Premature Ventricular Contraction

7/26/2019 Premature Ventricular Contraction

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PREMATURE VENTRICULAR CONTRACTION

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 Q! comple"es#$ith the Q! $idth usually % &' msec. hese comple"es are not preceded by a P-$ave and the -

$ave is usually lar*e and opposite in direction to the ma+or deflection of the Q!.

he clinical si*nificance of PVCs is dependent on PVC fre,uency# comple"ity and hemodynamic

response.

Pathophysioogy! PVCs reflect the enhanced activity of ventricular pacemaker cells. !u**ested

mechanisms for PVCs are reentry# tri**ered activity and enhanced automaticity.

eentry occurs $hen there is an ar

ea of one-$ay block in the Purkin+e fibers and a second area of slo$ conduction. urin* ventricular

activation# the area of slo$ conduction activates the blocked part of the system after the remainder of

the ventricle has recovered. his results in an e"tra beat. eentry can produce sin*le ectopic beats or

can tri**er paro"ysmal tachycardia.

ri**ered beats are felt to be due to after depolarizations tri**ered by the precedin* action potential.

nhanced automaticity su**ests that there is an ectopic focus of pacemaker cells $ithin the ventricle

that have a subthreshold potential for firin*. he

heart/s basic rhythm raises these cells to threshold# $hich precipitates an ectopic beat.

.

"r#$u#ncy!

In th# U%&%! 0ne of the most common arrhythmias# PVCs occur in patients $ith and $ithout

heart disease. 1n healthy# middle-a*ed males# more than 23 $ill sho$ PVCs on routine

4olter monitorin*. 1n patients $ith prior myocardial infarction (51)# more than 63 $ill

sho$ evidence of PVCs on 4olter.

.Mortaity'Mor(idity! he clinical si*nificance of PVCs depends on the clinical conte"t in $hich

they are occurrin*.

PVCs in youn* healthy patients $ithout underlyin* structural heart disease are not associated

$ith any increased rate of mortality.

PVCs occurrin* in older patients# in particular those $ith underlyin* heart disease# are

clinically si*nificant.

7 PVC fre,uency of % &8hour# the presence of runs of PVCs# multiple ventricular

morpholo*ies and PVCs occurrin* early in the cardiac cycle (-on- phenomenon) areassociated $ith increased mortality and subse,uent arrhythmic events.


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)! Ventricular ectopy may be hi*her in males than in females of the same a*e.

Ag#!PVC fre,uency increases $ith a*e# reflectin* the increased prevalence of cardiac disease in

older populations.

.

CLINICAL

*istory!

Patients are usually asymptomatic.

Palpitations and neck8chest discomfort can be caused by cannon a $aves or by the increased

force of contraction due to poste"trasystolic potentiation of contractility.

he patient may report feelin* the heart has stopped after a PVC.

1n patients $ith fre,uent PVCs or bi*eminy# syncope can be reported due to inade,uate stroke

volume or decreased cardiac output due to effectively halvin* the heart rate.

9on* runs of PVCs can also result in hypotension.

"ercise can increase or decrease the PVC rate.

Physica!

Cannon a $aves may be observed in the +u*ular venous pulse# if the timin* of the PVC causes

an atrial contraction a*ainst a closed tricuspid valve.

Compensatory pauses follo$in* a premature beat $ill be detected on auscultation.

he ectopic beat may produce a diminished or absent pulse# dependent on the force of the

ventricular contraction.

Caus#s!

Cardiac:

o 7cute myocardial infarction8ischemia

o 5yocarditis

o Cardiomyopathy# dilated or hypertrophic

o 4ypoma*nesemia# hypokalemia# hypercalcemia

o 5itral Valve Prolapse


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4ypo"ia

5edications (e.*.# di*o"in# sympathomimetics# tricyclic antidepressants# aminophylline#

caffeine)

1llicit substances (e.*.# cocaine# amphetamines# alcohol# tobacco)

+OR,UP

La( &tudi#s!

!erum electrolytes# in particular potassium consider checkin* ma*nesium level# especially in

patients $ith lo$ potassium.

1n selected patients# a dru* screen may be helpful.

;or patients on medication $ith kno$n pre-arrhythmic effects (e.*.# di*o"in or theophylline)#

dru* levels may be useful.

.I-aging &tudi#s!

lectrocardio*raphy (C


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o PVCs may appear in a pattern of bi*eminy# tri*eminy or ,uadri*eminy# $hich

describe a pattern of PVCs occurin* every other# every third or every fourth beat#

respectively.

o PVCs $ith identical morpholo*y on a tracin* are called monomorphic or unifocal. 1f

the PVCs demonstrate t$o or more different morpholo*ies# they are referred to asmultiform# pleomorphic or polymorphic.

o PVCs are usually described in terms of the 9o$n *radin* system for premature beats.

he hi*her the *rade# the more serious the ectopy.

o o premature beats

!V.

o !7C


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o here is no indication for routine P! in lo$-risk patients after 51. 9o$ risk refers to

simple ectopy# *ood 9V function and lo$ C4; class.

o 1t is indicated in hi*h-risk patients $ith comple" ectopy.

o P! is felt to be beneficial in those patients $ith sustained ventricular tachycardia*reater than 'A hours after an 51.

TREATMENT

Pr#hospita Car#!

elemetry

1V access

0"y*en

9idocaine should be used for patients $ith comple" ectopy and hemodynamic instability. 1t is

not indicated routinely for chest pain.

E-#rg#ncy D#part-#nt Car#!

Dhether or not to treat PVCs in the emer*ency or outpatient settin*s depends on the clinical

scenario. 1n the absence of cardiac disease# isolated# asymptomatic ventricular ectopy

re*ardless of confi*uration or fre,uency# re,uires no treatment. Dith cardiac disease# certain

to"icities and electrolyte imbalances# treatment may be re,uired. elemetry# 1V access#

o"y*en and a t$elve lead C< should be established.

4ypo"ia: reat the underlyin* cause and provide o"y*en and the 7BCs.

ru* o"icity: !pecific therapy indicated for certain to"icities. "amples include di*o"in

(;ab antibodies)# tricyclics (bicarbonate) and aminophylline (*astrointestinal decontamination

and# possibly# hemodialysis).

Correct electrolyte imbalances# particularly those of ma*nesium# calcium and potassium.

7cute 1schemia81nfarction:

o arly dia*nosis and treatment of acute infarction8ischemia is the cornerstone of

therapy.

o he routine use of lidocaine and other type 1 anti-arrhythmic a*ents in the settin* of

acute myocardial infarction is no lon*er recommended due to to"icity.

o his includes patients $ith ectopy in the immediate period after receivin*

thrombolytic a*ents# in $hich comple" ectopy is fre,uently seen.


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o 0nly in the settin* of symptomatic# comple" ectopy is lidocaine likely to benefit a

patient havin* an infarction.

o Beta-blockers have proven efficacy in the settin* of acute myocardial infarction and

are safe to use.

.Consutations! Cardiolo*y involvement may be indicated if the patient is refractory to standard

therapy.

MEDICATION

herapy for comple" ventricular ectopy depends on the settin* and the underlyin* cause. 1n dru*

to"icity# specific therapies are available. Dith electrolyte imbalances# correction of abnormalities is

therapeutic. 9idocaine is the 0C in the settin* of comple" ectopy in the peri-51 period if the patient

is symptomatic# yet there is no firm evidence to support this practice.

ru* Cate*ory:Anti-arrhythmics- hese a*ents alter the electrophysiolo*ic mechanisms responsible

for premature ventricular contractions (PVCs).

Drug Na-#

9idocaine - 1t is a class 1B a*ent that stabilizes cell membranes and

blunt phase of the action potential. ;urthermore# it shortens

repolarization. he net effect is to decrease firin* of the ectopic foci

and allo$ a normal rhythm to reassert itself.

Adut Dos#

7dminister a bolus of &-&. m*8k* 1V and repeat# as necessary# usin*

&. m*8k* boluses ,@- min to a total of @ m*8k*. ;ollo$ $ith acontinuous 1V infusion of ' m*8min after return of perfusion.

1n the event that a continuous 1V infusion is not started# additional

boluses of . m*8k* should be administered ,& min to maintain the

medication/s effect.

1f endotracheal administration is done# the dose used should be '-'.

times the 1V dose.

P#diatric Dos#

he endotracheal# intraosseous# and 1V loadin* dose for children is &

m*8k* and# if necessary# may repeat t$ice at , &-& min. ;ollo$in*the loadin* dose# start a continuous 1V infusion of '- mc*8k*8min.

Contraindications

7ll fibrinolytics are contraindicated in the follo$in* situations:

9idocaine is contraindicated for patients $ith documented

hypersensitivity to amide-type local anesthetics. 1ts use should be

avoided in patients $ith 7dams-!tokes syndrome and Dolf-Parkinson

$hite syndrome. 1t should also be avoided in patients $ith severe

sinoatrial# atrioventricular (7V) or intraventricular block# if an

artificial pacemaker is not in place.


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Int#ractions

Dhen taken concomitantly $ith cimetidine or beta-blockers# lidocaine

plasma concentrations can reach to"ic levels. 1n addition# $hen the

dru* is taken $ith procainamide and tocainide# the combination may

result in additive cardiodepressant action. 9idocaine may also

increase the effects of succinylcholine.

Pr#gnancy B - Esually safe but benefits must out$ei*h the risks.

Pr#cautions

o not use a dru* solution that contains preservatives. "ercise

caution also $hen the dru* is administered to patients $ith heart

failure# hepatic disease# hypo"ia# hypovolemia or shock# respiratory-

depression# and bradycardia.

he elderly may also be at increased risk for C>! and cardiac side

effects due to increased half-life or decreased clearance of the dru*.

4i*h plasma concentrations can cause seizures# heart block# and 7V

conduction abnormalities. 1n addition# the use of lidocaine has been

associated $ith mali*nant hyperthermic crisis.

.

Drug Na-#

Procainamide - 1t is a Class 1-7 antiarrhythmic used for PVCs. 1tincreases the refractory period of the atria and ventricles. 5yocardiac

e"citability is reduced by an increase in the threshold for e"citation

and inhibition of ectopic pacemaker activity.

Adut Dos#

Ese continued 1V infusion rates of @ m*8min until either the

arrhythmia is suppressed# the patient becomes hypotensive# the Q!

$idens 3 above baseline# or a ma"imum dose of &F m*8k* is

administered.

0nce arrhythmia is suppressed# may infuse at a continuous rate of &-Am*8min

P#diatric Dos#

!afety and efficacy in children have not been established. 4o$ever#

the follo$in* doses have been su**ested.

po: & to m*8k*8d divided ,@-2h

o not e"ceed A *8d

15: ' to @ m*8k*8d divided ,A-2h


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o not e"ceed A *8d

1V: @-2 m*8k*8dose infused over min

he maintenance dose is ' to 6 mc*8k*8min administered as acontinuous infusion.

o not e"ceed & m*8dose or ' *8d

Contraindications

o not administer to patients dia*nosed $ith complete heart block or

second or third de*ree heart block if a pacemaker is not in place.

7void also in patients $ith torsade de pointes. o not use in patients

$ith documented hypersensitivity to procainamide or related dru*s or

patients dia*nosed $ith systemic lupus erythematosus.

Int#ractions

1ncreased levels of procainamide metabolite >7P7 can be e"pected in

patients takin* cimetidine# amiodarone# trimethoprim# ranitidine# beta-

blockers# and ,uinidine.

Procainamide may also increase the effect of skeletal muscle

rela"ants# ,uinidine and lidocaine and neuromuscular blockers.

0flo"acin inhibits the tubular secretion of procainamide and may

increase peak plasma concentrations and bioavailability. 1n addition#

$hen the dru* is taken concurrently $ith sparflo"acin# it may increase

the risk of cardioto"icity.

Pr#gnancy C - !afety for use durin* pre*nancy has not been established.

Pr#cautions

he lon*-term use of this dru* leads to the development of a positive

antinuclear antibody test in 3 of the patients. his may result in

lupus erythematosus-like syndrome in about '3 to @3 of the

patients.

;atal blood dyscrasias have also been reported $ith therapeutic doses.

he plasma concentration of procainamide and its active metabolite#>7P7 # may also be increased in renal failure.

4i*h or to"ic concentrations may induce 7V block or abnormal

automaticity. Ese caution in patients $ith complete 7V block# di*italis

into"ication# or*anic heart disease# renal disease# and hepatic

insufficiency.

Drug Na-# Bretylium - 1t is a class 111 anti-arrhythmic a*ent used in the treatmentof PVCs and it should be avoided as an initial treatment because of its


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side effects and initial catecholamine-releasin* properties.

1ts use is limited to PVCs that are refractory to class 1 anti-

arrhythmics. 1t increases the fibrillation threshold# and causes a

refractory period by decreasin* potassium conductance.

Adut Dos#

7dminister an 1V dose of m*8k* (undiluted) over & min. 1f PVCs

persist# administer & m*8k* (undiluted) over & min

1f necessary# repeat ,&-@ min

o not e"ceed @-@ m*8k*

he maintenance dose# $hen the treatment has become effective# is &

to ' m*8min

P#diatric Dos#

!afety and efficacy in children have not been established. 1t has been

administered to a limited number of pediatric patients# but such use

has been inade,uate to define proper dosa*e and limitations.

>onetheless# the follo$in* doses have been su**ested.

& m*8k* over & min and repeat# as necessary# ,& min

o not e"ceed @ m*8k*

he maintenance dose is to & m*8k*8dose ,2h

Contraindications

o not administer to patients $ith complete heart block or second or

third de*ree heart block if a pacemaker is not in place. 7void also in

patients $ith torsade de pointes.

o not use in patients $ith documented hypersensitivity to

procainamide or related dru*s# or patients dia*nosed $ith systemic

lupus erythematosus. 1t should also be avoided in di*italis-induced

arrhythmias.

Int#ractions

1ncreased to"icity has been reported $hen this dru* is taken $ithpressor catecholamines# and di*italis. 1n addition# the risk of

cardioto"icity# $hen taken concurrently $ith sparflo"acin may

increase.


Pr#cautions 4ypotension is associated $ith the use of this dru*# especially in

patients $ith a fi"ed cardiac output (e.*.# aortic stenosis). Ese caution

in patients $ith renal insufficiency# severe pulmonary hypertension#


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and aortic stenosis.

he dru* has a prolon*ed half-life in the elderly and thus# $hen renal

clearance is &- ml8min# administer '3 to 3 of the dose. apid

1V in+ection may also result in transient hypertension# nausea andvomitin*. 9imit the in+ection to ml (undiluted) at each site.

ru* Cate*ory:Beta-Blockers- his cate*ory of dru*s has the potential to suppress ventricular

ectopy due to ischemia or e"cess catecholamines. 1n the settin* of myocardial ischemia beta-blockers

have antiarrhythmic properties and reduce myocardial o"y*en demand# secondary to elevations in

heart rate and inotropy.

Drug Na-#5etoprolol - 1t is a selective beta & -adrener*ic receptor blocker. 1t

decreases the automaticity of contractions.

Adut Dos# @ 1V bolus in+ections of m* each , ' min

P#diatric Dos# !afety and efficacy in children have not been established.

Contraindications

7void use in patients $ith documented hypersensitivity to this dru* or

related products and those dia*nosed $ith uncompensated con*estiveheart failure# cardio*enic shock# bradycardia# and 7-V conduction

abnormalities.

Int#ractions

7luminum salts# barbiturates# >!71s# penicillins# calcium salts#

cholestyramine# and rifampin may decrease its bioavailability and

plasma levels# possibly resultin* in a decreased pharmacolo*ic effect.

Conversely# loop diuretics# 570 inhibitors# haloperidol# and

hydralazine may increase metoprolol levels and thus its to"icity or

pharmacolo*ic effects.


Pr#cautions Beta-adrener*ic blockade may blunt the si*ns and symptoms of acute

hypo*lycemia. 1n addition# beta-adrener*ic blockers may mask

clinical si*ns (e*# tachycardia) of developin* or continuin*

hyperthyroidism. 7brupt $ithdra$al may e"acerbate symptoms of

hyperthyroidism# includin* thyroid storm. 5onitor the patient closely

and $ithdra$ the dru* slo$ly.


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urin* 1V administration# carefully monitor blood pressure# heart

rate# and C


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Pr#cautions

Beta-adrener*ic blockade may blunt the si*ns and symptoms of acutehypo*lycemia. 1n addition# beta-adrener*ic blockers may mask the

clinical si*ns (e*# tachycardia) of developin* or continuin*

hyperthyroidism. 7brupt $ithdra$al may e"acerbate symptoms of

hyperthyroidism# includin* thyroid storm.

Drug Na-#

Propranolol - 1t is a class 11 anti-arrhythmic nonselective beta-

adrener*ic receptor blocker. 1t has membrane-stabilizin* activity anddecreases the automaticity of contractions.

Adut Dos#

7dminister &-@ m* under careful monitorin* and do not e"ceed &

m*8min to avoid lo$erin* blood pressure and causin* a cardiac

standstill.

7llo$ time for the dru* to reach the site of action# particularly $hen

slo$ circulation is present. 1f necessary# *ive a second dose after '

min. hereafter# do not *ive additional dru* in less than Ah.

o not *ive additional propranolol after the desired alteration if the

desired rate and8or rhythm are achieved. ransfer to oral therapy as

soon as possible. he usual dose-ran*e is &-@ m* tid-,id.

P#diatric Dos#

1V use in children is not recommended. 4o$ever# an unlabeled dose

of .&-.& m*8k*8dose to a ma"imum of & m*8dose# by slo$ push has

been used for arrhythmias. ransfer to oral therapy as soon as

possible.

he usual pediatric dosa*e ran*e is '-A m*8k*8d divided bid (ie# & to '

m*8k* t$ice daily).

Contraindications


related products and those dia*nosed $ith uncompensated con*estive

heart failure# cardio*enic shock# bradycardia# and 7-V conduction

abnormalities.

Int#ractions 7luminum salts# >!71s# penicillins# barbiturates# calcium salts#

cholestyramine# and rifampin may decrease its bioavailability# and

plasma levels# possibly resultin* in a decreased pharmacolo*iceffects. Conversely# loop diuretics# haloperidol# hydralazine# and


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570 inhibitors may increase metoprolol levels# and thus its to"icity

or pharmacolo*ic effects.


Pr#cautions

Beta-adrener*ic blockade may suppress the si*ns and symptoms of

acute hypo*lycemia. 1n addition# beta-adrener*ic blockers may mask

the clinical si*ns (e*# tachycardia) of developin* or continuin*

hyperthyroidism. he abrupt $ithdra$al of this medication may

e"acerbate symptoms of hyperthyroidism# includin* thyroid storm.

ru* Cate*ory:Electrolytes- hese a*ents are considered to be therapeutic alternatives for refractoryPVCs. Patients $ith persistent or recurrent PVCs follo$in* antiarrhythmic administration# should be

assessed for underlyin* electrolyte abnormalities as a cause for their refractory dysrhythmia.

4ypoma*nesemia is associated $ith the onset of PVCs.

Drug Na-#

5orphine sulfate - 1t acts as an anti-arrhythmic a*ent and diminishes

the fre,uency of PVCs# particularly $hen it is secondary to acute

ischemia.

Adut Dos#

7dminister &- ' * diluted in & ml of D over a period of &-' min

for refractory V; and kno$n or suspected hypoma*nesemia (5* G'

less than &.A m,89).

o not e"ceed a dose of @-A *8d# or a rate of infusion for

maintenance of &-' *8h

Contraindications

7void use in patients $ith documented hypersensitivity to ma*nesium

and in those dia*nosed $ith heart block# 7ddison/s disease#

myocardial dama*e# or severe hepatitis.

Int#ractions

Concurrent use $ith nifedipine may cause hypotension and

neuromuscular blockade. 5a*nesium may also increase the

neuromuscular blockade seen $ith amino*lycosides and other a*ents

causin* neuromuscular anta*onism. 1n addition# it may increase the

C>! effects of C>! depressants. 5a*nesium also increases the

to"icity of C>! depressants# betamethasone# and cardioto"icity of

ritodrine.

Pr#gnancy 7 - !afe in pre*nancy


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Pr#cautions

5a*nesium may alter cardiac conduction leadin* to heart block indi*italized patients. espiratory rate# deep tendon refle"# and renal

function should be monitored $hen this electrolyte is administered

parenterally. Ese caution $hen administerin* the ma*nesium dose

since it may produce si*nificant hypertension or asystole.

ru* Cate*ory: Calcium channel blockers- 1n specialized automatic and conductin* cells in the heart#

calcium is involved in the *eneration of the action potential. he calcium channel blockers share the

ability to inhibit movement of calcium ions across the cell membrane. his effect can depress both

impulse formation (automaticity) and conduction velocity.

Drug Na-#

Verapamil - 1t can diminish PVCs associated $ith perfusion therapy

and decrease the risk of ventricular fibrillation and ventricular

tachycardia. By interruptin* reentry at the 7V node# verapamil can

restore normal sinus rhythm in patients $ith paro"ysmal

supraventricular tachycardias (P!V).

Adut Dos# 6-&2 m* tid

P#diatric Dos# !afety and efficacy in children have not been established.

Contraindications


related products and in those dia*nosed $ith severe C4;# sick sinus

syndrome or second- or third-de*ree 7V block# and hypotension (less

than H mm 4* systolic).

Int#ractions

!erum verapamil levels may be decreased by hydantoins. 9oss ofclinical effectiveness of oral verapamil may occur. he 1V route may

bypass this interaction.


Pr#cautions !everal cases of hepatocellular in+ury have been associated $ith

verapamil use. his medication may increase the activity of

transaminases $ith and $ithout concomitant elevations in alkalinephosphatase and bilirubin. levations have been transient and may


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disappear $ith continued verapamil treatment. 5onitor liver function#

periodically# in patients treated $ith this medication.

.

"OLLO+.UP

Prognosis!

1n asymptomatic patients $ithout underlyin* heart disease# the lon*-term pro*nosis is similarto that of the *eneral population. 7symptomatic patients $ith e+ection fractions *reater than

A3 demonstrate an appro"imately @.3 incidence of sustained ventricular tachycardia or

cardiac arrest. hus# in patients $ith absence of heart disease on noninvasive $ork-up#

reassurance is appropriate.

1n the settin* of acute coronary ischemia8infarction# patients $ith simple PVCs rarely

pro*ress to mali*nant arrhythmias. 4o$ever# persistent comple" ectopy after a myocardial

infarction is associated $ith increased risk of sudden death and may be an indication for P!.

Patients $ith underlyin* chronic structural heart disease (e.*.# cardiomyopathy# infarction# and

valvular disease) and comple" ectopy (or % & PVCs8hour) have a si*nificantly increased

mortality.

o here is also a poor understandin* of the role of anti-arrhythmic therapy in the

months post myocardial infarction. he Cardiac 7rrhythmia !uppression rial

(C7!) studied patients $ith ventricular ectopy post 51# to see if anti-arrhythmic

therapy improved survival. espite suppression of ectopy on 4olter monitorin*#

patients treated $ith encainide# flecainide or moricizine actually had hi*her rates of

sudden death and all-cause mortality. ecent studies have su**ested a role for

amiodarone in this patient population# and have demonstrated si*nificant reductions

in post-51 ventricular arrhythmias and death.

o 9eft ventricular function has a much stron*er association $ith increased mortalitythan do PVCs. PVCs are felt by many to reflect the severity of heart disease# rather

than havin* a precipitatin* role in arrhythmo*enesis as $as once thou*ht.

P! has a primary role in risk stratification of patients $ith fre,uent or comple"

PVCs. Patients $ith PVCs that are noninducible (i.e.# unable to tri**er ventricular

tachycardia durin* stimulation) have a lo$ risk of sudden death.

MI&CELLANEOU&


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&p#cia Conc#rns!

Pediatrics:

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

o 7bout '3 of healthy boys# a*e &-&@# sho$ PVCs on routine 4olter.

o PVCs in healthy ne$borns *enerally resolve by the t$elfth $eek and usually re,uire

no treatment once the presence of a normal heart is confirmed.

o his is probably related to developmental factors associated $ith the autonomic

nervous system.

o 1n older children# PVCs are often related to transient or e"o*enous factors includin*

mild viral myocarditis# e"cessive caffeine or sympathomimetic dru*s (cold or asthma

medications). hey usually resolve $ithout treatment.

Dhen comple" ectopy is seen in pre*nancy# or immediately after# obtain an C< for possible

peripartum cardiomyopathy.

Patients $ith presentations that indicate an ischemic basis for their PVCs (e.*.# chest pain#

dyspnea# and syncope) or are hemodynamically unstable# should be closely monitored $hile

in the and admitted to an appropriate monitored settin*.

BIBLIO/RAP*0

Burkart ;# Pfisterer 5# Iio$ski D : ffect of antiarrhythmic therapy on mortality in survivors

of myocardial infarction $ith asymptomatic comple" ventricular arrhythmias: Basel

7ntiarrhythmic !tudy of 1nfarct !urvival (B7!1!). J 7m Coll Cardiol &HH &2: &F&&-&F&6.

Cairns J7# Connolly !J# oberts : andomized trial of outcome after myocardial infarction

in patients $ith fre,uent or repetitive ventricular premature depolarizations: C7517. 9ancet

&HHF @AH: 2F-26'.

Califf 5# 5cIinnis 7# Burks J: Pro*nostic implications of ventricular arrhythmias durin*

'A hour ambulatory monitorin* in patients under*oin* cardiac catheterization for coronary

artery disease. 7m J Cardiol &H6' : '@-@&.

4allstrom 7P# Bi**er J# oden : Pro*nostic si*nificance of ventricular premature

depolarizations measured & year after myocardial infarction in patients $ith early

postinfarction asymptomatic ventricular arrhythmia. J 7m Coll Cardiol &HH' ': 'H-'2A.

4ammill !C # rusty J5# Dood 9: 1nfluence of ventricular function and presence or

absence of coronary artery disease on results of electrophysiolo*ic testin* for asymptomatic

nonsustained ventricular tachycardia. 7m J Cardiol &HH 2: F''-F'6.


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4ar*arten I# Chapman P# !tueven 47: Prehospital prophylactic lidocaine does not

favorably affect outcome in patients $ith chest pain. 7nn 5ed &HH &H: &'FA-&'FH.

Iennedy 47# Dhitlock J7# !pra*ue 5I: 9on* term follo$-up of asymptomatic healthy

sub+ects $ith fre,uent and comple" ectopy. >J5 &H6 @&': &H@-&HF.

9o$n B# Dolf 5: 7pproaches to sudden death from coronary heart disease. Circulation &F&

AA: &@-&A'.

5a**ioni 7P# Kuanetti # 0lsson

Premature Ventricular Contraction

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