The Mechanisms of Atrial Fibrillation

Chen, Peng‐Sheng; Chou, Chung-Chuan; Tan, Alex Y.; Zhou, Shengmei; Fishbein, Michael C.; Hwang, Chun; Karagueuzian, Hrayr S.; Lin, Shien‐Fong

doi:10.1111/j.1540-8167.2006.00626.x

Cited by 51 publications

(29 citation statements)

References 65 publications

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“…By necessitating more rapid fluid removal in a compressed timeframe, shorter dialysis sessions expose patients to greater fluid shifts with attendant myocardial stunning and ischemia (15), intradialytic hypotension, hemodynamic destabilization (16), and resultant interruptions of end-organ perfusion. The cumulative consequences of these cardiac stresses have been linked to maladaptive changes in left ventricular geometry such as hypertrophy and fibrosis with derivative heart failure and conduction system abnormalities (15,(17)(18)(19)(20)(21)(22). Shorter dialysis sessions may also detrimentally affect survival through limiting removal of phosphorus, b2-microglobulin, and other middle molecules (23)(24)(25).…”

Section: Discussionmentioning

confidence: 99%

“…Chronic volume overload promotes maladaptive cardiac structural changes (e.g., left ventricular hypertrophy and fibrosis) through direct activation of the mammalian target of rapamycin pathway (26-28) and through upregulation of the sympathetic nervous system and renin-angiotensin-aldosterone pathways (29,30). This, in turn, distorts cardiac conduction pathway architecture and predisposes patients to arrhythmias and sudden cardiac death (18)(19)(20)(21)(22). Delineating the independent associations of IDWG and DSL with mortality has important therapeutic implications.…”

Section: Discussionmentioning

confidence: 99%

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Disentangling the Ultrafiltration Rate–Mortality Association

Flythe

Curhan

Brunelli

2013

Clinical Journal of the American Society of Nephrology

103

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SummaryBackground and objectives Rapid ultrafiltration rate is associated with increased mortality among hemodialysis patients. Ultrafiltration rates are determined by interdialytic weight gain and session length. Although both interdialytic weight gain and session length have been linked to mortality, the relationship of each to mortality, independent of the other, is not adequately defined. This study was designed to evaluate whether shorter session length independent of weight gain and larger weight gain independent of session length are associated with increased mortality.Design, setting, participants, & measurements Data were taken from a national cohort of 14,643 prevalent, thriceweekly, in-center hemodialysis patients dialyzing from 2005 to 2009 (median survival time, 25 months) at a single dialysis organization. Patients with adequate urea clearance and delivered dialysis session $240 and ,240 minutes were pair-matched on interdialytic weight gain (n=1794), and patients with weight gain #3 and .3 kg were pair-matched on session length (n=2114); mortality associations were estimated separately.Results Compared with delivered session length $240, session length ,240 minutes was associated with increased all-cause mortality (adjusted hazard ratio [95% confidence interval], 1.32 [1.03 to 1.69]). Compared with weight gain #3, weight gain .3 kg was associated with increased mortality (1.29 [1.01 to 1.65]). The associations were consistent across strata of age, sex, weight, and weight gain and session length. Secondary analyses demonstrated dose-response relationships between both and mortality.Conclusions Among patients with adequate urea clearance, shorter dialysis session length and greater interdialytic weight gain are associated with increased mortality; thus, both are viable targets for directed intervention.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Disentangling the Ultrafiltration Rate–Mortality Association

Flythe

Curhan

Brunelli

2013

Clinical Journal of the American Society of Nephrology

103

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“…Fibrosis also promotes arrhythmia. If fibrous tissue with high electrical resistance is interposed between cardiomyocytes, it will cause local delay in the spread of the action potential favoring the development of reentry types of arrhythmia, both ventricular and atrial (28,29).…”

Section: Cardiac Fibrosis and Microvessel Diseasementioning

confidence: 99%

The Challenge of Sudden Death in Dialysis Patients

Ritz¹,

Wanner²

2008

Clinical Journal of the American Society of Nephrology

114

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A 60-yr-old patient with ESRD (82 kg/168 cm), hypertension for the previous 18 yr, and type 2 diabetes is found dead in bed by his wife at home on a Saturday morning. The patient's history is notable for having started dialysis 34 weeks previously. His last dialysis had been the previous day (on a Friday afternoon). Predialysis potassium had been 5.7 mmol/L, the dialysate K ϩ was 2.0 mmol/L, and Mg 2ϩ was 0.5 mmol/L. Autopsy was not performed.Before his morbid event, the patient had been doing well on dialysis. He had less than 6 episodes of hypotension (Ͻ100 mmHg) per month. His average predialytic weight gain was 4 kg, and, with fluctuations, his average predialysis BP was 155/65 mmHg. While continuing on gliquidone (an oral sulfonylurea hypoglycemic drug that does not accumulate in renal failure), he had no episodes of hypoglycemia, and his last glycosylated hemoglobin level was 7.2%. His medical history is of hypertension, type 2 diabetes, and left ventricular hypertrophy (LVH) with an ejection fraction of 55%. His electrocardiogram showed signs of LVH and flat T waves. He had no history of hypoglycemic episodes and no evidence of retinopathy. He reported no episodes of arrhythmia or precordial pain. A predialysis chest x-ray 2 wk before the terminal event had shown pulmonary congestion. His medications included 0.25 g/d calcitriol, calcium carbonate, 10 mg of folate, 80 mg of verapamil, and no ␤ blockers. In addition, he received varying doses of darbepoietin and iron gluconate as required. He did not receive a statin. Dr. Eberhard Ritz: This case, unfortunately, is the usual presentation of patients on dialysis who succumb to sudden death: There are few, if any, specific premonitory symptoms or signs, cardiac standstill is usually the presenting symptom, and autopsy is not performed, so more specific information on underlying cardiac pathology, if any, is not available. The lack of pathoanatomic confirmation of the underlying pathology or pathologies-as in this case-continues to remain a problem that in the future should come onto the radar screen of nephrologists.Nevertheless, this case presentation raises a number of unresolved issues and provides an occasion to discuss how the currently unsatisfactory results might be improved in the future. In this context, it is of interest to have a look at the recent 4D study.

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“…An attractive but disputed hypothesis is that cardiac muscle in pulmonary veins contains pacemaker cells that would generate spontaneous activity (5,24). Quantitative surveys of ion channel currents in isolated cardiac myocytes have looked for differences that might account for an increased tendency toward automatic activity in the pulmonary vein (1,12,21).…”

mentioning

confidence: 99%

Catecholaminergic automatic activity in the rat pulmonary vein: electrophysiological differences between cardiac muscle in the left atrium and pulmonary vein

Doisne¹,

Maupoil²,

Cosnay³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Doisne N, Maupoil V, Cosnay P, Findlay I. Catecholaminergic automatic activity in the rat pulmonary vein: electrophysiological differences between cardiac muscle in the left atrium and pulmonary vein. Am J Physiol Heart Circ Physiol 297: H102-H108, 2009. First published May 8, 2009 doi:10.1152/ajpheart.00256.2009.-Ectopic activity in cardiac muscle within pulmonary veins (PVs) is associated with the onset and the maintenance of atrial fibrillation in humans. The mechanism underlying this ectopic activity is unknown. Here we investigate automatic activity generated by catecholaminergic stimulation in the rat PV. Intracellular microelectrodes were used to record electrical activity in isolated strips of rat PV and left atrium (LA). The resting cardiac muscle membrane potential was lower in PV [Ϫ70 Ϯ 1 (SE) mV, n ϭ 8] than in LA (Ϫ85 Ϯ 1 mV, n ϭ 8). No spontaneous activity was recorded in PV or LA under basal conditions. Norepinephrine (10 Ϫ5 M) induced first a hyperpolarization (Ϫ8 Ϯ 1 mV in PV, Ϫ3 Ϯ 1 mV in LA, n ϭ 8 for both) then a slowly developing depolarization (ϩ21 Ϯ 2 mV after 15 min in PV, ϩ1 Ϯ 2 mV in LA) of the resting membrane potential. Automatic activity occurred only in PV; it was triggered at approximately Ϫ50 mV, and it occurred as repetitive bursts of slow action potentials. The diastolic membrane potential increased during a burst and slowly depolarized between bursts. Automatic activity in the PV was blocked by either atenolol or prazosine, and it could be generated with a mixture of cirazoline and isoprenaline. In both tissues, cirazoline (10 Ϫ6 M) induced a depolarization (ϩ37 Ϯ 2 mV in PV, n ϭ 5; ϩ5 Ϯ 1 mV in LA, n ϭ 5), and isoprenaline (10 Ϫ7 M) evoked a hyperpolarization (Ϫ11 Ϯ 3 mV in PV, n ϭ 7; Ϫ3 Ϯ 1 mV in LA, n ϭ 6). The differences in membrane potential and reaction to adrenergic stimulation lead to automatic electrical activity occurring specifically in cardiac muscle in the PV. atrium; norepinephrine; electrophysiology; atrial fibrillation; thoracic veins THE CAUSE OF FOCAL ELECTRICAL activity in myocardial sleeves within the pulmonary veins (6, 14) which can trigger and sustain atrial fibrillation in humans is unknown.A number of themes have been developed to address possible causes of ectopic activity in the pulmonary veins. An attractive but disputed hypothesis is that cardiac muscle in pulmonary veins contains pacemaker cells that would generate spontaneous activity (5, 24). Quantitative surveys of ion channel currents in isolated cardiac myocytes have looked for differences that might account for an increased tendency toward automatic activity in the pulmonary vein (1,12,21). Extensive studies have been made to determine whether cardiac muscle in pulmonary veins is more prone than the left atrium to develop arrhythmogenic phenomena such as early and delayed afterdepolarizations (EADs and DADs) due to differences in Ca 2ϩ handling and/or tachycardia-triggered activity (5, 34). The irregular orientation of cardiac muscle fibers in the pulmonary vein has been suggested to lead t...

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The Mechanisms of Atrial Fibrillation

Cited by 51 publications

References 65 publications

Disentangling the Ultrafiltration Rate–Mortality Association

Disentangling the Ultrafiltration Rate–Mortality Association

The Challenge of Sudden Death in Dialysis Patients

Catecholaminergic automatic activity in the rat pulmonary vein: electrophysiological differences between cardiac muscle in the left atrium and pulmonary vein

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