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Fibrillation
Fibrillation
Fibrillation
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Fibrillation is the rapid, irregular, and unsynchronized contraction of muscle fibers. An important occurrence is with regard to the heart.

Cardiology

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There are two major classes of cardiac fibrillation: atrial fibrillation and ventricular fibrillation.

Fibrillation may sometimes be used after heart surgery to stop the heart from beating while any minor leaks are stitched up.

Musculoskeletal

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Fibrillation also occurs with individual skeletal muscle fibers.[7] This happens when muscle fibers lose contact with their innervating axon producing a spontaneous action potential, "fibrillation potential" that results in the muscle fiber's contraction. These contractions are not visible under the skin and are detectable through needle electromyography (EMG) and ultrasound.[8] Fibrillations can occur in healthy individuals. If the fibrillations have irregular potentials, then they don't have pathological significance.[9] In other cases they are a major symptom in acute and severe peripheral nerve disorders, in myopathies in which muscle fibers are split or inflamed, and in lower motor neuron lesions.

They contrast with fasciculations that are visible spontaneous contractions involving small groups of muscle fibers. Fasciculations can be seen in lower motor neuron lesions as well, but they also do not necessarily denote pathology.

Terminology

[edit]

The word fibrillation (/ˌfɪbrɪlˈeɪʃən/) is related to the word fibril in the sense of muscle fibrils, the proteins that make up each muscle fiber (muscle cell).

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Fibrillation

View on Grokipedia
from Grokipedia
Fibrillation refers to abnormal quivering or twitching of muscle fibers in physiological contexts or the aggregation of proteins into fibrillar structures in biochemical and pathological contexts, often impairing normal function. In the medical context, it most prominently describes cardiac arrhythmias, where abnormal electrical signals cause the heart's chambers to quiver ineffectively rather than pump efficiently, potentially leading to severe complications such as , , or sudden . This condition affects millions worldwide, with alone being the most common sustained cardiac , impacting approximately 1% of the global population and rising in prevalence with age. The primary types of fibrillation are atrial and ventricular, distinguished by the affected heart chambers. (AFib) involves chaotic electrical activity in the upper chambers (atria), causing them to fibrillate at rates up to 600 beats per minute, which results in an irregularly irregular ventricular response and reduced cardiac efficiency. It is classified into subtypes such as paroxysmal (self-terminating within seven days), persistent (lasting longer than seven days), long-standing persistent (over 12 months), and permanent (requiring ongoing management). (VFib), by contrast, affects the lower chambers (ventricles) and is immediately life-threatening, as the heart cannot pump blood, leading to and within minutes if not treated with . Outside the heart, fibrillation manifests as spontaneous contractions of single fibers, often signaling from nerve damage in conditions like or , and is detectable via . In biochemistry, protein fibrillation refers to the misfolding and self-assembly of proteins into amyloid fibrils characterized by a cross-β sheet structure, implicated in diseases such as and . Fibrillation arises from various underlying factors, including structural heart changes, electrolyte imbalances, ischemia, and genetic predispositions. In AFib, common triggers include , heart valve disease, thyroid disorders, and excessive alcohol consumption, while VFib is frequently precipitated by or . Symptoms of cardiac fibrillation may include palpitations, , , , and , though some cases are asymptomatic until complications arise. Management focuses on restoring rhythm, controlling rate, preventing clots with anticoagulants, and addressing root causes through medications, , or implantable devices, significantly improving outcomes when detected early.

Introduction

Definition

Fibrillation refers to the rapid, irregular, and unsynchronized contraction of individual muscle fibers or the formation of fibrillar aggregates in proteins, resulting in a loss of coordinated activity and diminished functional efficiency. In muscular contexts, it manifests as quivering or twitching of single fibers without effective overall contraction, while in proteins, it involves the self-assembly of misfolded polypeptides into elongated, β-sheet-rich fibrils that can disrupt cellular processes. This process differs from related phenomena such as flutter, which involves organized, rapid, and regular electrical impulses leading to a more patterned rhythm, and , which entails visible, spontaneous contractions of multiple muscle fibers due to intact innervation rather than isolated fiber activity. The hallmark of fibrillation is its chaotic nature, where individual units operate independently, precluding the synchronized action essential for normal . Physiologically, fibrillation impairs organ function by eliminating effective mechanical output; for instance, in cardiac tissue, it prevents coordinated pumping, potentially leading to hemodynamic instability, whereas in , it contributes to weakness through ineffective force generation.

Etymology and Terminology

The term "fibrillation" originates from the Latin word fibrilla, a of fibra meaning "," referring to small fibrous structures, and it entered English medical lexicon in the early around 1839–1842 as a description of irregular quivering or twitching in muscle fibers. Initially applied to observable contractions without coordination, the word encapsulated the visual resemblance to fine, independent fiber movements, drawing from earlier anatomical observations of fibrillar components in tissues. In 19th-century , "fibrillation" evolved from a broad descriptor of "trembling" or uncoordinated muscle activity—such as the heart's auricles observed by in 1628—to a more specific term for cardiac irregularities by the late 1800s. This shift accelerated in the early with the advent of ; Willem Einthoven's 1906 publication of the first ECG tracing of enabled precise classification of arrhythmias as chaotic, fibrillatory patterns rather than mere or tremors. By the mid-20th century, the terminology had standardized in to denote disorganized electrical impulses causing ineffective contractions. Contemporary definitions, as established by authoritative bodies, distinguish fibrillation across contexts while maintaining its core connotation of fibrillar disarray. In , the describes fibrillation—particularly atrial and ventricular forms—as irregular, often rapid heart rhythms resulting from chaotic electrical activity in the atria or ventricles, leading to quivering rather than coordinated pumping. In biochemistry, it refers to the pathological aggregation of proteins into insoluble, beta-sheet-rich , where soluble monomers misfold and stack into rigid, fiber-like structures resistant to degradation. Common terminological confusions arise with related terms like "," which denotes the pathological thickening and scarring of due to excessive fibrous deposition, unrelated to dynamic twitching or aggregation. Similarly, "" describes the enzymatic breakdown of clots in blood coagulation, a degradative process distinct from the formative or arrhythmic aspects of fibrillation. These distinctions underscore the importance of contextual precision in medical to avoid misinterpretation in clinical and research settings.

Cardiac Fibrillation

Atrial Fibrillation

Atrial fibrillation (AFib or AF) is an irregular and often rapid heart rhythm that is a supraventricular tachyarrhythmia characterized by chaotic and rapid electrical impulses originating in the atria, leading to ineffective atrial contraction and an irregular ventricular response. The atrial rate during AF typically ranges from 300 to 600 beats per minute, while the ventricular rate varies depending on atrioventricular node conduction, often resulting in rates of 100 to 180 beats per minute if untreated. This disorganized activity causes loss of coordinated atrial systole, which can impair cardiac hemodynamics and contribute to the condition's chronic progression. Epidemiologically, AF affects approximately 10.5 million people in the United States as of 2024 estimates, with prevalence increasing markedly with age to about 13% in individuals over 65 years. Due to population aging and rising cardiovascular risk factors, projections from 2020 estimate 6 to 16 million cases in the US by 2050. Globally, AF prevalence has risen progressively, with an estimated 59 million cases worldwide as of 2019, underscoring its growing public health burden. Common causes and risk factors for AF include , , , , and excessive alcohol consumption, which can trigger or exacerbate atrial remodeling and electrical instability. Genetic predispositions also play a role, with mutations in genes such as KCNQ1—encoding a subunit—linked to familial forms of the by altering dynamics. Advanced age, , , and further elevate risk, often through shared pathways of atrial and . Patients with may experience symptoms such as palpitations, fatigue, and dyspnea on exertion, reflecting reduced cardiac output and irregular rhythm. However, up to 30% of cases are , particularly in early or paroxysmal stages, allowing the condition to progress undetected until complications arise. Diagnosis relies on (ECG), which reveals absent P waves, fibrillatory waves, and irregularly irregular RR intervals, confirming the . Additionally, wearable devices such as smartwatches can detect AFib using photoplethysmography or single-lead ECG, providing immediate alerts to users to seek medical help. The CHA2DS2-VASc score is used to stratify risk, incorporating factors like congestive , , age ≥75 years (2 points), , prior (2 points), , age 65-74 years, and sex category (: 1 point), guiding anticoagulation decisions. Major complications of AF include , which increases risk fivefold (4-5 times) and can contribute to heart attack due to in the atria promoting clot formation, and tachycardia-induced leading to heart failure. Without intervention, AF doubles overall mortality risk and heightens susceptibility to systemic emboli beyond the . Management emphasizes stroke prevention, rate or rhythm control, and risk factor modification. Recent 2024 ESC guidelines highlight the importance of lifestyle interventions, such as regular equivalent to 150–300 minutes per week of moderate-intensity exercise and , in preventing progression. Anticoagulation with direct oral anticoagulants (DOACs) like or is recommended for most patients based on CHA2DS2-VASc score ≥2 in men or ≥3 in women to reduce thromboembolic events. Rate control uses beta-blockers (e.g., metoprolol) or non-dihydropyridine (e.g., ) to maintain ventricular rates of 60-100 beats per minute at rest. Rhythm control involves antiarrhythmic drugs like or electrical for symptomatic patients, while targeting isolation is effective for refractory paroxysmal or persistent AF, improving in select cases.

Ventricular Fibrillation

Ventricular fibrillation (VF) is a severe characterized by rapid, chaotic electrical activity in the ventricles, resulting in disorganized quivering of the heart muscle that prevents effective pumping of blood and leads to immediate hemodynamic collapse and sudden . This condition differs from organized ventricular rhythms by producing no identifiable QRS complexes on , instead showing irregular, undulating waveforms at rates exceeding 300 beats per minute. Without prompt intervention, VF causes cessation of , leading to within seconds and within minutes due to lack of oxygenated blood flow to vital organs. The primary causes of VF include acute , which disrupts electrical conduction through ischemia, and other structural heart diseases such as or congenital defects that alter ventricular architecture. Risk factors encompass prior episodes of VF, imbalances like or hypomagnesemia, drug toxicities including or amphetamines, and inherited channelopathies such as or , which predispose the heart to re-entrant s. Additional triggers involve hypoxia, , , , or complications from , all of which can initiate the disorganized electrical activity. Symptoms of VF typically manifest abruptly with sudden collapse, loss of consciousness, absence of a detectable pulse, and no spontaneous breathing or only agonal gasps, often without warning in unwitnessed cases. Preceding prodromal signs, if present, may include chest pain, dizziness, nausea, shortness of breath, or palpitations, particularly in the context of an underlying myocardial infarction. Due to its rapid progression to cardiac arrest, many episodes are fatal before medical help arrives, emphasizing the need for bystander recognition of collapse as a potential VF event. Diagnosis of VF is primarily confirmed through (ECG), which reveals a characteristic pattern of fine or coarse fibrillatory waves without discernible P waves, QRS complexes, or T waves, reflecting the absence of coordinated ventricular . In emergency settings, automated external defibrillators (AEDs) or manual defibrillators analyze the rhythm and identify VF with high accuracy, often supplemented by pulse checks to confirm pulselessness. Additional diagnostic tools, such as blood tests for cardiac enzymes, echocardiograms to assess ventricular function, or coronary angiography to detect ischemia, are employed post-resuscitation to identify underlying causes. Treatment of VF requires immediate initiation of (CPR) at a rate of 100-120 compressions per minute to maintain circulation until can be performed, as delays beyond 3-5 minutes drastically reduce survival odds. with biphasic shocks of 120-200 joules is the cornerstone intervention, aiming to depolarize the myocardium and restore , often followed by administration of antiarrhythmic agents like (300 mg IV) or lidocaine if refractory. For secondary prevention in survivors, implantable cardioverter- (ICDs) are recommended to detect and automatically terminate recurrent VF episodes, while addressing reversible causes such as ischemia through or correction. Epidemiologically, VF accounts for approximately 18% of out-of-hospital cardiac arrests as an initial shockable rhythm as of 2020 data and is implicated in up to 70% of sudden cardiac death cases, contributing to an estimated 300,000 to 450,000 such deaths annually in the United States. Out-of-hospital survival rates for VF are generally below 10% without prompt AED use, though witnessed arrests with bystander intervention can achieve up to 30-35% survival to hospital discharge. These figures underscore VF's role as the leading cause of sudden cardiac death, with incidence rising in populations with or advanced age. If untreated, VF rapidly leads to complications including profound , resulting in irreversible brain damage after 4-6 minutes of , and multi-organ from prolonged ischemia affecting the kidneys, liver, and other tissues. Survivors of VF episodes face heightened risks of recurrent arrhythmias, , or neurological deficits, with overall mortality exceeding 50% in the first year post-event due to underlying cardiac pathology.

Muscular Fibrillation

Skeletal Muscle Fibrillation

Skeletal muscle fibrillation refers to the spontaneous, irregular contractions of individual muscle fibers resulting from , which are typically visible only under microscopic examination or detectable via (EMG) as small action potentials. These contractions arise independently of surrounding fibers and represent a hallmark electrophysiological sign of muscle fiber isolation from neural control. The involves the loss of innervation, leading to hypersensitivity of the muscle fiber membrane to and spontaneous depolarizations due to altered sodium and permeabilities, which generate rhythmic oscillations in . Following , such as from peripheral , these changes manifest within 1-4 weeks, progressing to muscle fiber if the condition becomes chronic, as the denervated fibers undergo structural degeneration without trophic support from the . Common causes include peripheral nerve damage from trauma or compression, motor neuron diseases like amyotrophic lateral sclerosis (), inflammatory neuropathies such as Guillain-Barré syndrome, and radiculopathies due to spinal root compression; it can also occur transiently during normal reinnervation processes after injury. In ALS, fibrillations often precede clinical weakness and are detected in limb muscles, serving as an early indicator of ongoing loss. Characteristics of skeletal muscle fibrillations include detection on EMG as low-amplitude potentials typically ranging from 20 μV to over 1000 μV (often 100–500 μV initially, decreasing with chronicity), that are distinct from larger fasciculations involving groups of fibers. These potentials are length-dependent, appearing first in distal muscles, and exhibit irregular firing rates without coordination with voluntary activity. Fibrillations are associated with conditions like , where they contribute to diagnostic criteria by indicating active ; Guillain-Barré , particularly in axonal variants with secondary ; and radiculopathies, where they signal root-level nerve involvement. Prognostically, isolated fibrillations may be benign and resolve with reinnervation, as seen in recovery from reversible nerve injuries, but persistent activity indicates ongoing and correlates with poorer outcomes in progressive disorders like , where they can endure for years without intervention.

Clinical Detection and Significance

Fibrillation potentials in skeletal muscle are primarily detected through needle electromyography (EMG), which identifies spontaneous electrical activity in resting muscle fibers. These potentials typically exhibit firing rates of 0.5-15 Hz and amplitudes ranging from 20 μV to over 1000 μV (often 100–500 μV initially, decreasing with chronicity), manifesting as brief, negative spikes indicative of denervation. Needle EMG is the gold standard for capturing this activity, as the electrode insertion provokes depolarizations in denervated fibers, allowing quantification of their density across multiple muscle sites. In severe cases, muscle ultrasound can visualize fibrillations as subtle, irregular ripples or oscillations within the muscle fascicles, offering a non-invasive adjunct with reported sensitivity of 45% and specificity up to 85% when assessed in real-time. The presence of fibrillation potentials on EMG serves as a key diagnostic criterion for active , distinguishing it from chronic or reinnervated states where such activity diminishes. Diagnostic accuracy is enhanced by interference pattern analysis during quantitative EMG, which measures the and firing rates of motor units to grade denervation severity on a scale from mild to severe based on potential density. This approach confirms involvement when fibrillations are widespread and persistent, typically appearing 1-4 weeks post-injury. Clinically, fibrillation potentials act as an early marker of lesions, such as those in peripheral neuropathies or radiculopathies, enabling timely intervention before significant occurs. In (ALS), their density provides a fibrillation score that tracks disease progression and correlates with reduced survival, as higher scores reflect more extensive and faster loss. Unlike neurogenic patterns, fibrillations help differentiate from myopathic processes, where short-duration motor unit potentials predominate without spontaneous activity. Prognostically, persistent fibrillation potentials beyond the expected reinnervation window—typically 3-6 months post-nerve injury—signal poor functional recovery, as they indicate ongoing axonal loss rather than regeneration. In contrast, their absence in conditions like underscores the specificity to pathology, as lesions do not generate potentials due to preserved peripheral innervation. Recent advances include quantitative EMG techniques that automate fibrillation detection and grading for more objective assessments, reducing inter-examiner variability. Correlations between EMG findings and quantitative MRI metrics, such as T2 relaxation times and apparent fiber density, enable non-invasive monitoring of progression, with MRI sensitivity complementing EMG in subacute phases. These tools are increasingly integrated into clinical trials for neuroprotective agents in , where serial EMG and MRI evaluate therapeutic efficacy by tracking changes in fibrillation density and muscle microstructure.

Protein Fibrillation

Mechanisms of Formation

Protein fibrillation typically proceeds through a nucleation-dependent mechanism, in which natively folded or partially unfolded proteins undergo misfolding to form unstable oligomers that serve as nuclei for further assembly into β-sheet-rich . These are stabilized primarily by hydrophobic interactions between non-polar side chains and hydrogen bonding between backbone atoms in the β-strands, leading to the characteristic cross-β architecture where β-strands are perpendicular to the fibril axis. The process unfolds in distinct kinetic stages: an initial lag phase dominated by slow , where monomers form transient oligomers; an elongation phase marked by rapid addition of monomers to growing fibril ends; and a final plateau phase where aggregation saturates due to monomer depletion. These stages are highly sensitive to environmental conditions, with lower promoting partial unfolding and accelerating , elevated temperatures enhancing molecular mobility to speed elongation, and higher protein concentrations shortening the lag phase by increasing . Several factors modulate the rate and extent of fibrillation. agents like (PEG) mimic cellular conditions and accelerate the lag phase by reducing the entropic penalty of nucleus formation. Metal ions such as Cu²⁺ catalyze aggregation by binding to specific residues, stabilizing misfolded intermediates and promoting oxidative cross-linking. Conversely, molecular chaperones like inhibit fibrillation by binding to early oligomers, preventing their conversion to nuclei and facilitating refolding or degradation. Detection and characterization of these processes rely on biophysical techniques. The thioflavin T (ThT) fluorescence assay monitors fibril formation in real time, as ThT binds selectively to β-sheet structures, exhibiting enhanced fluorescence upon incorporation into fibrils. (AFM) reveals fibril morphology, showing unbranched, linear structures with diameters typically ranging from 5 to 10 nm, consistent with paired protofilaments. Representative examples illustrate these mechanisms. In , amyloid-β (Aβ) peptides assemble into featuring a cross-β core, where in-register parallel β-sheets form through of hydrophobic segments followed by elongation at tips. Similarly, α-synuclein in undergoes fibrillation via a seeding mechanism, where preformed fragments act as templates to lower the nucleation barrier and propagate aggregation.

Implications in Disease

Protein fibrillation, the process by which proteins misfold and assemble into insoluble amyloid fibrils, is a central pathological feature in numerous human diseases, leading to tissue damage, , and progressive degeneration. These fibrils are highly stable and resistant to proteasomal or autophagic degradation, resulting in their extracellular deposition as plaques or intracellular accumulation as inclusions, which disrupt cellular and trigger inflammatory responses. In neurodegenerative disorders, such aggregates impair neuronal function and promote prion-like propagation across regions, exacerbating cognitive and motor decline. Similarly, in systemic amyloidoses, fibril deposition in vital organs like the heart, kidneys, and liver causes multisystem failure. In neurodegenerative diseases, protein fibrillation underlies conditions such as Alzheimer's disease (AD), where amyloid-β (Aβ) peptides and hyperphosphorylated tau form extracellular plaques and intracellular neurofibrillary tangles, respectively, leading to synaptic loss, neuronal apoptosis, and cognitive impairment. The toxic effects stem from soluble oligomers and fibrils disrupting mitochondrial function, inducing oxidative stress, and activating neuroinflammatory pathways via microglia. Parkinson's disease (PD) involves α-synuclein fibrillation into Lewy bodies, which propagates prion-like from the substantia nigra, causing dopaminergic neuron death, motor symptoms, and non-motor deficits like autonomic dysfunction. Other examples include Huntington's disease, driven by polyglutamine-expanded huntingtin fibrils that sequester chaperones and impair proteostasis, and amyotrophic lateral sclerosis (ALS), where TAR DNA-binding protein 43 (TDP-43) aggregates contribute to motor neuron degeneration. These fibrillar aggregates not only directly toxify cells but also facilitate intercellular spread via exosomes or tunneling nanotubes, amplifying disease progression across neural networks. Systemic amyloidosis represents another major implication, where circulating proteins fibrillate and deposit in multiple organs, often triggered by chronic , aging, or genetic mutations. In (primary), immunoglobulin light chains form fibrils that infiltrate the heart and kidneys, causing and renal failure with a median survival of 12-18 months without treatment. (secondary) arises from protein during prolonged (e.g., in ), leading to renal amyloid deposition and . (TTR) fibrillation in ATTR amyloidosis, either wild-type (senile) or mutant forms, predominantly affects the heart, resulting in and , as seen in familial cases where destabilized TTR tetramers dissociate into monomers prone to aggregation. Type 2 diabetes involves islet amyloid polypeptide (IAPP) fibrils in pancreatic β-cells, contributing to insulin secretion impairment and β-cell . Across these conditions, fibril-induced mechanical disruption of tissue architecture, combined with toxic oligomer-mediated and , drives irreversible organ damage. Therapeutically, understanding fibrillation's disease implications has spurred strategies targeting fibril formation, stability, or clearance, such as stabilizers for TTR in ATTR (e.g., , reducing cardiac events by 30% in trials) and immunotherapies against Aβ in (e.g., , approved in 2023 for early Alzheimer's and shown to slow cognitive decline). However, challenges persist due to the heterogeneity of toxic —oligomers versus mature fibrils—and the need for early biomarkers to halt propagation before widespread damage occurs.

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