Older Adults at Risk for Atrial Fibrillation Lack Knowledge and Confidence to Seek Treatment for Signs and Symptoms.

Early detection of atrial fibrillation (AF) is crucial for averting AF-related stroke and heart failure, but treatment is delayed when AF is not recognized. The critical need for early detection and treatment requires education to promote AF awareness. Knowledge deficits, attitudes, and beliefs about AF that should be addressed to improve awareness and reduce treatment-seeking delay in older adults at risk for developing AF have not been well documented. The purpose of this study was to describe knowledge, treatment-seeking attitudes, and beliefs about AF in adults ⩾ 65 years old and identify demographic characteristics associated with knowledge, attitudes, and beliefs. Patients with no history of AF recruited from an academic medical center were interviewed using the Knowledge, Attitudes, and Beliefs about Atrial Fibrillation Survey. Data were analyzed using descriptive statistics and independent t tests. Participants (N = 180) were 63% male with a mean age of ±3.± 6.0 years, and 52% held ⩾ 4-year college degree. About one third could not identify common symptoms of AF including palpitations (31%), chest pain (36%), dyspnea (30%), and fatigue (35%). A majority (84%) lacked confidence to recognize AF, and 58% were not sure when they should seek care for AF symptoms. Nearly a third (32%) believed palpitations are always present with AF, and 74% believed that low energy would not be their only symptom of AF. Higher scores for AF Symptom Knowledge (p = .02) were observed in females, and General Knowledge about AF was greater for younger participants (p < .001). Participants lacked knowledge and confidence to aid decision-making for treatment-seeking for symptoms of AF and held inaccurate beliefs about AF that could hinder early treatment-seeking. Programs to promote AF awareness should explain the spectrum of symptoms that may be manifested by AF and include action plans for responding to symptoms

Genetic Risk and Atrial Fibrillation in Patients with Heart Failure

Aims: To study the association between an atrial fibrillation (AF) genetic risk score with prevalent AF and all-cause mortality in patients with heart failure. Methods and results: An AF genetic risk score was calculated in 3759 European ancestry individuals (1783 with sinus rhythm, 1976 with AF) from the BIOlogy Study to TAilored Treatment in Chronic Heart Failure (BIOSTAT-CHF) by summing 97 single nucleotide polymorphism (SNP) alleles (ranging from 0–2) weighted by the natural logarithm of the relative SNP risk from the latest AF genome-wide association study. Further, we assessed AF risk variance explained by additive SNP variation, and performance of clinical or genetic risk factors, and the combination in classifying AF prevalence. AF was classified as AF or atrial flutter (AFL) at baseline electrocardiogram and/or a history of AF or AFL. The genetic risk score was associated with AF after multivariable adjustment. Odds ratio for AF prevalence per 1-unit increase genetic risk score was 2.12 (95% confidence interval 1.84–2.45, P = 2.15 × 10−24) in the total cohort, 2.08 (1.72–2.50, P = 1.30 × 10−14) in heart failure with reduced ejection fraction (HFrEF) and 2.02 (1.37–2.99, P = 4.37 × 10−4) in heart failure with preserved ejection fraction (HFpEF). AF-associated loci explained 22.9% of overall AF SNP heritability. Addition of the genetic risk score to clinical risk factors increased the C-index by 2.2% to 0.721. Conclusions: The AF genetic risk score was associated with increased AF prevalence in HFrEF and HFpEF. Genetic variation accounted for 22.9% of overall AF SNP heritability. Addition of genetic risk to clinical risk improved model performance in classifying AF prevalence

Genetic risk prediction of atrial fibrillation

Background—Atrial fibrillation (AF) has a substantial genetic basis. Identification of individuals at greatest AF risk could minimize the incidence of cardioembolic stroke. Methods—To determine whether genetic data can stratify risk for development of AF, we examined associations between AF genetic risk scores and incident AF in five prospective studies comprising 18,919 individuals of European ancestry. We examined associations between AF genetic risk scores and ischemic stroke in a separate study of 509 ischemic stroke cases (202 cardioembolic [40%]) and 3,028 referents. Scores were based on 11 to 719 common variants (≥5%) associated with AF at P-values ranging from <1x10-3 to <1x10-8 in a prior independent genetic association study. Results—Incident AF occurred in 1,032 (5.5%) individuals. AF genetic risk scores were associated with new-onset AF after adjusting for clinical risk factors. The pooled hazard ratio for incident AF for the highest versus lowest quartile of genetic risk scores ranged from 1.28 (719 variants; 95%CI, 1.13-1.46; P=1.5x10-4) to 1.67 (25 variants; 95%CI, 1.47-1.90; P=9.3x10-15). Discrimination of combined clinical and genetic risk scores varied across studies and scores (maximum C statistic, 0.629-0.811; maximum ΔC statistic from clinical score alone, 0.009-0.017). AF genetic risk was associated with stroke in age- and sex-adjusted models. For example, individuals in the highest versus lowest quartile of a 127-variant score had a 2.49-fold increased odds of cardioembolic stroke (95%CI, 1.39-4.58; P=2.7x10-3). The effect persisted after excluding individuals (n=70) with known AF (odds ratio, 2.25; 95%CI, 1.20-4.40; P=0.01). Conclusions—Comprehensive AF genetic risk scores were associated with incident AF beyond associations for clinical AF risk factors, though offered small improvements in discrimination. AF genetic risk was also associated with cardioembolic stroke in age- and sex-adjusted analyses. Efforts are warranted to determine whether AF genetic risk may improve identification of subclinical AF or help distinguish between stroke mechanisms

Type of atrial fibrillation and clinical outcomes in patients with heart failure and reduced ejection fraction

Background: Atrial fibrillation (AF) is common in heart failure (HF), but the outcome by type of AF is largely unknown. Objectives: This study investigated outcomes related to type of AF (paroxysmal, persistent or permanent, or new onset) in 2 recent large trials in patients with HF with reduced ejection fraction. Methods: The study analyzed patients in the PARADIGM-HF (Prospective comparison of ARNI with ACEI to Determine Impact on Global Mortality and morbidity in Heart Failure) and ATMOSPHERE (Aliskiren Trial to Minimize Outcomes in Patients with Heart Failure) trials. Multivariable Cox regression models were used to estimate hazard ratios (HRs) for outcomes related to AF type. Results: Of 15,415 patients, 5,481 (35.6%) had a history of AF at randomization, and of these, 1,645 (30.0%) had paroxysmal AF. Compared with patients without AF, patients with paroxysmal AF at randomization had a higher risk of the primary composite endpoint of cardiovascular death or HF hospitalization (HR: 1.20; 95% confidence interval [CI]: 1.09 to 1.32; p < 0.001), HF hospitalization (HR: 1.34; 95% CI: 1.19 to 1.51; < 0.001), and stroke (HR: 1.34; 95% CI: 1.02 to 1.76; p = 0.037), whereas the corresponding risks in patients with persistent or permanent AF were not elevated. Neither type of AF was associated with higher mortality. New onset AF was associated with the greatest risk of adverse outcomes: primary endpoint (HR: 2.21; 95% CI: 1.80 to 2.71), HF hospitalization (HR: 2.11; 95% CI: 1.58 to 2.81), stroke (HR: 2.20; 95% CI: 1.25 to 3.88), and all-cause mortality (HR: 2.26; 95% CI: 1.86 to 2.74), all p values < 0.001, compared with patients without AF. Anticoagulants were used less often in patients with paroxysmal (53%) and new onset (16%) AF than in patients with persistent or permanent AF (71%). Conclusions: Among HF patients with a history of AF, those with paroxysmal AF were at greater risk of HF hospitalization and stroke than were patients with persistent or permanent AF, underlining the importance of anticoagulant therapy. New onset AF was associated with increased risk of all outcomes. (Prospective comparison of ARNI with ACEI to Determine Impact on Global Mortality and Morbidity in Heart Failure [PARADIGM-HF]; NCT01035255) (Aliskiren Trial to Minimize Outcomes in Patients with Heart Failure [ATMOSPHERE]; NCT00853658

Influence of autonomic nervous system in the inducibility of atrial fibrillation.

Cílem této práce je zjištění změn předcházejícím fibrilaci síní. Pozorována je rovnováha mezi sympatikem a parasympatikem. Do experimentu výzkumného ústavu Cleavlendské kliniky bylo zapojeno šest psů různých ras. Signály EKG byly získány Holterovským 24hodinovým monitorováním. Pomocí 40 vysokofrekvenčních impulsů (TI) byla každých 30 minut vyvolávána AF. Z 24hodinového signálu byly extrahovány kratší epizody. Každá z těchto epizod obsahovala 10 minut předcházejících TI a 3 minuty následující po TI. Desetiminutové epizody byly zpracovány automaticky, byly detekovány QRS komplexy a RR intervaly a vypočteny HRV parametry. Přítomnost a délka trvání AF byly zjištěny manuálně z tříminutových intervalů následujících po TI. Byla-li vyvolána AF o délce trvání kratší než 30 sekund došlo ve srovnání s epizodami bez výskytu AF k významným změnám tří HRV parametrů. HF parametr poklesl pro epizody s výskytem AF. LF parametr byl naopak vyšší v epizodách s AF. Pro AF delší než 30 sekund nebyly významné změny pozorovány. Změny v epizodách s krátkou AF mohly být způsobeny změnami vlivu sympatiku a parasympatiku. Ke vzniku dlouhých AF je pravděpodobně zapotřebí i jiného vlivu, který nemusí nutně souviset s nervovým systémem. K dalším analýzám je zapotřebí většího množství signálů.The aim of this study is to investigate changes in sympatho-vagal balance before the initiation of AF. Six mongrel dogs from the Cleveland Clinic foundation were included in this study. ECG was recorded for 24 hours using telemetric Holter monitoring. AF was periodically induced every 30 min. by applying brief bursts of 40 high-frequency atrial train impulses (TI). From the 24 hours signals' traces shorter data episodes were extracted. Each episode consisted of 10 minutes preceding the atrial burst, and 3 minutes following the (TI). The 10 minutes episodes were processed automatically to determine the QRS complexes and RR intervals, and to calculate the HRV parameters. The presence and the duration of AF were determined by manual examination in each of the 3 minutes intervals following the delivery of TI. When the AF was generated, but episodes of AF were shorter than 30 seconds, three HRV parameters were significantly different than when AF was not generated. The HF component was lower in episodes that generated AF. The LF component was higher in episodes that generated AF. No significant differences were found when episodes of AF were longer than 30 seconds. Short episodes of AF could be generated when a certain disorder between sympathetic and parasympathetic tone is present. However in order to be able to generate longer AF episodes it is necessary another component not necessary related to the nervous system. Further analysis with a higher number of dogs should be needed.

Atrial fibrillation impairs the diagnostic performance of cardiac natriuretic peptides in dyspneic patients. results from the BACH Study (Biomarkers in ACute Heart Failure)

Objectives: The purpose of this study was to assess the impact of atrial fibrillation (AF) on the performance of mid-region amino terminal pro-atrial natriuretic peptide (MR-proANP) in comparison with the B-type peptides (BNP and NT-proBNP) for diagnosis of acute heart failure (HF) in dyspneic patients. Background: The effects of AF on the diagnostic and prognostic performance of MR-proANP in comparison with the B type natriuretic peptides have not been previously reported. Methods: A total of 1,445 patients attending the emergency department with acute dyspnea had measurements taken of MR-proANP, BNP, and NT-proBNP values on enrollment to the BACH trial and were grouped according to presence or absence of AF and HF. Results: AF was present in 242 patients. Plasma concentrations of all three peptides were lowest in those with neither AF nor HF and AF without HF was associated with markedly increased levels (p < 0.00001). HF with or without AF was associated with a significant further increment (p < 0.00001 for all three markers). Areas under receiver operator characteristic curves (AUCs) for discrimination of acute HF were similar and powerful for all peptides without AF (0.893 to 0.912; all p < 0.001) with substantial and similar reductions (0.701 to 0.757) in the presence of AF. All 3 peptides were independently prognostic but there was no interaction between any peptide and AF for prediction of all-cause mortality. Conclusions: AF is associated with increased plasma natriuretic peptide (MR-proANP, BNP and NT-proBNP) levels in the absence of HF. The diagnostic performance of all three peptides is impaired by AF. This warrants consideration of adjusted peptide thresholds for diagnostic use in AF and mandates the continued search for markers free of confounding by AF

Atrial Fibrillation and Myocardial Infarction: A Systematic Review and Appraisal of Pathophysiologic Mechanisms

A growing body of evidence suggests that atrial fibrillation (AF) is associated with myocardial infarction (MI). However, incidence and management of MI in AF is still undefined. METHODS AND RESULTS: We searched MEDLINE via PubMed and Cochrane database between 1965 and 2015. All observational clinical studies and interventional trials reporting 1-year incidence of MI in AF were included. We also discussed pathophysiological mechanisms, predictors, and therapeutic approaches to reduce the risk of MI in AF. Twenty-one observational studies and 10 clinical trials were included. The annual rate of MI in observational studies including AF patients ranged from 0.4% to 2.5%. Higher rates of MI were reported in AF patients with stable coronary artery disease (11.5%/year), vascular disease (4.47%/year), heart failure (2.9%/year), and in those undergoing coronary artery interventions (6.3%/year). However, lower annual rates have been described in AF patients from Eastern countries (0.2-0.3%/year), and in those enrolled in clinical trials (from 0.4 to 1.3%/year). CONCLUSIONS: AF patients had a significant residual risk of MI despite anticoagulant treatment. Coexistence of atherosclerotic risk factors and platelet activation account for the increased risk of MI in AF. Identification of high-risk AF patients is a needed first step to develop cost-effective approaches for prevention. A new score, the 2MACE score, has been recently developed to stratify MI risk in AF, and may help not only in allocating resources to high-risk groups, but also in design of studies examining novel therapies for prevention of MI in AF