" atrial fibrillation. In all groups, atrial mechanical function increases over time, ultimately achieving similar levels. Full recovery of atrial mechanical function, however, is achieved within 24 h in patients with brief atrial fibrillation, within 1 week in patients with moderate-duration atrial fibrillation and within 1 month in patients with prolonged atrial fibrillation. Recovery of left atrial mechanical function is related to the duration of atrial fibrillation before cardioversion. These findings have important implications for assessing the early hemodynamic benefit of successful cardioversion.

                Author and article information

                S. Karger AG
                December 2007
                10 July 2007
                : 109
                : 1
                : 33-40
                aDepartment of Medicine, Kyushu University, bFukuoka Wajiro Hospital and cIshihara Cardiovascular Hospital, Fukuoka, Japan
                105324 Cardiology 2008;109:33–40
                © 2007 S. Karger AG, Basel

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                Page count
                Figures: 3, Tables: 2, References: 30, Pages: 8
                Original Research


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