Premature ventricular contraction

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Radwa AbdElHaras Mohamed AbouZaied, M.B.B.S[2] Mugilan Poongkunran M.B.B.S [3] Homa Najafi, M.D.[4]

Premature ventricular contraction is a form of irregular heart beat in which the ventricle contracts prematurely. This results in a skipped beat followed by a stronger beat. Individuals may report a feeling that their heart stops after a premature ventricular contraction.

Premature ventricular contractions can be classified based upon the number of normal beats between them and defined accordingly into bigeminy, trigeminy, or quadrigeminy.

Premature ventricular contraction is a relatively common event where the heartbeat is initiated by Purkinje fibres in the ventricles rather than by the sinoatrial node, the normal heartbeat initiator. Re-entrant signalling and enhanced automaticity in some ectopic focus are the main pathophysiological explanations.

Premature ventricular contractions can occur in a healthy person of any age, however they are more common in patients with underlying heart disease such as ischemic heart disease and structural heart disease. Patients on tricyclic antidepressant are at risk of having PVCs.

A premature ventricular contraction originates in the ventricle, and this must be differentiated from an impulse that originates above the ventricle (i.e. it is supraventricular in origin) and conducts with a delay (i.e. a wide complex, it is aberrantly conducted).

The prevalence of premature ventricular contractions (PVCs) varies between 100 to 400 per 100,000 individuals worldwide on standard 12-lead electrocardiography and 4000 to 7500 per 100,000 individuals on 24- to 48-hour Holter monitoring. Patients of all age groups may develop PVC and the incidence increases with age. African- American individuals are more likely to develop PVCs. Men are more commonly developed the disease than women.

Premature ventricular contraction can occur due to activation of the sympathetic nervous system and the common risk factors are anxiety, physiological stress etc. Patient with copper deficiency are also prone to PVCs.

Premature ventricular contraction caries no risk of mortality in the absence of any underlying heart disease. Heart rate turbulence is a phenomenon representing the return to equilibrium of the heart rate after a PVC. These parameters correlate significantly with mortality after myocardial infarction.

Premature ventricular contraction patients may have no symptom at all or may present with exercise intolerance and chest pain. Sometimes patients may present with a non specific feeling of forceful beat which might need the use of Holter monitor to pick up PVCs.

Complete physical examination help determine any heart defects as a cause for premature ventricular contractions.

Many cases of premature ventricular contraction have no definite cause, it may be the result of various other problems. If PVC patients present with symptoms, a generalized approach is done to find the precipitating factors.

When looking at an electrocardiograph, premature ventricular contractions are easily spotted and therefore a definitive diagnosis can be made. The QRS and T waves look very different to normal readings. The spacing between the PVC and the preceding QRS wave is a lot shorter than usual and the time between the PVC and the proceeding QRS is a lot longer. However, the time between the preceding and proceeding QRS waves stays the same as normal due to the compensatory pause.

Isolated premature ventricular contractions with benign characteristics require no treatment. In healthy individuals, PVCs can often be resolved by restoring the balance of magnesium, calcium and potassium within the body.

Radiofrequency ablation is useful for treating patients with high frequency of premature ventricular contraction episodes.

The most effective treatment of premature ventricular contraction is the elimination of triggers particularly the cessation of the use of substances such as caffeine, and certain drugs.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Radwa AbdElHaras Mohamed AbouZaied, M.B.B.S[2]

• During the second century BC, Herophilus, a Greek anatomist and physician described what is known today as extrasystoles, which was called “intermittent pulse” by his successors.
• Later, Galen (132-201 AD) became interested in studying this abnormality and he hypothesized a link between intermittent pulse and death and was considered an ominous sign. His teachings remained unrevised till around the 17^th century.
• Between the 17^th and the 19^th century, authors, still influenced by Galen’s tenets, were more interested in describing the character of the intermittent pulse rather than researching the cause behind it. Writers during this period still linked intermittent pulse to subsequent cardiac or medical conditions and confirmed that is in fact a manifestation of disease.
• In 1899, Cushny and Wenckebach were the first known to postulate that intermittent pulse was actually caused by extrasystoles. This discovery was only made possible in the light of the development of the cardiac science of electrophysiology growing big in the 20^th century utilizing animal physiology labs. The theory was also approved at that time by by Hering, Pan and Trendelenburg. Wenckebach believed that intermittent pulse was not a caused by disturbance of pulse, but in fact a problem with cardiac function.
• Einthoven, 1906, unleashed a new era in the understanding of extra-systoles by recording the fist extrasystole using the string of a galvanometer.
• It was not before the 20^th century that the Galenic teachings were challenged by some authors like Mackenzie, Lewis and Osler, who described extra-systoles as a benign phenomenon in the absence of other cardiac manifestations. This belief started to grow in Cardiology texts during the late 1960’s, that extra-systoles can occur in normal persons and is not a manifestation of disease. In 1968, and by the development in the science of electrophysiology, it was possible to describe the origin of the extrasystole, and scientists were particularly concerned about those originating from the ventricles.
• In 1969, results of a widely publicized observation study which including an entire population of Tecumseh city (1959-1965), 2.8% was the incidence rate of death in subjects with ventricular ectopy in contrast to 1.3% among normal subjects, a difference not clinically significant. Many of the subjects with ventricular ectopy resulting in death were suffering coronary artery disease. Thus, this study made evident that not all patients exhibiting ventricular ectopy are alike and they can be sub-grouped into categories with different prognosis.
• However, in practice, clinicians in the late 1970’s still viewed all ventricular ectopy as a potential cause of sudden death and used to admit all patients to CCU to be treated with antiarrhythmic drugs. Premature ventricular conduction has since then being regarded as an area of debate given the clinical significance and versatility of patient subsets each exhibiting different prognosis.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2] Radwa AbdElHaras Mohamed AbouZaied, M.B.B.S[3]

Premature ventricular contractions can be classified based upon the number of normal beats between them.

• There are four different named patterns of regularly occurring PVCs.
• Depending whether there are 1, 2, or 3 normal beats between each PVC, the rhythm is called bigeminy, trigeminy, or quadrigeminy.
• Unifocal PVCs are triggered from a single site in the ventricle, causing the peaks on the ECG to look the same.
• Multifocal PVCs arise when more than one site in the ventricles initiate depolarization, causing each peak on the ECG to have a different shape. If 3 or more PVCs occur in a row it may be called ventricular tachycardia.

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According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].

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Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.

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The staging of [malignancy name] is based on the [staging system].

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There is no established system for the staging of [malignancy name].

There is no established system for the classification of [disease name].

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[Disease name] may be classified according to [classification method] into [number] subtypes/groups:

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[Disease name] may be classified into [large number > 6] subtypes based on:

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[Disease name] may be classified into several subtypes based on:

• [Classification method 1]
• [Classification method 2]
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Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.

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If the staging system involves specific and characteristic findings and features:

According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].

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The staging of [malignancy name] is based on the [staging system].

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There is no established system for the staging of [malignancy name].

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Radwa AbdElHaras Mohamed AbouZaied, M.B.B.S[2] Mugilan Poongkunran M.B.B.S [3]

Premature ventricular contraction is a relatively common event where the heartbeat is initiated by Purkinje fibres in the ventricles rather than by the sinoatrial node, the normal heartbeat initiator.

• Normally impulses pass through both ventricles almost simultaneously and the depolarization waves of the two ventricles partially cancel each other out in the ECG. However, when a PVC occurs the impulse nearly always travels in one direction, so there is no neutralisation effect and this results in the high voltage QRS wave in the electrocardiograph.
• There are two main physiological explanations for premature ventricular contractions:
  • 1. Re-entrant signalling
  • 2. Enhanced automaticity in some ectopic focus: The enhanced automaticity means that the ectopic centre fires more regularly than usual and is protected from depolarisation that results in premature contractions.

There are a number of different molecular explanations for PVCs. One explanation is most basically due to an increased amount of cyclic AMP(cAMP) in the ventricular cardiac myocytes leading to increased flow of calcium ions into the cell. This may happen for the following reasons:

• Activation of the sympathetic nervous system, due to anxiety or hypovolemia. This activation can cause a release of catecholamines such as epinephrine (adrenaline) which can bind to beta-1 adrenergic receptor (β₁ receptors) on cardiac myocytes, activating a type of guanosine nucleotide-binding protein called G_s protein.^[1] This type of protein stimulates the production of cAMP,^[2] ultimately increasing the flow of calcium ions from the extracellular space and from the sarcoplasmic reticulum into the cytosol.^[3]
  This has the effect of increasing the strength of contraction (inotropy) and depolarizing the myocyte more rapidly (chronotropy). The ventricular myocytes are therefore more irritable than usual, and may depolarize spontaneously before the SA node depolarizes. Other sympathomimetic molecules such as amphetamines and cocaine will also cause this effect.
• Phosphodiesterase inhibitors such as caffeine directly affect the G-coupled signal transduction cascade^[4] by inhibiting the enzyme that catalyzes the breakdown of cAMP,^[1] again leading to the increased concentration of calcium ions in the cytosol.
• Potassium ion concentrations are a major determinant in the magnitude of the electrochemical potential of cells, and hypokalemia makes it more likely that cells will depolarize spontaneously.
• Hypercalcemia has a similar effect, although clinically it is of less concern.
• Magnesium ions affect the flow of calcium ions, and they affect the function of the Na+/K+ ATPase, and are necessary for maintaining potassium levels. Hypomagnesemia therefore also makes spontaneous depolarization more likely.
• Existing damage to the myocardium can also provoke PVCs. The myocardial scarring that occurs in myocardial infarction and also in the surgical repair of congenital heart disease can disrupt the conduction system of the heart and may also irritate surrounding viable ventricular myocytes, make them more likely to depolarize spontaneously. Inflammation of the myocardium (as occurs in myocarditis) and systemic inflammation cause surges of cytokines, which can affect the electrical properties of myocytes and may be ultimately responsible for causing irritability of myocytes.

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Genes involved in the pathogenesis of [disease name] include:

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The development of [disease name] is the result of multiple genetic mutations such as:

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Conditions associated with [disease name] include:

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2] Radwa AbdElHaras Mohamed AbouZaied, M.B.B.S[3]

Premature ventricular contractions can occur in a healthy person of any age, however, they are more common in patients with underlying heart disease such as ischemic heart disease and structural heart disease. Patients on tricyclic antidepressant are at risk of having PVCs.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

• Acute cardiac allograft rejection
• Acute coronary syndrome
• Diabetic ketoacidosis
• NSTEMI
• Pulmonary embolism
• Short QT syndrome
• STEMI

• Alcohol
• Amiodarone
• Anxiety disorder
• Azithromycin
• Caffeine consumption
• Cocaine
• Congestive heart failure
• Dilated cardiomyopathy
• Hypercalcemia
• Hypertensive heart disease
• Hypokalemia
• Hypomagnesemia
• Inotropes
• Myocardial infarction
• Pseudoephedrine
• Pulmonary artery catheter
• Sympathomimetics
• Tobacco
• Tricyclic antidepressant
• Valvular heart disease

Disease name] may be caused by [cause1], [cause2], or [cause3].

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Common causes of [disease] include [cause1], [cause2], and [cause3].

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The most common cause of [disease name] is [cause 1]. Less common causes of [disease name] include [cause 2], [cause 3], and [cause 4].

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The cause of [disease name] has not been identified. To review risk factors for the development of [disease name], click here.

• Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of disease name, however complications resulting from untreated disease name is common.
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Common causes of [disease name] may include:

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• [Cause2]
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• [Disease name] is caused by an infection with [pathogen name].
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Less common causes of [disease name] include:

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• [Disease name] is caused by a mutation in the [gene name] gene.

List the causes of the disease in alphabetical order:

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2] Homa Najafi, M.D.[3] Sahar Memar Montazerin, M.D.[4]

A premature ventricular contraction originates in the ventricle, and this must be differentiated from an impulse that originates above the ventricle (i.e. it is supraventricular in origin) and conducts with a delay (i.e. a wide complex, it is aberrantly conducted).

Aberrant ventricular conduction is:

• A transient form of abnormal intraventricular conduction delay (#IVCD) and occurs when there is unequal refractoriness of the two bundles.
• The right bundle has a longer action potential duration, and is more vulnerable to conduction delay or failure.
• The refractory period is affected by the preceding cycle length.
• The refractory period is longer when there is a long preceding RR interval.
• Aberrant ventricular conduction is favored when a premature supraventricular impulse comes after a long preceding RR interval (Ashman phenomenon).
• If the underlying rhythm is sinus in origin, and if the abnormal QRS is preceded by a premature P wave, then the ectopic beat is likely to be supraventricular in origin.
• The absence of a fully compensatory pause further supports this diagnosis.
• If a retrograde P wave is identifiable after the QRS complex and the RP interval is less than 0.11 second, the premature beat is likely to have originated from the AV junction, since the RP interval is too short for VA conduction (unless an accessory pathway is present).
• A long RP interval of 0.20 seconds or longer is suggestive but not diagnostic of a PVC, since the retrograde conduction time of a junctional beat is less likely to exceed this duration.
• The beat is more likely to be due to aberrancy if the initial forces are similar to those of the sinus beat and if it has an RSR’ configuration in lead V1.
• If the QRS complexes in all the precordial leads are positive or all negative, then a PVC is more likely.
• Diagnosis of PVCs in the presence of atrial fibrillation:

  • Absence of P waves and the irregularity of the rhythm are the handicaps
  • A constant coupling time is suggestive of PVCs
  • Ashman phenomenon. Keep in mind that a long cycle length also favors the precipitation of a PVC, therefore this sign is helpful but not diagnostic of aberrancy.
  • PVC is favored if the abnormal complex terminates a short-long cycle.

[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].

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[Disease name] must be differentiated from [[differential dx1], [differential dx2], and [differential dx3].

[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].

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[Disease name] must be differentiated from [differential dx1], [differential dx2], and [differential dx3].

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As [disease name] manifests in a variety of clinical forms, differentiation must be established in accordance with the particular subtype. [Subtype name 1] must be differentiated from other diseases that cause [clinical feature 1], such as [differential dx1] and [differential dx2]. In contrast, [subtype name 2] must be differentiated from other diseases that cause [clinical feature 2], such as [differential dx3] and [differential dx4].

On the basis [symptom 1], [symptom 2], and [symptom 3], [disease name] must be differentiated from [disease 1], [disease 2], [disease 3], [disease 4], [disease 5], and [disease 6].

The table below provides information on the differential diagnosis of ventricular tachycardia in terms of ECG appearance:

Disease Name	Causes	ECG Characteristics	ECG view
Ventricular tachycardia [19][20][21][22][23]	Ischemic heart disease Illicit drug use such as cocaine and methamphetamine Structural heart diseases Electrolyte disturbances Congestive heart failure Myocarditis Obstructive sleep apnea Pulmonary artery catheter Long QT syndrome	Ventricular tachycardia originates from a ventricular focus. Lasts more than 30 seconds. Broad QRS complexes: rate of >90 BPM.	[24]
Ventricular fibrillation [17][25][26][27]	Acute coronary ischemia Cardiomyopathies Congenital heart disease Myocardial infarction Heart surgery Electrolyte abnormalities	Poorly identifiable QRS complexes and absent P waves The heart rate is >300 BPM Rhythm is irregular	[28]
Ventricular flutter [29][30][31]	Electrolyte disturbances Medications such as: Disopyramide Quinidine	The ECG shows: A typical sinusoidal pattern Frequency of 300 bpm	[32]
Asystole [33][34]	Hypovolemia Hypoxia Acidosis Hypothermia Hyperkalemia or Hypokalemia Hypoglycemia Cardiac Tamponade Tension pneumothorax Thrombosis Myocardial infarction Thrombosis Pulmonary embolism Cardiogenic shock Degeneration of the sinoatrial or atrioventricular nodes Ischemic stroke	There is no electrical activity in the asystole	[35]
Pulseless electrical activity [36][37]	Hypovolemia Hypoxia Hydrogen ions (Acidosis) Hypothermia Electrolyte disturbances Hypoglycemia Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers Tamponade Tension pneumothorax Thrombosis (Myocardial infarction) Thrombosis (Pulmonary embolism) Trauma (Hypovolemia from blood loss)	Several pattern are possible including: Normal sinus rhythm Sinus tachycardia, with discernible P waves and QRS complexes Bradycardia, with or without P waves	[38]
Torsade de Pointes [39][40][41]	*Electrolyte disturbances Medications such as: Amiodarone Azithromycin Clozapine Famotidine Flecainide Foscarnet Levofloxacin Lithium Mirtazipine Quetiapine Risperidone Tacrolimus Tamoxifen Ziprasidone	Paroxysms of VT with irregular RR intervals. A ventricular rate between 200 and 250 beats per minute. Two or more cycles of QRS complexes with alternating polarity. Changing amplitude of the QRS complexes in each cycle in a sinusoidal fashion. Prolongation of the QT interval. Is often initiated by a PVC with a long coupling interval, R on T phenomenon. There are usually 5 to 20 complexes in each cycle.	[42]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Homa Najafi, M.D.[2]Mugilan Poongkunran M.B.B.S [3]

The prevalence of premature ventricular contractions (PVCs) varies between 100 to 400 per 100,000 individuals worldwide on standard 12-lead electrocardiography and 4000 to 7500 per 100,000 individuals on 24- to 48-hour Holter monitoring. Patients of all age groups may develop PVC and the incidence increases with age. African- American individuals are more likely to develop PVCs. Men are more commonly developed the disease than women.

• The prevalence of PVCs varies between 100 to 400 per 100,000 individuals worldwide on standard 12-lead electrocardiography and 4000 to 7500 per 100,000 individuals on 24- to 48-hour Holter monitoring.^[1][2]

• Patients of all age groups may develop PVC.^[3]
• The incidence of PVCs increases with age.

• African- American individuals are more likely to develop PVCs.^[4]

• Men are more commonly developed PVCs than women.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Radwa AbdElHaras Mohamed AbouZaied, M.B.B.S[2] Mugilan Poongkunran M.B.B.S [3] Homa Najafi, M.D.[4]

Premature ventricular contraction can occur due to activation of the sympathetic nervous system and the common risk factors are anxiety, physiological stress etc. Patient with copper deficiency are also prone to PVCs.

• Anxiety/Stress
• Chocolate
• Caffeine
• Calcium/magnesium imbalance
• Dehydration
• Alcohol
• Exercise
• Hormonal imbalance
• Hypercapnia (CO₂ poisoning)
• Vagal hyperstimulation
• Lack of sleep/exhaustion
• Overeating
• Copper deficiency
• Monosodium glutamate (MSG)

There are no established risk factors for [disease name].

OR

The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.

There are no established risk factors for [disease name].

OR

The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

• Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.
• Common risk factors in the development of [disease name] include:
  • [Risk factor 1]
  • [Risk factor 2]
  • [Risk factor 3]

• Less common risk factors in the development of [disease name] include:
  • [Risk factor 1]
  • [Risk factor 2]
  • [Risk factor 3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2] Radwa AbdElHaras Mohamed AbouZaied, M.B.B.S[3]

Premature ventricular contraction caries no risk of mortality in the absence of any underlying heart disease. Heart rate turbulence is a phenomenon representing the return to equilibrium of the heart rate after a PVC. These parameters correlate significantly with mortality after myocardial infarction.

• In the absence of ischemic heart disease (CAD) or hypertension (HTN), there is no excess risk of mortality in patients with PVCs.
• On the other hand, PVCs in the presence of structural cardiac abnormalities or hypertension is associated with twice the expected mortality.
• The development of sustained ventricular tachycardia (VT) is most likely among those patients with greater than 12 PVCs/min, couplets, and multifocal PVCs.
• Complex ventricular ectopic activity (VEA) during acute phase of STEMI does not have any prognostic significance.
• Their presence 2 to 3 weeks after acute MI is associated with a 3 fold increase in the risk of sudden death.

1. Healthy patients
   • The most common arrhythmia in patients with and without CAD.
   • Less common in infants and children, more common in the elderly.
   • Usually originate from the RV.
   • In normal patients, they may be either precipitated or suppressed by exercise.
   • No relationship to coffee or smoking has been established.
   • Frequency decreases with sleep.
2. Coronary artery disease
   • Routine ECGs demonstrate PVCs in 10% of patients with CAD.
   • Incidence inreases to 60 to 88% when the monitoring is increased to 12 to 24 hours.
   • The frequency of complex VEA increases with increasing numbers of vessels involved. (40% with one, 53% with two, and 78% with three vessels involved has VEA).
   • Patients with CAD are more prone to develop VEA with exercise (incidence 4 times higher than age matched controls).
   • Reported incidence in acute MI varies, but is near 100%.
   • After the initial 6 hours, the frequency decreases.
   • Persistence of VEA is associated with larger infarct size.
   • In one study, patients with EFs of greater than 50% had no persistent VEA, and patients with EFs of less than 30% had frequent PVCs.
3. Other Organic Heart Diseases:
   • Occur on routine EKG in 1/3rd of patients.
   • 12% of patients with congested cardiomyopathy have PVC on routine tracings.
   • 1.6% of patients with IHSS have PVCs on routine EKG.
4. Drugs:
   • PVCs are the most common arrhythmia in patients with digoxin toxicity.
   • Other drugs that cause PVCs are quinidine, PCA, norpace, phenothiazines and tricyclic antidepressants.
5. Electrolyte Imbalance:
   • Hypokalemia, hypomagnesemia, and hypercalcemia are frequently associated with the appearance of ventricular arrhythmias.^{[1] [2]}

There is insufficient evidence to recommend routine screening for [disease/malignancy].

OR

According to the [guideline name], screening for [disease name] is not recommended.

OR

According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with [condition 1], [condition 2], and [condition 3].

There is insufficient evidence to recommend routine screening for [disease/malignancy].

OR

According to the [guideline name], screening for [disease name] is not recommended.

OR

According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with:

• [Condition 1]
• [Condition 2]
• [Condition 3]

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