Dataset Information

Liver Disease as a Predictor of New-Onset Atrial Fibrillation.

ABSTRACT: Background Impact of liver disease on development of atrial fibrillation ( AF ) is unclear. The purpose of the study was to evaluate prevalence of AF in the setting of liver disease and whether increasing severity of liver disease, using Model for End-Stage Liver Disease ( MELD ), is independently associated with increased risk of AF . Methods and Results Retrospective data analysis of 1727 patients with liver disease evaluated for liver transplantation between 2006 and 2015 was performed, and patient characteristics were analyzed from billing codes and review of medical records. Multivariable time-dependent Cox proportional hazards model was performed to determine effect of increasing MELD score on risk of developing AF . Prevalence of AF was 11.2%. Incidence of AF at median follow-up time of 1.04 years was 8.5%. Both prevalence and incidence of AF increased with increasing MELD scores. Prevalence of AF was 3.7%, 6.4%, 16.7%, and 20.2% corresponding with MELD quartiles 1 to 10, 11 to 20, 21 to 30, and >30, respectively. Compared with patients with MELD quartile 1 to 10, patients with MELD quartile of 11 to 20 had hazard ratio of 2.73 (confidence interval, 1.47-5.07), those in the MELD quartile of 21 to 30 had a hazard ratio of 5.17 (confidence interval, 2.65-10.09), and those with MELD values >30 had hazard ratio of 9.33 (confidence interval, 3.93-22.14) for development of new-onset AF . Other significant variables associated with new-onset AF were age, sleep apnea, valvular heart disease, hemodynamic instability, and reduced left ventricular ejection fraction <50% (hazard ratio, of 1.06, 2.17, 3.21, 2.00, and 2.44, respectively). Conclusions Prevalence and incidence of AF in patients with liver disease is high. Severity of liver disease, as measured by MELD , is an important predictor of new-onset AF . This novel finding suggests an interaction between inflammatory and neurohormonal changes in liver disease and pathogenesis of AF .

SUBMITTER: Huang WA

PROVIDER: S-EPMC6201455 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature

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Liver Disease as a Predictor of New-Onset Atrial Fibrillation.

Huang William A WA Dunipace Eric A EA Sorg Julie M JM Vaseghi Marmar M

Journal of the American Heart Association 20180801 15

Background Impact of liver disease on development of atrial fibrillation ( AF ) is unclear. The purpose of the study was to evaluate prevalence of AF in the setting of liver disease and whether increasing severity of liver disease, using Model for End-Stage Liver Disease ( MELD ), is independently associated with increased risk of AF . Methods and Results Retrospective data analysis of 1727 patients with liver disease evaluated for liver transplantation between 2006 and 2015 was performed, and p ...[more]

PMID: 30371253

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Project description:CONTEXT:Although the heritability of atrial fibrillation (AF) is established, the contribution of familial AF to predicting new-onset AF remains unknown. OBJECTIVE:To determine whether familial occurrence of AF is associated with new-onset AF beyond established risk factors. DESIGN, SETTING, AND PARTICIPANTS:The Framingham Heart Study, a prospective community-based cohort study started in 1948. Original and Offspring Cohort participants were aged at least 30 years, were free of AF at the baseline examination, and had at least 1 parent or sibling enrolled in the study. The 4421 participants in this analysis (mean age, 54 [SD, 13] years; 54% women) were followed up through December 31, 2007. MAIN OUTCOME MEASURES:Incremental predictive value of incorporating different features of familial AF (any familial AF, premature familial AF [onset ?65 years old], number of affected relatives, and youngest age of onset in a relative) into a risk model for new-onset AF. RESULTS:Across 11,971 examinations during the period 1968-2007, 440 participants developed AF. Familial AF occurred among 1185 participants (26.8%) and premature familial AF occurred among 351 participants (7.9%). Atrial fibrillation occurred more frequently among participants with familial AF than without familial AF (unadjusted absolute event rates of 5.8% and 3.1%, respectively). The association was not attenuated by adjustment for AF risk factors (multivariable-adjusted hazard ratio, 1.40; 95% confidence interval [CI], 1.13-1.74) or reported AF-related genetic variants. Among the different features of familial AF examined, premature familial AF was associated with improved discrimination beyond traditional risk factors to the greatest extent (traditional risk factors, C statistic, 0.842 [95% CI, 0.826-0.858]; premature familial AF, C statistic, 0.846 [95% CI, 0.831-0.862]; P = .004). Modest changes in integrated discrimination improvement were observed with premature familial AF (2.1%). Net reclassification improvement (assessed using 8-year risk thresholds of <5%, 5%-10%, and >10%) did not change significantly with premature familial AF (index statistic, 0.011; 95% CI, -0.021 to 0.042; P = .51), although categoryless net reclassification was improved (index statistic, 0.127; 95% CI, 0.064-0.189; P = .009). CONCLUSIONS:In this cohort, familial AF was associated with an increased risk of AF that was not attenuated by adjustment for AF risk factors including genetic variants. Assessment of premature familial AF was associated with a very slight increase in predictive accuracy compared with traditional risk factors.

Project description:RationaleAtrial fibrillation (AF) is encountered rarely in pregnancy. Management of maternal AF is challenging as it poses a threat to both maternal and fetal well-being.Patient concernsWe report a case of a 35 weeks pregnant woman who presented in emergency with sudden-onset palpitations and mild shortness of breath with no personal/family history of cardiac diseases.DiagnosesPatient's pulse was irregularly irregular with an average rate of 179 beats per minute. The obstetric examination was normal.DiagnosisHigh-sensitive cardiac troponin T (hs-cTnT) was elevated. The 12 lead electrocardiogram (ECG) confirmed AF. The obstetric ultrasound, electronic fetal heart rate (EFHR) trace, and maternal echocardiography were normal.InterventionsThe patient was admitted under joint cardiology and obstetric care and monitored with continuous telemetry. She was commenced on a therapeutic dose of low-molecular weight heparin (LMWH) and intravenous fluid. She received a single 200 Joule synchronized direct current (DC) shock under general anesthesia in operation theater, which reverted the rhythm back to normal. EFHR monitoring was normal pre- and post-DC cardioversion. We acknowledge the unwise use of therapeutic dose of LMWH before DC cardioversion (DCCV) because of a potential need for emergency cesarean delivery for maternal and/or fetal compromise.OutcomeThe patient remained well and in sinus rhythm after cardioversion. She was discharged home the following day on Flecainide (anti-arrhythmic) and therapeutic dose of low molecular weight heparin (LMWH) and followed up in outpatient clinics frequently. She had a baby at term and received prophylactic LMWH for 10 days post-cesarean. She was discharged from cardiology clinic when she was 10 weeks postnatal, and Flecainide was discontinued.LessonsWe are reporting this case because of the rarity of the condition and successful use of DCCV for treating maternal AF. High-sensitive cardiac troponin T (hs-cTnT) level is a useful laboratory indicator to gauge the severity of AF in pregnancy. We emphasize to make the arrangements for EFHR monitoring and potential cesarean delivery and advocate cautious use of thromboprophylaxis while planning for electrical cardioversion (ECV) for maternal AF.

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Dataset Information

Liver Disease as a Predictor of New-Onset Atrial Fibrillation.

Publications

Liver Disease as a Predictor of New-Onset Atrial Fibrillation.

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