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Atrial Fibrillation
ACC guidelines 2023
Dr Rajesh Ponnada
Cardiology Resident
Apollo Hospital, Visakhapatnam
Atrial Fibrillation
Electrophysiological abnormalities
(Impulse generation)
Structural abnormalities
Ectopic action potentials Reentrant activity
Atrial
Ectopy
Sufficient
Subtrate
Reentry
to persist
PV
Heterogeneity in IK1
Abnormal Ca2+ handling
Downregulation of connexin
Genetic,
Old Age,
Inflammation, SDB
(Atrial cardiomyopathy)
Prothrombotic LA
Electrical
remodeling,
Heterogenous
atrial conduction velocity
and repolarization
NLRP3 knockdown prevented A
Persistence of AF
The ANS as AF trigger
Modifiable AF risk factors promote ANS dysfunction
Incidence and prevalence Increasing
Increase in Aging Population
Increase in Obesity
Increased Survival in AF patients
Multi factorial
Increased Detection
Mortality
12%
Stroke
14%
dementia
8%
Heart failure
30%
MI
8%
CKD
8%
PAD
8%
SCD
12%
SEQUEL OF AF
0
1
2
3
4
5
6
Mortality Stroke dementia Heart failure MI CKD PAD SCD
Risk Probability
Age-Standardized Global Prevalence Rates of AF
and Atrial Flutter per 100,000, Both Sexes, 2020
Risk Factors for Diagnosed
AF
CVDs causing AF
Consider
Increased
Surveillance
Treat modifiable risk
Factors
Monitor AF burden clinically throughout
Risk of stroke Assessment, Pathophysiological
changes, Treatment of symptoms
S.O.S
S.O.S
Definitions
Term Definitions
AF A SVT with uncoordinated atrial activation and ineffective atrial contraction
Clinical AF
Subclinical AF
Atrial high-rate episodes
AF burden
First detected AF
Paroxysmal AF
Persistent AF
Long-standing persistent AF
Permanent AF
Risk Stratification and Population Screening
CHARGE-AF (Co- horts for Heart and Aging Research in
Genomic Epidemiology model for atrial fibrillation
Total points 0-8. For the C2HEST
score, the C statistic was 0.749, with
95% CI of 0.729–0.769.10 The incident
rate of AF increased significantly with
higher C2HEST scores.
AF Complicating ACS or Percutaneous Coronary Intervention (PCI)
Chronic Coronary Disease (CCD)
Peripheral Artery Disease (PAD)
Recommendations for CKD/Kidney Failure
Thank you…..

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Atrial fibrillation guidelines 2023 ppt Rajesh.pptx

Editor's Notes

  1. AF is a chaotic, rapid (300-500 bpm), and irregular atrial Rhythm AF is the result of either electrophysiological abnormalities that underlie impulse generation and/or structural abnormalities of cellular connections that typically facilitate rapid and uniform impulse conduction AF often is initiated from electrical activity originating from ectopic action potentials most commonly generated in the pulmonary veins (PVs) of the left atrium (LA), or in response to reentrant activity promoted by heterogeneous conduction due to interstitial fibrosis PV features that increase vulnerability for initiating ectopy include a higher resting membrane potential, stretchactivated channels,2 and pattern of cross myofiber orientation
  2. Downregulation of connexin results in decreased gap junctions, leading to slow heterogeneous atrial conduction velocity and repolarization, promoting regional functional conduction block that can support reentry. Connexin remodeling can be due to genetic or acquired factors, such as inflammatory state, older age, or sleep-disordered breathing (SDB Calcium mishandling from remodeling increases calcium load in the sarcoplasmic reticulum Remodeling in sarcoplasmic reticulum calcium ATPase underlies sequestration of intracellular Calcium milieu for delayed afterdepolarizations, the most likely trigger for AF initiation. Action potential alternans related to Ca2+ mishandling can be noted to precede AF onset and increases with age. The atria of patients with AF tend to have both shorter effective refractory periods and slower conduction, which enhances dispersion of repolarization and favor reentry PAC burden is associated with development of AF.2 Larger LA volume increased NT-proBNP levels, and impaired LA emptying are associated with increased PAC burden Atrial cardiomyopathy has been identified as “any complex of structural, architectural, contractile or electrophysiological changes affecting the atria with the potential to produce clinically relevant manifestations.” Prothrombotic changes are often evident in the LA, including increased endocardial expression of von Willebrand factor, vascular cell adhesion molecule-1 and monocyte chemoattractant protein-1 changes, which may increase risk of thrombus formation and stroke
  3. A suitable substrate for AF has a wavelength (wavelength ¼ refractory period conduction velocity) that is shorter than the dimensions of the tissue, with heterogenous conduction velocity and/or repolarization duration. Thus, an individual with large, fibrotic, and/or fatty atria is more likely to have persistent AF than one with a normal-sized atria with little interstitial fibrosis or adipose infiltration
  4. Sympathetic efferent stimulation releases noradrenaline, stimulating G-coupled b-adrenergic receptors, enhancing L-type calcium channels, and increasing inward current (automaticity/early afterdepolarization). Delayed afterdepolarization occurs via calcium overload and ryanodine-2 receptor dysfunction Parasympathetic stimulation shortens atrial effective refractory period by increasing IKACh (acetyl-choline receptor mediated inward rectifying potassium channel) activity. Atrial effective refractory period heterogeneity follows the pattern of autonomic innervation. Sympathetic and parasympathetic activity, alone or combined, can trigger AF. ANS maintains AF
  5. Atrial fibrillation (AF) is the most sustained common arrhythmia, and its incidence and prevalence are increasing in the globally .The increasing burden is multifactorial; causes include the aging of the population, rising tide of obesity, increasing detection, and increasing survival with AF and other forms of cardiovascular disease The estimated global prevalence was 50 million in 2020 with majority underdiagnosed
  6. SDI was made up of the geometric mean of 3 common indicators: the lag distributed income per capita, mean educational achievement for those aged $15 y, and total fertility rate <25 y. SDI ranged from 0 to 1, where 0 represents the theoretical minimum level of development, whereas 1 represents the theoretical maximum level of development
  7. AF is associated with a 1.5- to 2-fold increased risk of death; studies suggest that the mortality risk may be higher in women than in men.6 In meta-analyses, AF is also associated with increased risk of multiple adverse outcomes, including a 2.4-fold risk of stroke, 1.5-fold risk of cognitive impairment or dementia,1.5-fold risk of myocardial infarction 2-fold risk of sudden cardiac death, 5-fold risk of heart failure (HF), 1.6-fold risk of chronic kidney disease (CKD), and 1.3-fold risk of peripheral artery disease (PAD). In Medicare beneficiaries, the most frequent outcome in the 5 years after AF diag- nosis was death (19.5% at 1 year; 48.8% at 5 years)11; the next most common diagnosis was HF (13.7%), followed by new-onset stroke (7.1%), gastrointestinal hemorrhage (5.7%), and MI (3.9%
  8. Other atrial arrhythmias are often encountered in patients with AF