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Fibrillation

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 blood efficiently, potentially leading to severe complications such as stroke, heart failure, or sudden cardiac arrest.^[1] This condition affects millions worldwide, with atrial fibrillation alone being the most common sustained cardiac arrhythmia, impacting approximately 1% of the global population and rising in prevalence with age.^[2]^[3] The primary types of fibrillation are atrial and ventricular, distinguished by the affected heart chambers. Atrial fibrillation (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.^[4] 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).^[2] Ventricular fibrillation (VFib), by contrast, affects the lower chambers (ventricles) and is immediately life-threatening, as the heart cannot pump blood, leading to unconsciousness and death within minutes if not treated with defibrillation.^[1]^[5] Outside the heart, skeletal muscle fibrillation manifests as spontaneous contractions of single fibers, often signaling denervation from nerve damage in conditions like amyotrophic lateral sclerosis or muscular dystrophy, and is detectable via electromyography.^[6] 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 Alzheimer's disease and type 2 diabetes.^[7] Fibrillation arises from various underlying factors, including structural heart changes, electrolyte imbalances, ischemia, and genetic predispositions. In AFib, common triggers include hypertension, heart valve disease, thyroid disorders, and excessive alcohol consumption, while VFib is frequently precipitated by myocardial infarction or cardiomyopathy.^[4]^[5] Symptoms of cardiac fibrillation may include palpitations, fatigue, dizziness, shortness of breath, and chest pain, though some cases are asymptomatic until complications arise.^[3] Management focuses on restoring rhythm, controlling rate, preventing clots with anticoagulants, and addressing root causes through medications, catheter ablation, or implantable devices, significantly improving outcomes when detected early.^[2]^[8]

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.^[9]^[10] 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.^[11]^[12] This process differs from related phenomena such as flutter, which involves organized, rapid, and regular electrical impulses leading to a more patterned rhythm, and fasciculation, which entails visible, spontaneous contractions of multiple muscle fibers due to intact innervation rather than isolated fiber activity.^[13]^[14] The hallmark of fibrillation is its chaotic nature, where individual units operate independently, precluding the synchronized action essential for normal physiology. 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 skeletal muscle, it contributes to weakness through ineffective force generation.^[4]

Etymology and Terminology

The term "fibrillation" originates from the Latin word fibrilla, a diminutive of fibra meaning "fiber," referring to small fibrous structures, and it entered English medical lexicon in the early 19th century around 1839–1842 as a description of irregular quivering or twitching in muscle fibers.^[15]^[16] Initially applied to observable muscular contractions without coordination, the word encapsulated the visual resemblance to fine, independent fiber movements, drawing from earlier anatomical observations of fibrillar components in tissues.^[9] In 19th-century medical literature, "fibrillation" evolved from a broad descriptor of "trembling" or uncoordinated muscle activity—such as the heart's auricles observed by William Harvey in 1628—to a more specific term for cardiac irregularities by the late 1800s.^[17] This shift accelerated in the early 20th century with the advent of electrocardiography; Willem Einthoven's 1906 publication of the first ECG tracing of atrial fibrillation enabled precise classification of arrhythmias as chaotic, fibrillatory patterns rather than mere palpitations or tremors.^[18] By the mid-20th century, the terminology had standardized in cardiology 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 cardiology, the American Heart Association 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.^[3]^[19] In biochemistry, it refers to the pathological aggregation of proteins into insoluble, beta-sheet-rich amyloid fibrils, where soluble monomers misfold and stack into rigid, fiber-like structures resistant to degradation.^[20] Common terminological confusions arise with related terms like "fibrosis," which denotes the pathological thickening and scarring of connective tissue due to excessive fibrous deposition, unrelated to dynamic twitching or aggregation. Similarly, "fibrinolysis" describes the enzymatic breakdown of fibrin 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 nomenclature to avoid misinterpretation in clinical and research settings.

Cardiac Fibrillation

Atrial Fibrillation

Atrial fibrillation (AF) 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.^[21]^[2]^[22] 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.^[23]^[24]^[25]^[26] Common causes and risk factors for AF include hypertension, heart failure, valvular heart disease, hyperthyroidism, 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 potassium channel subunit—linked to familial forms of the arrhythmia by altering repolarization dynamics. Advanced age, obesity, diabetes, and sleep apnea further elevate risk, often through shared pathways of atrial fibrosis and inflammation.^[2]^[27]^[28] Patients with AF 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 asymptomatic, particularly in early or paroxysmal stages, allowing the condition to progress undetected until complications arise.^[4]^[2] Diagnosis relies on electrocardiography (ECG), which reveals absent P waves, fibrillatory waves, and irregularly irregular RR intervals, confirming the arrhythmia. The CHA2DS2-VASc score is used to stratify stroke risk, incorporating factors like congestive heart failure, hypertension, age ≥75 years (2 points), diabetes, prior stroke (2 points), vascular disease, age 65-74 years, and sex category (female: 1 point), guiding anticoagulation decisions.^[29]^[30] Major complications of AF include thromboembolism, which increases stroke risk fivefold due to blood stasis in the atria promoting clot formation, and tachycardia-induced cardiomyopathy leading to heart failure. Without intervention, AF doubles overall mortality risk and heightens susceptibility to systemic emboli beyond the brain.^[3]^[31] 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 physical activity equivalent to 150–300 minutes per week of moderate-intensity exercise and weight management, in preventing progression. Anticoagulation with direct oral anticoagulants (DOACs) like apixaban or warfarin 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 calcium channel blockers (e.g., diltiazem) to maintain ventricular rates of 60-100 beats per minute at rest. Rhythm control involves antiarrhythmic drugs like amiodarone or electrical cardioversion for symptomatic patients, while catheter ablation targeting pulmonary vein isolation is effective for refractory paroxysmal or persistent AF, improving quality of life in select cases.^[32]^[33]^[34]^[35]

Ventricular Fibrillation

Ventricular fibrillation (VF) is a severe cardiac arrhythmia 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 cardiac arrest.^[19]^[36] This condition differs from organized ventricular rhythms by producing no identifiable QRS complexes on electrocardiography, instead showing irregular, undulating waveforms at rates exceeding 300 beats per minute.^[36] Without prompt intervention, VF causes cessation of cardiac output, leading to unconsciousness within seconds and death within minutes due to lack of oxygenated blood flow to vital organs.^[5] The primary causes of VF include acute myocardial infarction, which disrupts electrical conduction through ischemia, and other structural heart diseases such as cardiomyopathy or congenital defects that alter ventricular architecture.^[5]^[36] Risk factors encompass prior episodes of VF, electrolyte imbalances like hypokalemia or hypomagnesemia, drug toxicities including cocaine or amphetamines, and inherited channelopathies such as long QT syndrome or Brugada syndrome, which predispose the heart to re-entrant arrhythmias.^[19]^[5] Additional triggers involve hypoxia, acidosis, sepsis, electrocution, or complications from cardiac surgery, all of which can initiate the disorganized electrical activity.^[36] 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.^[19]^[5] 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.^[36] 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.^[5] Diagnosis of VF is primarily confirmed through electrocardiography (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 depolarization.^[37]^[36] 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.^[19] 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.^[37]^[36] Treatment of VF requires immediate initiation of cardiopulmonary resuscitation (CPR) at a rate of 100-120 compressions per minute to maintain circulation until defibrillation can be performed, as delays beyond 3-5 minutes drastically reduce survival odds.^[19]^[37] Defibrillation with biphasic shocks of 120-200 joules is the cornerstone intervention, aiming to depolarize the myocardium and restore sinus rhythm, often followed by administration of antiarrhythmic agents like amiodarone (300 mg IV) or lidocaine if refractory.^[36] For secondary prevention in survivors, implantable cardioverter-defibrillators (ICDs) are recommended to detect and automatically terminate recurrent VF episodes, while addressing reversible causes such as ischemia through angioplasty or electrolyte correction.^[37]^[36] 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.^[38]^[36]^[39] 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.^[36] These figures underscore VF's role as the leading cause of sudden cardiac death, with incidence rising in populations with coronary artery disease or advanced age.^[39] If untreated, VF rapidly leads to complications including profound cerebral hypoxia, resulting in irreversible brain damage after 4-6 minutes of arrest, and multi-organ failure from prolonged ischemia affecting the kidneys, liver, and other tissues.^[5] Survivors of VF episodes face heightened risks of recurrent arrhythmias, heart failure, or neurological deficits, with overall mortality exceeding 50% in the first year post-event due to underlying cardiac pathology.^[36]

Muscular Fibrillation

Skeletal Muscle Fibrillation

Skeletal muscle fibrillation refers to the spontaneous, irregular contractions of individual muscle fibers resulting from denervation, which are typically visible only under microscopic examination or detectable via electromyography (EMG) as small action potentials.^[6] These contractions arise independently of surrounding fibers and represent a hallmark electrophysiological sign of muscle fiber isolation from neural control.^[40] The pathophysiology involves the loss of motor neuron innervation, leading to hypersensitivity of the muscle fiber membrane to acetylcholine and spontaneous depolarizations due to altered sodium and potassium channel permeabilities, which generate rhythmic oscillations in membrane potential.^[6] Following denervation, such as from peripheral nerve injury, these changes manifest within 1-4 weeks, progressing to muscle fiber atrophy if the condition becomes chronic, as the denervated fibers undergo structural degeneration without trophic support from the nerve.^[40] Common causes include peripheral nerve damage from trauma or compression, motor neuron diseases like amyotrophic lateral sclerosis (ALS), 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.^[41] In ALS, fibrillations often precede clinical weakness and are detected in limb muscles, serving as an early indicator of ongoing motor neuron loss.^[42] 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.^[6]^[43] These potentials are length-dependent, appearing first in distal muscles, and exhibit irregular firing rates without coordination with voluntary activity.^[44] Fibrillations are associated with conditions like ALS, where they contribute to diagnostic criteria by indicating active denervation; Guillain-Barré syndrome, particularly in axonal variants with secondary denervation; and radiculopathies, where they signal root-level nerve involvement.^[42]^[41]^[45] Prognostically, isolated fibrillations may be benign and resolve with reinnervation, as seen in recovery from reversible nerve injuries, but persistent activity indicates ongoing denervation and correlates with poorer outcomes in progressive disorders like ALS, where they can endure for years without intervention.^[6]

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.^[43]^[6] 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.^[46] 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.^[47] The presence of fibrillation potentials on EMG serves as a key diagnostic criterion for active denervation, distinguishing it from chronic or reinnervated states where such activity diminishes.^[48] Diagnostic accuracy is enhanced by interference pattern analysis during quantitative EMG, which measures the recruitment and firing rates of motor units to grade denervation severity on a scale from mild to severe based on potential density.^[49] This approach confirms lower motor neuron involvement when fibrillations are widespread and persistent, typically appearing 1-4 weeks post-injury.^[50] Clinically, fibrillation potentials act as an early marker of lower motor neuron lesions, such as those in peripheral neuropathies or radiculopathies, enabling timely intervention before significant atrophy occurs.^[6] In amyotrophic lateral sclerosis (ALS), their density provides a fibrillation score that tracks disease progression and correlates with reduced survival, as higher scores reflect more extensive denervation and faster motor neuron loss.^[51] Unlike neurogenic patterns, fibrillations help differentiate denervation from myopathic processes, where short-duration motor unit potentials predominate without spontaneous activity.^[46] 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.^[40] In contrast, their absence in conditions like stroke underscores the specificity to lower motor neuron pathology, as upper motor neuron lesions do not generate denervation potentials due to preserved peripheral innervation.^[52] Recent advances include quantitative EMG techniques that automate fibrillation detection and grading for more objective assessments, reducing inter-examiner variability.^[49] Correlations between EMG findings and quantitative MRI metrics, such as T2 relaxation times and apparent fiber density, enable non-invasive monitoring of denervation progression, with MRI sensitivity complementing EMG in subacute phases.^[53] These tools are increasingly integrated into clinical trials for neuroprotective agents in ALS, where serial EMG and MRI evaluate therapeutic efficacy by tracking changes in fibrillation density and muscle microstructure.^[51]

Protein Fibrillation

Mechanisms of Formation

Protein fibrillation typically proceeds through a nucleation-dependent polymerization 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 fibrils. These fibrils 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.^[54] The process unfolds in distinct kinetic stages: an initial lag phase dominated by slow nucleation, 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 pH promoting partial unfolding and accelerating nucleation, elevated temperatures enhancing molecular mobility to speed elongation, and higher protein concentrations shortening the lag phase by increasing collision frequency.^[55]^[56] Several factors modulate the rate and extent of fibrillation. Macromolecular crowding agents like polyethylene glycol (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 Hsp70 inhibit fibrillation by binding to early oligomers, preventing their conversion to nuclei and facilitating refolding or degradation.^[57]^[58] 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. Atomic force microscopy (AFM) reveals fibril morphology, showing unbranched, linear structures with diameters typically ranging from 5 to 10 nm, consistent with paired protofilaments.^[59]^[60] Representative examples illustrate these mechanisms. In Alzheimer's disease, amyloid-β (Aβ) peptides assemble into fibrils featuring a cross-β core, where in-register parallel β-sheets form through nucleation of hydrophobic segments followed by elongation at fibril tips. Similarly, α-synuclein in Parkinson's disease undergoes fibrillation via a seeding mechanism, where preformed fibril fragments act as templates to lower the nucleation barrier and propagate aggregation.^[61]^[62]

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, organ dysfunction, 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 homeostasis and trigger inflammatory responses. In neurodegenerative disorders, such aggregates impair neuronal function and promote prion-like propagation across brain regions, exacerbating cognitive and motor decline. Similarly, in systemic amyloidoses, fibril deposition in vital organs like the heart, kidneys, and liver causes multisystem failure.^[63]^[20] 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.^[64]^[63]^[65] Systemic amyloidosis represents another major implication, where circulating proteins fibrillate and deposit in multiple organs, often triggered by chronic inflammation, aging, or genetic mutations. In AL amyloidosis (primary), immunoglobulin light chains form fibrils that infiltrate the heart and kidneys, causing cardiomyopathy and renal failure with a median survival of 12-18 months without treatment. AA amyloidosis (secondary) arises from serum amyloid A protein during prolonged inflammation (e.g., in rheumatoid arthritis), leading to renal amyloid deposition and proteinuria. Transthyretin (TTR) fibrillation in ATTR amyloidosis, either wild-type (senile) or mutant forms, predominantly affects the heart, resulting in restrictive cardiomyopathy and heart failure, 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 apoptosis. Across these conditions, fibril-induced mechanical disruption of tissue architecture, combined with toxic oligomer-mediated inflammation and apoptosis, drives irreversible organ damage.^[20]^[66]^[67] Therapeutically, understanding fibrillation's disease implications has spurred strategies targeting fibril formation, stability, or clearance, such as stabilizers for TTR in ATTR (e.g., tafamidis, reducing cardiac events by 30% in trials) and immunotherapies against Aβ in AD (e.g., lecanemab, approved in 2023 for early Alzheimer's and shown to slow cognitive decline). However, challenges persist due to the heterogeneity of toxic species—oligomers versus mature fibrils—and the need for early biomarkers to halt propagation before widespread damage occurs.^[63]^[68]^[69]

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