Atrial fibrillation and heart failure: A contemporary review of current management approaches
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ABSTRACT:
SUBMITTER: Lee J
PROVIDER: S-EPMC8710620 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Chronic heart failure (CHF) remains the only cardiovascular disease with an increasing hospitalization burden and an ongoing drain on health care expenditures. The prevalence of CHF increases with advancing life span, with diastolic heart failure predominating in the elderly population. Primary prevention of coronary artery disease and risk factor management via aggressive blood pressure control are central in preventing new occurrences of left ventricular dysfunction. Optimal therapy for CHF involves identification and correction of potentially reversible precipitants, target-dose titration of medical therapy, and management of hospitalizations for decompensation. The etiological phenotype, absolute decrease in left ventricular ejection fraction and a widening of QRS duration on electrocardiography, is commonly used to identify patients at increased risk of progression of heart failure and sudden death who may benefit from prophylactic implantable cardioverter-defibrillator placement with or without cardiac resynchronization therapy. Patients who transition to advanced stages of disease despite optimal traditional medical and device therapy may be candidates for hemodynamically directed approaches such as a left ventricular assist device; in selected cases, listing for cardiac transplant may be warranted.
| S-EPMC2813829 | biostudies-other
Project description:Atrial fibrillation is increasingly encountered in patients with heart failure. Both diseases have seen tremendous rises in incidence in recent years. In general, the treatment of atrial fibrillation is focused on relieving patients from atrial fibrillation-related symptoms and risk reduction for thromboembolism and the occurrence or worsening of heart failure. Symptomatic relief may be accomplished by either (non-)pharmacological rate or rhythm control in combination with optimal therapy of underlying cardiovascular morbidities and risk factors. Atrial fibrillation ablation has been performed in patients without overt heart failure successfully for many years. However, in recent years, attempts have been made for patients with heart failure as well. In this review, we discuss the current literature describing the treatment of atrial fibrillation in heart failure. We highlight the early rate versus rhythm control studies, the importance of addressing underlying conditions and treatment of risk factors. A critical evaluation will be performed of the catheter ablation studies that have been performed so far in light of larger (post-hoc) ablation studies. Furthermore, we will hypothesise the role of patient selection as next step in optimising outcome for patient with atrial fibrillation and heart failure.
| S-EPMC8899490 | biostudies-literature
Project description:Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice. Its increasing prevalence, particularly among the elderly, renders it one of the most serious current medical epidemics. Several management questions confront the clinician treating a patient with AF: Should the condition be treated? Is the patient at risk of death or serious morbidity as a result of this diagnosis? If treatment is necessary, is rate control or rhythm control superior? Which patients need anticoagulation therapy, and for how long? This review of articles obtained by a search of the PubMed and MEDLINE databases presents the available evidence that can guide the clinician in answering these questions. After discussing the merits of available therapy, including medications aimed at controlling rate, rhythm, or both, we focus on the present status of ablative therapy for AF. Catheter ablation, particularly targeting the pulmonary veins, is being increasingly performed, although the precise indications for this approach and its effectiveness and safety are being actively investigated. We briefly discuss other invasive options that are less frequently used, such as pacemakers, defibrillators, left atrial appendage closure devices, and the surgical maze procedure.
| S-EPMC2704137 | biostudies-literature
Project description:Atrial fibrillation (AF) and heart failure (HF) contribute to about 45% of all cardiovascular disease (CVD) deaths in the USA and around the globe. Due to the complex nature, progression, inherent genetic makeup, and heterogeneity of CVDs, personalized treatments are believed to be critical. To improve the deciphering of CVD mechanisms, we need to deeply investigate well-known and identify novel genes that are responsible for CVD development. With the advancements in sequencing technologies, genomic data have been generated at an unprecedented pace to foster translational research. Correct application of bioinformatics using genomic data holds the potential to reveal the genetic underpinnings of various health conditions. It can help in the identification of causal variants for AF, HF, and other CVDs by moving beyond the one-gene one-disease model through the integration of common and rare variant association, the expressed genome, and characterization of comorbidities and phenotypic traits derived from the clinical information. In this study, we examined and discussed variable genomic approaches investigating genes associated with AF, HF, and other CVDs. We collected, reviewed, and compared high-quality scientific literature published between 2009 and 2022 and accessible through PubMed/NCBI. While selecting relevant literature, we mainly focused on identifying genomic approaches involving the integration of genomic data; analysis of common and rare genetic variants; metadata and phenotypic details; and multi-ethnic studies including individuals from ethnic minorities, and European, Asian, and American ancestries. We found 190 genes associated with AF and 26 genes linked to HF. Seven genes had implications in both AF and HF, which are SYNPO2L, TTN, MTSS1, SCN5A, PITX2, KLHL3, and AGAP5. We listed our conclusion, which include detailed information about genes and SNPs associated with AF and HF.
| S-EPMC10239148 | biostudies-literature
Project description: Not available
| S-EPMC7719059 | biostudies-literature
Project description:A retained intracardiac catheter fragment left in situ for 2 years was incidentally found in a patient presenting with worsening heart failure and atrial fibrillation. This case describes the diagnostic evaluation of this rare event, with successful endovascular retrieval and resolution of his symptoms. (Level of Difficulty: Advanced.).
| S-EPMC8642736 | biostudies-literature
Project description:Atrial fibrillation is the most common sustained cardiac arrhythmia, and affected individuals suffer from increased rates of heart failure, stroke, and death. Despite the enormous clinical burden that it exerts on patients and health care systems, contemporary treatment strategies have only modest efficacy that likely stems from our limited understanding of its underlying pathophysiology. Epidemiological studies have provided unequivocal evidence that the arrhythmia has a substantial heritable component. Subsequent investigations into the genetics underlying atrial fibrillation have suggested that there is considerable interindividual variability in the pathophysiology characterizing the arrhythmia. This heterogeneity may partly account for the poor treatment efficacy of current therapies. Subdividing atrial fibrillation into mechanistic subtypes on the basis of genotype illustrates the heterogeneous nature of the arrhythmia and may ultimately help guide treatment strategies. A pharmacogenetic approach to the management of atrial fibrillation may lead to dramatic improvements in treatment efficacy and improved patient outcomes.
| S-EPMC4051329 | biostudies-literature
Project description:In patients with atrial fibrillation (AF) and heart failure (HF) with or without systolic dysfunction, either rhythm control or rate control is an acceptable primary therapeutic option. If a rate control strategy is chosen, treatment with a beta-blocker is almost always required to achieve rate control. Adequate ventricular rate control is usually a resting rate of less than 100 beats per minute, but lower resting rates may be appropriate. Non-dihydropyridine calcium channel blockers are often contraindicated when AF is associated with HF with systolic dysfunction. There have been recent debates on a possible reduced efficacy of beta-blockers as well as safety issues with digoxin when treating HF patients with AF. The benefit of beta-blockers on survival may be lower in patients with HF with reduced ejection fraction when AF is present. Digoxin does not improve survival but may help to obtain satisfactory rate control in combination with a beta-blocker. Digoxin may be useful in the presence of hypotension or an absolute contraindication to beta-blocker treatment.
| S-EPMC5490978 | biostudies-other
Project description:While the interplay between heart failure (HF) and atrial fibrillation (AF) has been extensively studied, little is known regarding HF and atrial flutter (AFL), which may be managed differently. We reviewed the incidence, prevalence, and predictors of HF in AFL and vice versa, and the outcomes of treatment of AFL in HF. A systematic literature review of PubMed/Medline and EMBASE yielded 65 studies for inclusion and qualitative synthesis. No study described the incidence or prevalence of AFL in unselected patients with HF. Most cohorts enrolled patients with AF/AFL as interchangeable diagnoses, or highly selected patients with tachycardia-induced cardiomyopathy. The prevalence of HF in AFL ranged from 6% to 56%. However, the phenotype of HF was never defined by left ventricular ejection fraction (LVEF). No studies reported the predictors, phenotype, and prognostic implications of AFL in HF. There was significant variation in treatments studied, including the proportion that underwent ablation. When systolic dysfunction was tachycardia-mediated, catheter ablation demonstrated LVEF normalization in up to 88%, as well as reduced cardiovascular mortality. In summary, AFL and HF often coexist but are understudied, with no randomized trial data to inform care. Further research is warranted to define the epidemiology and establish optimal management.
| S-EPMC8712920 | biostudies-literature
Project description:AimsWe sought to define the underlying mechanisms for atrial fibrillation (AF) during chronic heart failure (HF).Methods and resultsPreliminary studies showed that 4 months of HF resulted in irreversible systolic dysfunction (n = 9) and a substrate for sustained inducible AF (>3 months, n = 3). We used a chronic (4-month) canine model of tachypacing-induced HF (n = 10) to assess atrial electrophysiological remodelling, relative to controls (n = 5). Left ventricular fractional shortening was reduced from 37.2 +/- 0.83 to 13.44 +/- 2.63% (P < 0.05). Left atrial (LA) contractility (fractional area change) was reduced from 34.9 +/- 7.9 to 27.9 +/- 4.23% (P < 0.05). Action potential durations (APDs) at 50 and 90% repolarization were shortened by approximately 60 and 40%, respectively, during HF (P < 0.05). HF-induced atrial remodelling included increased fibrosis, increased I(to), and decreased I(K1), I(Kur), and I(Ks) (P < 0.05). HF induced increases in LA Kv channel interacting protein 2 (P < 0.05), no change in Kv4.3, Kv1.5, or Kir2.3, and reduced Kir2.1 (P < 0.05). When I(Ca-L) was elicited by action potential (AP) clamp, HF APs reduced the integral of I(Ca) in control myocytes, with a larger reduction in HF myocytes (P < 0.05). I(CaL) measured with standard voltage clamp was unchanged by HF. Incubation of myocytes with N-acetylcysteine (a glutathione precursor) attenuated HF-induced electrophysiological alterations. LA angiotensin-1 receptor expression was increased in HF.ConclusionChronic HF causes alterations in ion channel expression and ion currents, resulting in attenuation of the APD and atrial contractility and a substrate for persistent AF.
| S-EPMC2761201 | biostudies-literature