Left Atrial Activity Following Cardioversion

Logan, W.F.W.E.; Rowlands, Dewi K.; Howitt, G.; Holmes, A.M.

doi:10.1016/s0140-6736(65)91427-3

Cited by 70 publications

(24 citation statements)

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“…Parallel evidence from experimental AF demonstrated that loss of atrial contractility after cardioversion is followed by a partial or full functional recovery even though the amount of fibrosis persists. 24,25 However, improvement in LA function in our study was limited (Table 4 and Figure 2) and did not occur in patients with the longest AFr duration of Ն59 days. The data again imply that there is a limit to LA dilation beyond which the atrium is no longer responsive to a pharmacological intervention or, less likely, that a longer exposure is necessary to achieve a therapeutic response.…”

mentioning

confidence: 55%

Left Atrial Remodeling and Response to Valsartan in the Prevention of Recurrent Atrial Fibrillation

Staszewsky

Wong

Masson

et al. 2011

Circ: Cardiovascular Imaging

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on behalf of GISSI-AF Investigators* Background-Left atrial (LA) dilation precedes or appears early after the onset of atrial fibrillation (AF) and factors in perpetuating the arrhythmia. Angiotensin receptor blockers were proposed for reversing LA remodeling. We evaluated the effect of valsartan on LA remodeling in patients with a recent episode of AF and the effect of LA size on AF recurrence (AFr). Methods and Results-LA and left ventricular (LV) echocardiographic variables were measured at baseline and 6 and 12 months in 340 patients from GISSI-AF, a trial testing valsartan prevention of AFr. Reversal of remodeling was considered as a decrease in LA size over 12 months. Changes in patients with and without recurrence and the relationship to duration of AFr were analyzed. Patients were 68.4Ϯ8.8 years old, with history of hypertension (85.3%) and cardioversion in the previous 2 weeks (87.4%) or Ն2 AFr in the previous 6 months (40.4%). Baseline LA maximal volume (LAVmax) was severely increased (Ͼ40 mL/m 2 ); LV dimensions and function were relatively normal. Over 12 months, 54.4% of patients had AFr. LAVmax was unchanged by rhythm, time, or randomized treatment. Higher baseline LAVmax and lower LA emptying fraction were linearly related to increasing AFr duration during follow-up. T he hypothesis that long-term renin-angiotensin system (RAS) inhibition could reverse the left atrial (LA) remodeling process and thereby contribute to the prevention of atrial fibrillation recurrence (AFr) was formally tested in the double-blind, randomized, Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico-Atrial Fibrillation (GISSI-AF) trial. 1,2 The entirely neutral results of the study were somewhat surprising, 3 given the wealth of positive evidence. Data from experimental AF implicated RAS in the remodeling associated with atrial electric heterogeneity, ab- Received March 7, 2011; accepted August 9, 2011 Clinical Perspective on p 728 Conclusions-GISSI-AFPost hoc analyses of clinical trials in patients with left ventricular dysfunction showed that ACE inhibitors and angiotensin receptor blockers (ARBs) reduced the onset of new AF, 10,11 and, in prospective studies of patients after cardioversion of paroxysmal and persistent AF, RAS inhibitors in addition to amiodarone prevented recurrences of AF. 12 We report the results from the GISSI-AF echo study that explored whether the expected effect of valsartan to reverse LA remodeling would prevent AF recurrences. In addition, left atrial volume (LAV) and LV anatomy and function were assessed to estimate left ventricular resistance to LA emptying. MethodsThe GISSI-AF trial was a double-blind, randomized, placebocontrolled, multicenter study that enrolled 1442 patients in sinus rhythm with a history of AF to test whether the ARB valsartan could reduce the recurrence of AF (see Expanded Methods, Patients in the GISSI-AF Main Study, in the online-only Data Supplement). The primary end points were time to the first recurrence of AF and the proportion of patients w...

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confidence: 55%

Left Atrial Remodeling and Response to Valsartan in the Prevention of Recurrent Atrial Fibrillation

Staszewsky

Wong

Masson

et al. 2011

Circ: Cardiovascular Imaging

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“…Afterward, AF was maintained for 5 days. During these 5 days, the maintenance of AF was briefly interrupted at 6,12,24,48,72,96, and 120 h of AF. Thirty minutes after spontaneous termination of AF, the atrial contractile function was studied at different pacing rates.…”

Section: Methodsmentioning

confidence: 99%

“…It has been proposed that mild impairment of ventricular pump function due to the high ventricular rate during AF might increase end-diastolic ventricular and atrial pressures (12). An alternative explanation might be that the pronounced atrial contractile dysfunction of the atria induced by AF (6,7,10) underlies the dilatation of fibrillating atria. In theory, loss of contractility in fibrillating atria is expected to increase atrial compliance and size.…”

mentioning

confidence: 99%

Loss of atrial contractility is primary cause of atrial dilatation during first days of atrial fibrillation

Schotten¹,

Haan²,

Neuberger³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Allessie. Loss of atrial contractility is primary cause of atrial dilatation during first days of atrial fibrillation. Am J Physiol Heart Circ Physiol 287: H2324 -H2331, 2004. First published July 15, 2004 doi: 10.1152/ajpheart.00581.2004.-Atrial fibrillation (AF) induces a progressive dilatation of the atria which in turn might promote the arrhythmia. The mechanism of atrial dilatation during AF is not known. To test the hypothesis that loss of atrial contractile function is a primary cause of atrial dilatation during the first days of AF, eight goats were chronically instrumented with epicardial electrodes, a pressure transducer in the right atrium, and piezoelectric crystals to measure right atrial diameter. AF was induced with the use of repetitive burst pacing. Atrial contractility was assessed during sinus rhythm, atrial pacing (160-, 300-, and 400-ms cycle length), and electrically induced AF. The compliance of the fibrillating right atrium was measured during unloading the atria with diuretics and loading with 1 liter of saline. All measurements were repeated after 6, 12, and 24 h of AF and then once a day during the first 5 days of AF. Recovery of the observed changes after spontaneous cardioversion was also studied. After 5 days of AF, atrial contractility during sinus rhythm or slow atrial pacing was greatly reduced. During rapid pacing (160 ms) or AF, the amplitude of the atrial pressure waves had declined to 20% of control. The compliance of the fibrillating atria increased twofold, whereas the right atrial pressure was unchanged. As a result, the mean right atrial diameter increased by ϳ12%. All changes were reversible within 3 days of sinus rhythm. We conclude that atrial dilatation during the first days of AF is due to an increase in atrial compliance caused by loss of atrial contractility during AF. Atrial compliance and size are restored when atrial contractility recovers after cardioversion of AF. stunning; remodeling; atrial tachyarrhythmias A RELATIONSHIP between atrial size and atrial fibrillation (AF) was first proposed by Fraser and Turner in 1955 (1), who showed that AF was more common in patients with enlarged atria than in patients with normal atrial size. In the 1990s, large prospective trials established left atrial enlargement as an independent risk factor for the development of AF (13,14). Today, it is generally accepted that AF is not only a consequence but also a cause of atrial dilatation. In patients with "lone AF," Sanfilippo et al. (9) demonstrated that AF resulted in progressive atrial dilatation, which in turn, might contribute to the self-perpetuating nature of the arrhythmia.The mechanism of atrial dilatation related to AF is still unclear. It has been proposed that mild impairment of ventricular pump function due to the high ventricular rate during AF might increase end-diastolic ventricular and atrial pressures (12). An alternative explanation might be that the pronounced atrial contractile dysfunction of the atria induced by AF (6, 7, 10) underlies the dilatation of ...

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“…It has long been recognized that AF causes atrial hypocontractility, 16 and the role of atrial contractile dysfunction in the thromboembolic complications of AF is well appreciated. 8 Even very short-term AF (5 to 15 minutes) can cause contractile dysfunction, but normal contraction resumes within minutes of rhythm reversion after such brief episodes, whereas persistent hypocontractility (lasting Ն24 hours) follows AF episodes lasting days to weeks.…”

Section: Previous Studies Of Atrial Hypocontractility Mechanismsmentioning

confidence: 99%

Multiple Potential Molecular Contributors to Atrial Hypocontractility Caused by Atrial Tachycardia Remodeling in Dogs

Wakili

Yeh

et al. 2010

Circ: Arrhythmia and Electrophysiology

109

102

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Background-Atrial fibrillation impairs atrial contractility, inducing atrial stunning that promotes thromboembolic stroke.Action potential (AP)-prolonging drugs are reported to normalize atrial hypocontractility caused by atrial tachycardia remodeling (ATR). Here, we addressed the role of AP duration (APD) changes in ATR-induced hypocontractility. Methods and Results-ATR (7-day tachypacing) decreased APD (perforated patch recording) by Ϸ50%, atrial contractility (echocardiography, cardiomyocyte video edge detection), and [Ca 2ϩ ] i transients. ATR AP waveforms suppressed [Ca 2ϩ ] i transients and cell shortening of control cardiomyocytes; whereas control AP waveforms improved [Ca 2ϩ ] i transients and cell shortening in ATR cells. However, ATR cardiomyocytes clamped with the same control AP waveform had Ϸ60% smaller [Ca 2ϩ ] i transients and cell shortening than control cells. We therefore sought additional mechanisms of contractile impairment. Whole-cell voltage clamp revealed reduced I CaL ; I CaL inhibition superimposed on ATR APs further suppressed [Ca 2ϩ ] i transients in control cells. Confocal microscopy indicated ATR-impaired propagation of the Ca 2ϩ release signal to the cell center in association with loss of t-tubular structures. Myofilament function studies in skinned permeabilized cardiomyocytes showed altered Ca 2ϩ sensitivity and force redevelopment in ATR, possibly due to hypophosphorylation of myosin-binding protein C and myosin light-chain protein 2a (immunoblot). Hypophosphorylation was related to multiple phosphorylation system abnormalities where protein kinase A regulatory subunits were downregulated, whereas autophosphorylation and expression of Ca 2ϩ -calmodulin-dependent protein kinase II␦ and protein phosphatase 1 activity were enhanced. Recovery of [Ca 2ϩ ] i transients and cell shortening occurred in parallel after ATR cessation. Conclusions-Shortening of APD contributes to hypocontractility induced by 1-week ATR but accounts for it only partially. Additional contractility-suppressing mechanisms include I CaL current reduction, impaired subcellular Ca 2ϩ signal transmission, and altered myofilament function associated with abnormal myosin and myosin-associated protein phosphorylation. The complex mechanistic basis of the atrial hypocontractility associated with AF argues for upstream therapeutic targeting rather than interventions directed toward specific downstream pathophysiological derangements. 3 This study aimed to (1) evaluate the role of APD changes in hypocontractility induced by 1-week ATR, (2) determine whether APD changes alone were insufficient to account for contraction abnormalities, and (3) assess in detail other potential contributors. MethodsThis section includes essential methodologies. Additional details are found in the online-only Data Supplement. Animal ModelAll animal care and handling procedures were in accordance with National Institutes of Health guidelines (http://oacu.od.nih.gov/ training/index.htm) and were reviewed and appr...

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Left Atrial Activity Following Cardioversion

Cited by 70 publications

References 0 publications

Left Atrial Remodeling and Response to Valsartan in the Prevention of Recurrent Atrial Fibrillation

Left Atrial Remodeling and Response to Valsartan in the Prevention of Recurrent Atrial Fibrillation

Loss of atrial contractility is primary cause of atrial dilatation during first days of atrial fibrillation

Multiple Potential Molecular Contributors to Atrial Hypocontractility Caused by Atrial Tachycardia Remodeling in Dogs

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