Dott. Maurizio M. Ciammaichella

Dirigente Medico
Responsabile UAS “Trombosi Venosa Profonda ed Embolia Polmonare”
Responsabile CDF BLSD IRC “Emersan Lateranum”
U.O.C. Medicina Interna I° per l'Urgenza

(Direttore: Dott. G. Cerqua)
A.C.O. S. Giovanni - Addolorata - Roma

PREMATURE VENTRICULAR CONTRACTION

KEY-WORDS: Premature ventricular contraction

INTRODUCTION
CLINICAL
WORKUP
TREATMENT
MEDICATION
FOLLOW-UP
MISCELLANEOUS
BIBLIOGRAPHY

INTRODUCTION

Background: Premature ventricular contraction (PVC) is an ectopic cardiac pacemaker located in the ventricle. PVCs are characterized by the premature occurrence of bizarre-shaped QRS complexes, with the QRS width usually > 120 msec. These complexes are not preceded by a P-wave and the T-wave is usually large and opposite in direction to the major deflection of the QRS.

The clinical significance of PVCs is dependent on PVC frequency, complexity and hemodynamic response.

Pathophysiology: PVCs reflect the enhanced activity of ventricular pacemaker cells. Suggested mechanisms for PVCs are reentry, triggered activity and enhanced automaticity.

Reentry occurs when there is an ar

ea of one-way block in the Purkinje fibers and a second area of slow conduction. During ventricular activation, the area of slow conduction activates the blocked part of the system after the remainder of the ventricle has recovered. This results in an extra beat. Reentry can produce single ectopic beats or can trigger paroxysmal tachycardia.

Triggered beats are felt to be due to after depolarizations triggered by the preceding action potential.

Enhanced automaticity suggests that there is an ectopic focus of pacemaker cells within the ventricle that have a subthreshold potential for firing. The

heart's basic rhythm raises these cells to threshold, which precipitates an ectopic beat.

Frequency:

In the U.S.: One of the most common arrhythmias, PVCs occur in patients with and without heart disease. In healthy, middle-aged males, more than 60% will show PVCs on routine Holter monitoring. In patients with prior myocardial infarction (MI), more than 80% will show evidence of PVCs on Holter.

.Mortality/Morbidity: The clinical significance of PVCs depends on the clinical context in which they are occurring.

PVCs in young healthy patients without underlying structural heart disease are not associated with any increased rate of mortality.

PVCs occurring in older patients, in particular those with underlying heart disease, are clinically significant.
A PVC frequency of > 10/hour, the presence of runs of PVCs, multiple ventricular morphologies and PVCs occurring early in the cardiac cycle (R-on-T phenomenon) are associated with increased mortality and subsequent arrhythmic events.

Sex: Ventricular ectopy may be higher in males than in females of the same age.

Age: PVC frequency increases with age, reflecting the increased prevalence of cardiac disease in older populations.

CLINICALPATHOPHYSIOLOGY

History:

Patients are usually asymptomatic.

Palpitations and neck/chest discomfort can be caused by cannon a waves or by the increased force of contraction due to postextrasystolic potentiation of contractility.

The patient may report feeling the heart has stopped after a PVC.

In patients with frequent PVCs or bigeminy, syncope can be reported due to inadequate stroke volume or decreased cardiac output due to effectively halving the heart rate.

Long runs of PVCs can also result in hypotension.
Exercise can increase or decrease the PVC rate.

Physical:

Cannon a waves may be observed in the jugular venous pulse, if the timing of the PVC causes an atrial contraction against a closed tricuspid valve.

Compensatory pauses following a premature beat will be detected on auscultation.

The ectopic beat may produce a diminished or absent pulse, dependent on the force of the ventricular contraction.

Causes:

Cardiac:

Acute myocardial infarction/ischemia

Myocarditis

Cardiomyopathy, dilated or hypertrophic

Hypomagnesemia, hypokalemia, hypercalcemia

Mitral Valve Prolapse

Hypoxia

Medications (e.g., digoxin, sympathomimetics, tricyclic antidepressants, aminophylline, caffeine)

Illicit substances (e.g., cocaine, amphetamines, alcohol, tobacco)

WORKUP

Lab Studies:

Serum electrolytes, in particular potassium; consider checking magnesium level, especially in patients with low potassium.

In selected patients, a drug screen may be helpful.

For patients on medication with known pre-arrhythmic effects (e.g., digoxin or theophylline), drug levels may be useful.

.Imaging Studies:

Electrocardiography (ECG):

An ECG should be obtained in patients with complex ectopy to rule out structural heart disease.

This will be useful not only in evaluating the ejection fraction, which is important prognostically, but any valvular disease and evidence of hypertrophy.

An ECG is essential to the diagnosis and work-up of PVCs.

Instances in which the ECG can be very helpful in determining the cause of ventricular ectopy include: acute ischemia/infarction (ST segment, T-wave changes), electrolyte abnormalities (hyperacute T-waves, QT prolongation drug effects (QRS widening and QT prolongation) or hypertrophy.

Electrocardiographic findings in PVCs may include any of the following:

a. They are premature in relation to the next expected beat of the basic rhythm.

b. The pause following the premature beat is usually a fully compensatory pause.

c. The R-R interval surrounding the premature beat is equal to double the basic R-R interval, showing that the ectopic beat did not reset the sinus node.

PVCs may appear in a pattern of bigeminy, trigeminy or quadrigeminy, which describe a pattern of PVCs occuring every other, every third or every fourth beat, respectively.

PVCs with identical morphology on a tracing are called monomorphic or unifocal. If the PVCs demonstrate two or more different morphologies, they are referred to as multiform, pleomorphic or polymorphic.

PVCs are usually described in terms of the Lown grading system for premature beats. The higher the grade, the more serious the ectopy.

Grade 0 = No premature beats

Grade 1 = Occasional (< 30 per hour)

Grade 2 = Frequent (> 30 per hour)

Grade 3 = Multiform

Grade 4 = Repetitive (A = Couplets, B = Salvos of = or > 3)

Grade 5 = R-on-T

Other Tests:

Holter 24-hour monitors are useful in quantifying and characterizing ventricular ectopy.

Holters have also been used to determine treatment efficacy in patents with frequent or complex PVCs.

Suppression of ectopy on Holter monitoring is not always predictive of survival.

The most important role for Holter monitoring is risk stratification of patients with a recent myocardial infarction or known left ventricular dysfunction.

Signal Averaged ECG (SAECG):

SAECGs may have a future role in identifying patients at risk for complex ventricular ectopy and NSVT.

SAECGs may have a role in identifying patients with complex ectopy who may benefit from EPS.

.Procedures:

Exercise Stress Testing (EST) is best used complementary to Holter monitoring. In patients with complex ectopy, EST can unmask nonsustained ventricular tachycardia triggered by increased catecholamines or myocardial ischemia.

The role of electrophysiologic studies (EPS) in complex ventricular ectopy is an area of both intense research and debate. A joint AHA/ACC statement suggested the following:

There is no indication for routine EPS in low-risk patients after MI. Low risk refers to simple ectopy, good LV function and low CHF class.

It is indicated in high-risk patients with complex ectopy.
EPS is felt to be beneficial in those patients with sustained ventricular tachycardia greater than 24 hours after an MI.

TREATMENT

Prehospital Care:

Telemetry

IV access

Oxygen

Lidocaine should be used for patients with complex ectopy and hemodynamic instability. It is not indicated routinely for chest pain.

Emergency Department Care:

Whether or not to treat PVCs in the emergency or outpatient settings depends on the clinical scenario. In the absence of cardiac disease, isolated, asymptomatic ventricular ectopy regardless of configuration or frequency, requires no treatment. With cardiac disease, certain toxicities and electrolyte imbalances, treatment may be required. Telemetry, IV access, oxygen and a twelve lead ECG should be established.

Hypoxia: Treat the underlying cause and provide oxygen and the ABCs.

Drug Toxicity: Specific therapy indicated for certain toxicities. Examples include digoxin (Fab antibodies), tricyclics (bicarbonate) and aminophylline (gastrointestinal decontamination and, possibly, hemodialysis).

Correct electrolyte imbalances, particularly those of magnesium, calcium and potassium.

Acute Ischemia/Infarction:

Early diagnosis and treatment of acute infarction/ischemia is the cornerstone of therapy.

The routine use of lidocaine and other type I anti-arrhythmic agents in the setting of acute myocardial infarction is no longer recommended due to toxicity.

This includes patients with ectopy in the immediate period after receiving thrombolytic agents, in which complex ectopy is frequently seen.

Only in the setting of symptomatic, complex ectopy is lidocaine likely to benefit a patient having an infarction.
Beta-blockers have proven efficacy in the setting of acute myocardial infarction and are safe to use.

.Consultations: Cardiology involvement may be indicated if the patient is refractory to standard therapy.

MEDICATION

Therapy for complex ventricular ectopy depends on the setting and the underlying cause. In drug toxicity, specific therapies are available. With electrolyte imbalances, correction of abnormalities is therapeutic. Lidocaine is the DOC in the setting of complex ectopy in the peri-MI period if the patient is symptomatic, yet there is no firm evidence to support this practice.

Drug Category: Anti-arrhythmics - These agents alter the electrophysiologic mechanisms responsible for premature ventricular contractions (PVCs).

Drug Name	Lidocaine - It is a class IB agent that stabilizes cell membranes and blunt phase 0 of the action potential. Furthermore, it shortens repolarization. The net effect is to decrease firing of the ectopic foci and allow a normal rhythm to reassert itself.
Adult Dose	Administer a bolus of 1-1.5 mg/kg IV and repeat, as necessary, using 1.5 mg/kg boluses q3-5 min to a total of 3 mg/kg. Follow with a continuous IV infusion of 2 mg/min after return of perfusion. In the event that a continuous IV infusion is not started, additional boluses of 0.5 mg/kg should be administered q10 min to maintain the medication's effect. If endotracheal administration is done, the dose used should be 2-2.5 times the IV dose.
Pediatric Dose	The endotracheal, intraosseous, and IV loading dose for children is 1 mg/kg and, if necessary, may repeat twice at q 10-15 min. Following the loading dose, start a continuous IV infusion of 20-50 mcg/kg/min.
Contraindications	All fibrinolytics are contraindicated in the following situations: Lidocaine is contraindicated for patients with documented hypersensitivity to amide-type local anesthetics. Its use should be avoided in patients with Adams-Stokes syndrome and Wolf-Parkinson white syndrome. It should also be avoided in patients with severe sinoatrial, atrioventricular (AV) or intraventricular block, if an artificial pacemaker is not in place.
Interactions	When taken concomitantly with cimetidine or beta-blockers, lidocaine plasma concentrations can reach toxic levels. In addition, when the drug is taken with procainamide and tocainide, the combination may result in additive cardiodepressant action. Lidocaine may also increase the effects of succinylcholine.
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Do not use a drug solution that contains preservatives. Exercise caution also when the drug is administered to patients with heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression, and bradycardia. The elderly may also be at increased risk for CNS and cardiac side effects due to increased half-life or decreased clearance of the drug. High plasma concentrations can cause seizures, heart block, and AV conduction abnormalities. In addition, the use of lidocaine has been associated with malignant hyperthermic crisis.

Drug Name	Procainamide - It is a Class I-A antiarrhythmic used for PVCs. It increases the refractory period of the atria and ventricles. Myocardiac excitability is reduced by an increase in the threshold for excitation and inhibition of ectopic pacemaker activity.
Adult Dose	Use continued IV infusion rates of 30 mg/min until either the arrhythmia is suppressed, the patient becomes hypotensive, the QRS widens 50% above baseline, or a maximum dose of 17 mg/kg is administered. Once arrhythmia is suppressed, may infuse at a continuous rate of 1-4 mg/min
Pediatric Dose	Safety and efficacy in children have not been established. However, the following doses have been suggested. po: 15 to 50 mg/kg/d divided q3-6h Do not exceed 4 g/d IM: 20 to 30 mg/kg/d divided q4-6h Do not exceed 4 g/d IV: 3-6 mg/kg/dose infused over 5 min The maintenance dose is 20 to 80 mcg/kg/min administered as a continuous infusion. Do not exceed 100 mg/dose or 2 g/d
Contraindications	Do not administer to patients diagnosed with complete heart block or second or third degree heart block if a pacemaker is not in place. Avoid also in patients with torsade de pointes. Do not use in patients with documented hypersensitivity to procainamide or related drugs or patients diagnosed with systemic lupus erythematosus.
Interactions	Increased levels of procainamide metabolite NAPA can be expected in patients taking cimetidine, amiodarone, trimethoprim, ranitidine, beta-blockers, and quinidine. Procainamide may also increase the effect of skeletal muscle relaxants, quinidine and lidocaine and neuromuscular blockers. Ofloxacin inhibits the tubular secretion of procainamide and may increase peak plasma concentrations and bioavailability. In addition, when the drug is taken concurrently with sparfloxacin, it may increase the risk of cardiotoxicity.
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	The long-term use of this drug leads to the development of a positive antinuclear antibody test in 50% of the patients. This may result in lupus erythematosus-like syndrome in about 20% to 30% of the patients. Fatal blood dyscrasias have also been reported with therapeutic doses. The plasma concentration of procainamide and its active metabolite, NAPA , may also be increased in renal failure. High or toxic concentrations may induce AV block or abnormal automaticity. Use caution in patients with complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency.

Drug Name	Bretylium - It is a class III anti-arrhythmic agent used in the treatment of PVCs and it should be avoided as an initial treatment because of its side effects and initial catecholamine-releasing properties. Its use is limited to PVCs that are refractory to class I anti-arrhythmics. It increases the fibrillation threshold, and causes a refractory period by decreasing potassium conductance.
Adult Dose	Administer an IV dose of 5 mg/kg (undiluted) over 1 min. If PVCs persist, administer 10 mg/kg (undiluted) over 1 min If necessary, repeat q15-30 min Do not exceed 30-35 mg/kg The maintenance dose, when the treatment has become effective, is 1 to 2 mg/min
Pediatric Dose	Safety and efficacy in children have not been established. It has been administered to a limited number of pediatric patients, but such use has been inadequate to define proper dosage and limitations. Nonetheless, the following doses have been suggested. 10 mg/kg over 1 min and repeat, as necessary, q15 min Do not exceed 30 mg/kg The maintenance dose is 5 to 10 mg/kg/dose q6h
Contraindications	Do not administer to patients with complete heart block or second or third degree heart block if a pacemaker is not in place. Avoid also in patients with torsade de pointes. Do not use in patients with documented hypersensitivity to procainamide or related drugs, or patients diagnosed with systemic lupus erythematosus. It should also be avoided in digitalis-induced arrhythmias.
Interactions	Increased toxicity has been reported when this drug is taken with pressor catecholamines, and digitalis. In addition, the risk of cardiotoxicity, when taken concurrently with sparfloxacin may increase.
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Hypotension is associated with the use of this drug, especially in patients with a fixed cardiac output (e.g., aortic stenosis). Use caution in patients with renal insufficiency, severe pulmonary hypertension, and aortic stenosis. The drug has a prolonged half-life in the elderly and thus, when renal clearance is 10-50 ml/min, administer 25% to 50% of the dose. Rapid IV injection may also result in transient hypertension, nausea and vomiting. Limit the injection to 5 ml (undiluted) at each site.

Drug Category: Beta-Blockers - This category of drugs has the potential to suppress ventricular ectopy due to ischemia or excess catecholamines. In the setting of myocardial ischemia beta-blockers have antiarrhythmic properties and reduce myocardial oxygen demand, secondary to elevations in heart rate and inotropy.

Drug Name	Metoprolol - It is a selective beta 1 -adrenergic receptor blocker. It decreases the automaticity of contractions.
Adult Dose	3 IV bolus injections of 5 mg each q 2 min
Pediatric Dose	Safety and efficacy in children have not been established.
Contraindications	Avoid use in patients with documented hypersensitivity to this drug or related products and those diagnosed with uncompensated congestive heart failure, cardiogenic shock, bradycardia, and A-V conduction abnormalities.
Interactions	Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease its bioavailability and plasma levels, possibly resulting in a decreased pharmacologic effect. Conversely, loop diuretics, MAO inhibitors, haloperidol, and hydralazine may increase metoprolol levels and thus its toxicity or pharmacologic effects.
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Beta-adrenergic blockade may blunt the signs and symptoms of acute hypoglycemia. In addition, beta-adrenergic blockers may mask clinical signs (eg, tachycardia) of developing or continuing hyperthyroidism. Abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm. Monitor the patient closely and withdraw the drug slowly. During IV administration, carefully monitor blood pressure, heart rate, and ECG.

Drug Name	Esmolol - It is an excellent drug for use in patients at risk for experiencing complications from beta-blockade. This is particularly true in patients with mild-moderate LV dysfunction, reactive airway disease, and peripheral vascular disease. The short half-life of 8 min allows for titration to desired effect, and the ability to stop quickly if needed.
Adult Dose	Initially administer a loading dose infusion of 500 mcg/kg/min for 1 min followed by a 4 min maintenance infusion of 50 mcg/kg/min. Repeat the loading dose and follow with a maintenance infusion of 100 mcg/kg/min if an adequate therapeutic effect is not observed within 5 min. Continue the titration procedure, repeating the loading infusion and increasing the maintenance infusion by increments of 50 mcg/kg/min (for 4 min). As the desired heart rate or a therapeutic end-point (eg, lowered blood pressure) is approached, omit the loading infusion and reduce the incremental dose in maintenance infusion from 50 mcg/kg/min to 25 mcg/kg/min or lower. Also, if desired, increase the interval between the titration steps from 5 to 10 min.
Pediatric Dose	Safety and efficacy in children have not been established. The suggested dose is 100-500 mcg/kg administered over 1 min
Contraindications	Avoid use in patients with documented hypersensitivity to this drug or related products and in those diagnosed with cardiogenic shock, congestive heart failure, bradycardia, and A-V conduction abnormalities.
Interactions	Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease its bioavailability and plasma levels, possibly resulting in a decreased pharmacologic effect. Conversely, loop diuretics, haloperidol, hydralazine, and MAO inhibitors may increase metoprolol levels and thus its toxicity or pharmacologic effects.
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Beta-adrenergic blockade may blunt the signs and symptoms of acute hypoglycemia. In addition, beta-adrenergic blockers may mask the clinical signs (eg, tachycardia) of developing or continuing hyperthyroidism. Abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm.

Drug Name	Propranolol - It is a class II anti-arrhythmic nonselective beta-adrenergic receptor blocker. It has membrane-stabilizing activity and decreases the automaticity of contractions.
Adult Dose	Administer 1-3 mg under careful monitoring and do not exceed 1 mg/min to avoid lowering blood pressure and causing a cardiac standstill. Allow time for the drug to reach the site of action, particularly when slow circulation is present. If necessary, give a second dose after 2 min. Thereafter, do not give additional drug in less than 4h. Do not give additional propranolol after the desired alteration if the desired rate and/or rhythm are achieved. Transfer to oral therapy as soon as possible. The usual dose-range is 10-30 mg tid-qid.
Pediatric Dose	IV use in children is not recommended. However, an unlabeled dose of 0.01-0.1 mg/kg/dose to a maximum of 1 mg/dose, by slow push has been used for arrhythmias. Transfer to oral therapy as soon as possible. The usual pediatric dosage range is 2-4 mg/kg/d divided bid (ie, 1 to 2 mg/kg twice daily).
Contraindications	Avoid use in patients with documented hypersensitivity to this drug or related products and those diagnosed with uncompensated congestive heart failure, cardiogenic shock, bradycardia, and A-V conduction abnormalities.
Interactions	Aluminum salts, NSAIDs, penicillins, barbiturates, calcium salts, cholestyramine, and rifampin may decrease its bioavailability, and plasma levels, possibly resulting in a decreased pharmacologic effects. Conversely, loop diuretics, haloperidol, hydralazine, and MAO inhibitors may increase metoprolol levels, and thus its toxicity or pharmacologic effects.
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Beta-adrenergic blockade may suppress the signs and symptoms of acute hypoglycemia. In addition, beta-adrenergic blockers may mask the clinical signs (eg, tachycardia) of developing or continuing hyperthyroidism. The abrupt withdrawal of this medication may exacerbate symptoms of hyperthyroidism, including thyroid storm.

Drug Category: Electrolytes - These agents are considered to be therapeutic alternatives for refractory PVCs. Patients with persistent or recurrent PVCs following antiarrhythmic administration, should be assessed for underlying electrolyte abnormalities as a cause for their refractory dysrhythmia. Hypomagnesemia is associated with the onset of PVCs.

Drug Name	Morphine sulfate - It acts as an anti-arrhythmic agent and diminishes the frequency of PVCs, particularly when it is secondary to acute ischemia.
Adult Dose	Administer 1- 2 g diluted in 100 ml of D5W over a period of 1-2 min for refractory VF and known or suspected hypomagnesemia (Mg +2 less than 1.4 mEq/L). Do not exceed a dose of 30-40 g/d, or a rate of infusion for maintenance of 1-2 g/h
Contraindications	Avoid use in patients with documented hypersensitivity to magnesium and in those diagnosed with heart block, Addison's disease, myocardial damage, or severe hepatitis.
Interactions	Concurrent use with nifedipine may cause hypotension and neuromuscular blockade. Magnesium may also increase the neuromuscular blockade seen with aminoglycosides and other agents causing neuromuscular antagonism. In addition, it may increase the CNS effects of CNS depressants. Magnesium also increases the toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine.
Pregnancy	A - Safe in pregnancy
Precautions	Magnesium may alter cardiac conduction leading to heart block in digitalized patients. Respiratory rate, deep tendon reflex, and renal function should be monitored when this electrolyte is administered parenterally. Use caution when administering the magnesium dose since it may produce significant hypertension or asystole.

Drug Category: Calcium channel blockers - In specialized automatic and conducting cells in the heart, calcium is involved in the generation of the action potential. The calcium channel blockers share the ability to inhibit movement of calcium ions across the cell membrane. This effect can depress both impulse formation (automaticity) and conduction velocity.

Drug Name	Verapamil - It can diminish PVCs associated with perfusion therapy and decrease the risk of ventricular fibrillation and ventricular tachycardia. By interrupting reentry at the AV node, verapamil can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardias (PSVT).
Adult Dose	80-160 mg tid
Pediatric Dose	Safety and efficacy in children have not been established.
Contraindications	Avoid use in patients with documented hypersensitivity to this drug or related products and in those diagnosed with severe CHF, sick sinus syndrome or second- or third-degree AV block, and hypotension (less than 90 mm Hg systolic).
Interactions	Serum verapamil levels may be decreased by hydantoins. Loss of clinical effectiveness of oral verapamil may occur. The IV route may bypass this interaction.
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Several cases of hepatocellular injury have been associated with verapamil use. This medication may increase the activity of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin. Elevations have been transient and may disappear with continued verapamil treatment. Monitor liver function, periodically, in patients treated with this medication.

FOLLOW-UP

Prognosis:

In asymptomatic patients without underlying heart disease, the long-term prognosis is similar to that of the general population. Asymptomatic patients with ejection fractions greater than 40% demonstrate an approximately 3.5% incidence of sustained ventricular tachycardia or cardiac arrest. Thus, in patients with absence of heart disease on noninvasive work-up, reassurance is appropriate.

In the setting of acute coronary ischemia/infarction, patients with simple PVCs rarely progress to malignant arrhythmias. However, persistent complex ectopy after a myocardial infarction is associated with increased risk of sudden death and may be an indication for EPS.

Patients with underlying chronic structural heart disease (e.g., cardiomyopathy, infarction, and valvular disease) and complex ectopy (or > 10 PVCs/hour) have a significantly increased mortality.

There is also a poor understanding of the role of anti-arrhythmic therapy in the months post myocardial infarction. The Cardiac Arrhythmia Suppression Trial (CAST) studied patients with ventricular ectopy post MI, to see if anti-arrhythmic therapy improved survival. Despite suppression of ectopy on Holter monitoring, patients treated with encainide, flecainide or moricizine actually had higher rates of sudden death and all-cause mortality. Recent studies have suggested a role for amiodarone in this patient population, and have demonstrated significant reductions in post-MI ventricular arrhythmias and death.

Left ventricular function has a much stronger association with increased mortality than do PVCs. PVCs are felt by many to reflect the severity of heart disease, rather than having a precipitating role in arrhythmogenesis as was once thought.

EPS has a primary role in risk stratification of patients with frequent or complex PVCs. Patients with PVCs that are noninducible (i.e., unable to trigger ventricular tachycardia during stimulation) have a low risk of sudden death.

MISCELLANEOUS

Special Concerns:

Pediatrics:

PVCs are less common in children than in adults but do occur in normal children.

About 20% of healthy boys, age 10-13, show PVCs on routine Holter.

PVCs in healthy newborns generally resolve by the twelfth week and usually require no treatment once the presence of a normal heart is confirmed.

This is probably related to developmental factors associated with the autonomic nervous system.

In older children, PVCs are often related to transient or exogenous factors including mild viral myocarditis, excessive caffeine or sympathomimetic drugs (cold or asthma medications). They usually resolve without treatment.

When complex ectopy is seen in pregnancy, or immediately after, obtain an ECG for possible peripartum cardiomyopathy.
Patients with presentations that indicate an ischemic basis for their PVCs (e.g., chest pain, dyspnea, and syncope) or are hemodynamically unstable, should be closely monitored while in the ED and admitted to an appropriate monitored setting.

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