taking a diagnostic approach

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SUMMARYNearly all pediatric murmurs areheard in normal hearts and arenot due to cardiac disorders.These murmurs usually can beclassified by distinctive featuresand distinguished from organicmurmurs by skillful clinicalexamination. This articlereviews the various types ofinnocent heart murmurs inchildren, discusses theirdifferential diagnoses, andsuggests an approach to sortingout pediatric murmurs.

RESUMEChez les enfants, presque tousles souffles sont entendus dansdes coeurs normaux et ils nesont pas causes par despathologies cardiaques. On peuthobituellement classifier cessouffles selon leurscaracteristiques distinctes, etl'examen clinique minutieuxpermet de les distinguer dessouffles organiques. Cet articlepasse en revue les divers typesde souffles anorganiques chezles enfants, discute dudiagnostic differentiel etpropose une approche pour biendistinguer les soufflespediatriques.Con Fam Physician 1995;41:1507-151 2.

Innocent heart murmurs

in child

Taking a diagnostic approach

NORMAN R. SAUNDERS, MD, FRCPC

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PPROXIMATELY HALF OF ALL

children have a detectablemurmur when the pre-cordium is auscultated.' Yet

the incidence of congenital heart diseaseis only 0.8%. Thus, the problem for pri-mary care physicians is to distinguishmurmurs related to an underlying heartdefect from murmurs created by thenormal flow ofblood within a structural-ly sound cardiovascular system.

Early and accurate identification ofcongenital heart defects allows forappropriate endocarditis prophylaxisand can lead to early treatment, whichcan prevent increased morbidity andmortality. Incorrect labeling of ahealthy heart as abnormal causes con-siderable patient morbidity throughpsychological impact, needless restric-tion from sports participation, andinsurability.3'4 Although accurate diag-nosis is important, investigating everymurmur will alarm parents needlesslyand add to the burden of a stressedhealth care system. This paper aims toprovide primary care physicians withan effective approach to assessing heartmurmurs detected in children.

Dr Saunders is an Assistant Professor ofPediatrics at the Universi_y of Toronto and is aStaffPediatrician at the Hospitalfor SickChildren in Toronto.

History and physical examinationIt is important to remember that theheart is a muscular pump. If the heartis malformed and, as a result, producesa murmur, several clues in the historyand physical examination of thepatient probably suggest the presenceofpump malfunction.

History. A patient's family history aswell as prenatal and postnatal recordcan help identify a serious heart mur-mur. For example, having a sibling witha ventricular septal defect (VSD)results in a recurrence risk of 6%.2 Ahistory of intrauterine insult shouldcreate suspicion that a murmur isorganic. For example, it has long beenknown that infection with rubella canproduce structural cardiovasculardefects. Also, it is wise to suspect anymurmur detected in a baby with a lowbirth weight. Postnatal symptoms of apoorly functioning heart that shouldactively be sought include poor feed-ing, failure to thrive, frequent lowerrespiratory tract infections (all associat-ed with increased left to right shunt-ing), excess diaphoresis, diminishedexercise tolerance, and precordial pain.

Nonauscultatoryfindings. To assessthe cardiac status of a child, it is helpfulto divide the physical examination into

Canadian Family Physician VOL41: September 1995 1507

general appearance, nonauscultatorycardiac findings, and auscultation. Thegeneral examination often suggeststhat a murmur is indeed pathological.For example, the presence of dysmor-phism, such as Down's syndrome,would increase one's concern if a mur-

mur were noted. Tachycardia or

tachypnea at rest sometimes accompa-

ny left to right shunting or failure.Unusually full pulses imply aortic run-

off seen in patent ductus arteriosus.Weak femoral pulses are, of course, a

sign of aortic coarctation.The chest wall could reveal a pre-

cordial bulge due to chronic cardiacenlargement or, perhaps, a hyperdynamic

heart. Palpating the precordium can

reveal a thrill, which implies an organ-

ic murmur. Thus, before the examineractually listens to the heart, much can

be learned about its functioning.Conversely, if a cardiac defect isminor, nonauscultatory findings are

usually normal.

Auscultation. As in adult patients,more will be learned when listening to

children's hearts when one dissects thefindings by focusing on each heartsound individually than when listeningfor clicks and then searching for mur-

murs in both systole and diastole. Forexample, an abnormally loud second

1508 Canadian Famif Physician VOL41: September 1995

CME

Innocent heart murmurs in children

heart sound (S2) implies pulmonaryhypertension, whereas a widely splitand fixed S2 is heard when an atrialseptal defect (ASD) is present.Discovering a click can help distinguishmild semilunar valve stenosis or mitralvalve prolapse from an innocent mur-

mur. Remembering to auscultate thenewborn's head can result in earlydiagnosis of an intracranial arteriove-nous malformation.

Innocent heart murmurs tend todisplay certain identifying features.Most arise from turbulence at the ori-gin of the great vessels. Generally,they are of short duration, are low inintensity and poorly transmitted,occur in early systole, and are of thecrescendo-decrescendo type. Theyvary with position, being best heardwhen the child is supine. Most impor-tantly, patients with an innocent heartmurmur display no associated cardiacabnormalities.On the other hand, an underlying

heart defect is likely present wheneverthe murmur seems very loud, is dias-tolic or pansystolic, or occurs late insystole; it is especially likely if associat-ed cardiac findings are abnormal.

Nearly all innocent heart murmurs

heard in childhood are classified as one

of five distinguishable types: Still'smurmur (also known as the vibratorysystolic murmur), the physiological pul-monary systolic ejection murmur, thesupraclavicular arterial bruit, thevenous hum, and peripheral pul-monary stenosis of infancy. Each has itsown distinctive features and differentialdiagnoses.

Still's (vibratory systolic)murmur

Features. The vibratory systolic or

Still's murmur is a common, low-fre-quency, early systolic ejection murmur

that is best heard at the left lower ster-nal border and extending to the apex

cordis. The murmur is most likely tobe noted after infancy and has a peakincidence in 3- to 7-year-olds. A vibra-tory or buzzing quality to the murmuris best appreciated listening with the

bell of the stethoscope while thepatient is supine. The intensity of Still'smurmur will be reduced by theValsalva maneuver (Figure 1).

Differential diagnoses. The chiefdifferential diagnoses of Still's murmurare idiopathic hypertrophic subaorticstenosis and a small VSD.'

Idiopathic hypertrophic subaortic stenosis:This familial cardiomyopathy can

cause a relatively quiet murmur in themiddle of the left sternal border. It isassociated with outflow obstructiondue to ventricular hypertrophy,arrhythmias, and even sudden death.Clinically, it can be distinguished fromStill's murmur by the Valsalva maneu-

ver. In idiopathic hypertrophic subaor-tic stenosis, the murmur intensifies

with the Valsalva maneuver becausereduced venous return causes the out-flow tract to narrow. Still's murmur is

reduced by the Valsalva maneuver.

Furthermore, the murmur of idiopath-ic hypertrophic subaortic stenosis lacksthe low-pitched musical quality of theStill's; pulses tend to be brisk, and theelectrocardiogram displays left ventric-ular hypertrophy.

Small ventricular septal defect: Murmurcharacteristics of a VSD generallyvary with the size of the defect. Asmall or closing VSD can be difficultto distinguish from the innocent vibra-tory systolic murmur, as it can presentas an early systolic murmur maximalin the third left interspace. Generally,however, murmurs associated with theVSD are pansystolic and more regur-

gitant in quality.

Physiological pulmonary systolicejection murmurFeatures. The physiological pul-monary systolic ejection murmur is an

early systolic crescendo-decrescendosound heard best with the diaphragmin the left second interspace (Figure 2).It is usually Grade 2 in intensity withlimited radiation. It is louder whenpatients lie supine or during inspira-

tion and is more obvious in slightlybuilt subjects or in situations of

(Canadian Family Plhysician VOL 41 September 1995 1509

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increased cardiac output, such as feveror exercise.

Differential diagnoses. Atrial septaldefects and pulmonary stenosis causephysiological pulmonary systolic ejec-tion murmurs.

Atrial septal defect: It is, perhaps, mostimportant not to mistake an ASD foran innocent pulmonic murmur.Although the ASD's murmur is also aGrade 2 to 3 systolic ejection murmurmaximal in the left second intercostalspace, several associated findings helpto distinguish it. The right ventricularimpulse is prominent; the second com-ponent of the first heart sound is loud,and the second heart sound is fixedand widely split. The ECG often showssigns of right conduction delay with orwithout right axis deviation or ventric-ular hypertrophy.

Pulmonary stenosis: The murmur ofpulmonary stenosis. sometimes resem-bles that of the physiological pul-monary murmur. Yet it is commonlyassociated with a click or thrill or awider radiation, which helps separate itfrom its innocent counterpart.

Other diagnoses: Other entities to con-sider include small VSD and mitral ortricuspid insufficiency, which should bedistinguishable by their clinical find-ings (especially the more blowing pan-systolic nature).

Supraclavicular arterial bruitFeatures. The supraclavicular arteri-al bruit is a relatively harsh, early sys-tolic murmur heard best with the bellof the stethoscope above the clavicles(Figure 3), particularly on the rightside. It is louder when patients sit, andits intensity can be reduced by hyper-extending patients' shoulders withtheir elbows bent. The murmur isheard at any age, but especially mid-childhood. It is thought to result fromturbulence in the brachiocephalic orcarotid arteries.6

Differential diagnosis. Be careful tocheck for a thrill in the suprasternalnotch; this usually implies a pathological

murmur, particularly aortic valvestenosis. This malformation, as well asbicuspid aortic valve, is often associat-ed with an ejection click; clicks shouldactively be sought. Furthermore, themurmur in aortic valve lesions tends tobe loudest below the right clavicle andis not diminished by shoulder hyperex-tension.

Venous humFeatures. The cervical venous hum isa relatively high-frequency, soft, blow-ing, continuous murmur heard bestwhen the patient is sitting down. It is acommon murmur, most frequentlynoted when the child is between 3 and8 years. Although potentially bilateral,it is most prominent to the right of thesternum anywhere from the supraclav-icular area to the base (Figure 4). It canbe intensified by rotating the patient'shead to the contralateral side while lis-tening with the bell in the supraclavic-ular space. Digital compression of theipsilateral internal jugular vein willreduce or eliminate the murmur whenauscultating in the same position. Thehum is much quieter when the patientis in the supine position.

Differential diagnosis. The cervicalvenous hum should be differentiatedfrom a patent ductus arteriosus.Whereas the venous hum is diminishedwhen the patient is supine and can beobliterated by compressing the internaljugular vein, the patent ductus arterio-sus is not and cannot. The venous humis similar to the continuous ductal mur-mur except that the diastolic compo-nent is high-pitched and the hum istruly a continuous ceaseless murmur,whereas the diastolic component of theductal murmur is low-pitched anddecrescendo.7 Patent ductus arteriosusis frequently associated with boundingpulses and a hyperdynamic left cardiacimpulse.

Innocent peripheralpulmonary stenosisFeatures. In newborns, particularly inpremature infants, the relatively dilated

1510 Canadian Famiy Physician VOL 41: September 1995

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main pulmonary artery branches tosmaller lateral vessels at sharp angles,creating turbulence and thus an audi-ble sound, the murmur of peripheralpulmonary stenosis (Figure 5), in some

babies. It is a short midsystolic ejectionmurmur of medium pitch and intensi-ty. It is heard in the pulmonic area insystole but is equally loud when auscul-tated in the axillae. The sound fre-quency of the murmur is similar to thatof a neonate's breath sounds and couldbe missed, particularly if the axillae are

not auscultated.

Differential diagnosis. The mur-

mur of innocent peripheral stenosisshould radiate widely and disappearwithin a few months. If it does not,then one is probably dealing withanother process associated with a pul-monic murmur, eg, pulmonary stenosis(valvular, supravalvular, or subvalvu-lar), ASD, patent ductus arteriosus, or

anomalous pulmonary venous return.True pulmonary branch stenosis, as

opposed to the innocent transientinfantile peripheral pulmonary steno-sis, frequently is accompanied by a his-tory of maternal rubella exposure.

Valvular stenosis often has an associat-ed click. Wide and fixed splitting of thesecond heart sound should accompany

an ASD, and ductal murmurs tend tobe harsh and continuous.

InvestigationsNewburger et al8 found little likelihoodthat ECG, chest x-ray, or M-modeechocardiogram results would alter thediagnosis of innocent heart murmur

made on the basis of a proper historyand physical examination. Smythe etal9 reported that the clinical examina-tion by a pediatric cardiologist, used toidentify the origin of childhood mur-

murs, had a sensitivity of 96%, speci-ficity of 95%, positive predictive valueof 88%, and negative predictive valueof 98%. In this study, the ECGchanged no diagnosis from innocent topathological. Generally, the chest x-ray,

ECG, and even the echocardiogramserve more to identify the specific

nature of already suspected disordersthan to screen murmurs thought to beinnocent based upon clinical examina-tion.

ManagementPrimary care physicians can effective-ly screen for heart murmurs in chil-dren. Congenital heart disease will beidentified in 46% of cases by the firstweek, in 88% of children by 1 year,

and in 98% by 4 years of age.'0

Furthermore, although less than 1%of children have congenital heart dis-ease, the incidence at initial assess-

ment by a pediatric cardiologist is

approximately 30% to 35%o.8,9'lWhen a careful history and physi-

cal examination clearly support thediagnosis of innocent heart murmur,neither further investigation nor refer-al is indicated. It is sufficient toinform the parents and the child,when appropriate, of the presence ofthe murmur in as reassuring a man-

ner as possible. Thereafter, the mur-

mur can be monitored at routineperiodic checkups.

In some situations, one cannot becertain of a murmur's innocence. Ifthe child has historical risk factors forcongenital heart disease, if the exam-

ination is suboptimal due to non-

compliance, or if the findings are

equivocal, a chest x-ray and ECG are

indicated. Afterward, if the physicianremains uncertain about the murmur

or suspects an organic lesion, referralto a pediatric cardiologist is advised. Areferral could also be required ifparental anxiety remains excessive.

In general, the younger the patient,the more prompt should be the refer-ral.'2 Neonates with suspected congeni-tal heart disease should be referred as

soon as possible, whereas older asymp-tomatic children can safely wait weeksfor assessment by a cardiologist withlittle likelihood of adverse effect.

Correspondence to: Dr Norman RSaunders, 586 Eglinton Ave E, Suite 404,Toronto, ON M4P IP2

Continued on page 1512

Canadian Family Physician VOL41: September 1995 1511

CME


cilazapril

Th.rup.utk aussiflcotionAngiotensin Connefting Enzyme Inhibitor

lkstios Ai Cac Use

Mild to moderate essential hypertension. May use alone or in combination withthiazide diuretics. Use not recommended in congestive heor failure or renovascularhypertension as safety and efficacy not esteblished. Safety and efficacy of concomituntuse with ontihypertensive agents other than thiazide diuretics not established. Whenused in pregnancy during the second and third trimesters, ACE inhibtiors can causeinjury or even death of the developing fetus. When pregnancy is detected 'Inhibece'should be discontinued as soon as possible.

Contrd tkafo.sHypersensotivtiy to this product and history of angioedema related to previous treatmentwith an angiotensin converting enzyme inhibitor.

Anaioedema: Angioedema has been reported. Discontinue, institute appropriatetherapy without delay, ond fallow corefully until the swelling subsides. When tongue,gbttis or larynx involved, odminister subcuteneors adrenaline (0.5 mL 1:1000)promptly when indkated. Patients with history of angioedema unrelatd to ACEinhibitor may be at increased risk.Hvpotension: Symptomatic hypotension has been repored, after first dose ou whendose increased. More likely with sodium or volume depftion. Potients with congestivoheart foilure may expeoience excessive hypotension and should ster therapy underclose medical supervision ond be folbwed for the first two weeks of treatment andwhen increasing the dose of Inhiboce' and/or diurefic.Neutropenio/Agranulocvtosis: Leucopenia and neutropenia have been reported.Monitor whhte blood cell counts periodically.Use in Preanancy: ACE inhibitors can souse fetel and neonatel morbidty and mortalitywhen administered to pregnant women. Discontinue as soon us possible whenpregnancy detected. Consuo product monogmph for situations in which no ahemativetreatment can be fosnd, and for infants with a history of in utero exposure.

Pr.coutissImpnired Renal Function: Use with coution. Monitor patients closely assessing renalfunction before and duoing thempy. Dosoge reducton and/or discontinuation ofconcomitent diuretic and/or cilazopsil may be required. In patients with severe heardisease, treatment wthh ACE inhibinors may resuh in oliunao and/or azotemia ondacute renal foilure and/or death. Increases in blood urea nitrogen and/or serumcreatinine observed in potients with renol artery stenosis. Inaease in blood ureantirogen and creatinine observed with concomtnant use of diuretic.Anaphvlactoid Reoctions duron Membrane Exposure: Anophyctoid rections havebeen reported in patients dialysed wih highflux (polyocrylontrile) membranes. Dialysisshould be stopped immediately.AnaohvIactoid Reoacions duoina Desershrization: There have been isolated reportsof potients expesiencing susteined lie-threatening naphyloctoid reoctions whilerecehang ACE inhibitors duoing desenstizing treatment with hymenoptem(bees and wasps) venom.Hyverkalemia: Elevated serum potassium observed. Consider oddtiional risk factors.Vavular Stenosis: Potients with aortic stenosis might be at nsk of decreasedcoronary perfusion.Sumerv/Anesthesia: Arterial hypotension may resuh.Impoired Liver Function: Hepotits, jaundice, elevations in liver enzymes and/or serumbilirunin reported duoing thempy with ACE inhibitors. Liver function tests, othernecessary irwestigations and/or discontinuation of thempy should be considered. Nostudies in potients with cirrhosis and/or liver dysfunction. Therefore, use with coution.Couah: Consider possible drug involvement as port of differentiol diagnosis.Nursina Mothers: Not known if excreted in breast milk. Use with coution.Pediatric Use: Safety and efficacy not established. Not recommended.Eldedo: Greater sensitivity cannot be ruled out.

Drug lbterotionsDiuretic Themwy: Occunence of hypotension. Minimize by discontinuing diuretic usincreasing sob intake, prior to intilation of treatment with Inhibuce' and/or reducingintial dose of Inhibace'.Aaents Increasina Serum Potassium: Elvotion of serum potassium has been reported.Use potassium spesing diuretics with coution and monitor frequently.Aaents Cousina Renin Release: Antihypertensive effect is ougmented.Acents Affectina Somoathetic Activit: Use with coution.Inhibitors of Endoeeous Prostealondin Synthesis: Indomethadn may reducethe antihypertensive effect of cilozopril but there is no evidence of attenuationof blood pressure lowering effects of daozopril when its odministmtion precedesthe ndministmtion of the NSAID.Pboexin: No phanvacodynamic us phanvucokiretic interaction.Lithium Salts: Lithium elimination may be reduced. Therefore, monitorseram ltithium levels.

Adverse ReaotdesThe most frequent adverse reactions (2,586 hypertensive participants) reported incontrolled clinical trials were: headache (5.1%), dizziness (3.0/o), fatigue (2.1%),cough (1.8%) and nousea (1.3%). 2.4% disconfinued. The most severe adversereocfions reported in 5,450 hypertensive patients were ongioedema/face edema(0.1%), postuml hypotension (0.3%), ortostatic hypotension (2.1%), myocardialinforction (0.1%), cerebrovascular disorder (0.04%), renal foilure (0.09%), andthrombwaytopenk purpum (0.02%). For adverse reoctions occurong in <1% of thepotients consut product monograph.Abnormal Labomtory Findinas: Leucopenia 0.2%, neutropenia 0.4%, changesin liver funcfion enzymes 0.1% - 1.1%, changes in renol function tests 0.6% orless, hyperkoemia (>5.5 mEq/L) 0.7%, serum creafinine >2 mg/dL 1.3%,proteinuria 0.5%.

Dosg And Ad imstratliIndividualize dosoge. Initial dose 2.5 tog per day. Usesl dose mnge 2.5 mg to 5 mgper day in a single daily dose. U seisfactory control is not maintained for 24 hours,consider twice daily odministrtion with the senme total daily dose or an inaeased dose,maximum dose of 10 mg duUy.If blood pressure is not adequately controlled with Inhibace' alone, a non-potassiumrspasing diuretic may be administered concomitantly.Diuretic-Treated Patents: Discontinue diuretic two to three days oefore 'Inhiboce'. Stertat 0.5 mg (hal of a mg tebhet) once doily and monitor the patient after the firstdose until stabilized. Thereafter, adiust the dose according to individual response.Dosoae in EldWAv Patienis (Over 65 Years): Insitah treatment with 1.25 mg(huff of a 2.5 mg tablet) once daily or less and adjust wtih caution.

Dosue Adiustment in Renal Imnairment (induding patients on diolysis):

Creatinine Clearance Initial Dose of 'Inhibace' Maximol Dose of Inhibace'

>40 ml/min 1 mg once daily 5 mg once daily10 - 40 mV/min 0.5 mg once doily 2.5 mg once daily<10 mIL/min 0.25 -0.5 mg once or twice a week according

to blood pressure response

Dosoae Adiustment in Hepatic Impairment Initiote treotment with cautionat a dose af 0.5 mg once daily.

Av&hqInhiboce' (dlazapdl) is available in film-coatd tablets containing:

1 ma cilazapril yellow, oval shaped, single scored bicorvex thlets,imprinted CIL 1.

2.5 ma cilazon)l pinkish-erown, oval shaped, single scored biconex tablets,impdnted CIL 2,5.

5 ma cilazazdl reddish-brown, oval shaped, single scored biconvex tablets,impdnted ROCHE 5.

Botfes of 100 tohlets.Schedule F Drug.

Product Monogmph avoiloble upon request.

1. Clozel JP, et al. Vascukaf protection with cilzopdl in hypertension.I Cadoor Flnol 1992;19(suppl 5):28s-33s.

2. Cozel JP, et al. Effects af chronic ACE inhihtiio on cardiac hypetrophy and coronaryvascular reverse in spontoneamly hypertensive mts with developed hypertesion.J of lypertesion 1989;7:2672175.

3. Clozel JP, et al. Decreases af vascular hypertrophy in four different types af atoresin spDntnesous hypertensive mts. Am IJMeed 1989;87suppl 6B):92s-95s.

4. lnhibace' Product Monograph.5. Lacourdcre Y et al. Anthihypertensive effects of cilazopril, 2.5 and S mg, once daily

versus pbcebo on amWatory olood pressure folbwing single and repetidoseadministration. I Caodioesc mleonocol 1991;18:219-223.

6. Jackson B, Cubela R, Johnston C. Angiotensin converting enzyme (ACE),chamcterization hy 12514MK351A binding studies of plasma and tissue ACEduodng variation of s utot in the rat. I of HIypeneosimo 1986;4:759-765.

7. Higashimore K, Gante J, Holzemonn 6, Inagami T. Signifance of vascular renin forInca) gonertion af angiotersins. Hypertension 1991;17(3):270-277.

8. Based on 1994 Price Lists and Ontorio Dreg Denefit Formulary withJanuary 15, 1995 Supplement and 1995 Ouebec Formulary.

MEMBER

/ > © 1995, Hoffmann-La Roche Lmited< Roche v e Registered Trademark af Hoffmanr La Roche lmited

a Mississauga, Ontudao lSN 617

CME

References1. Friedman S, Robie WA, Harris TN.Occurrence of innocent adventiouscardiac sounds in childhood. Pediatrics1949;4:782-9.

2. HoffmanJIE. Congenital heart disease:incidence and inheritance. Pediatr ClinNorth Am 1990;37:25-43.

3. Engle MA. Insurability and employability:congenital heart disease and innocentmurmurs. Circulation 1977;56:143-5.

4. Bergman AB, Stamm SJ. The morbidityof cardiac nondisease in school children.NEnglJ Med 1967;276:1008-13.

5. Danforth DA, McNamara DG. Innocentheart murmurs and heart sounds. In:Garson A, BrickerJT, McNamara DG,editors. The science and practice ofpediatriccardiology. Philadelphia: Lea and Febiger,1990: 1919-28.

6. Park MK. Physical examination. In:Park MK, editor. Pediatric cardiologyforpractitioners. 2nd ed. Chicago: Year BookMedical Publishers, Inc, 1988:9-33.

7. McNamara DG. Value and limitationsof auscultation in the management of con-genital heart disease. Pediatr Clin North Am1990;37:93-113.

8. NewburgerJW, Rosenthal A,Williams RG, Fellows K, Miettinen OS.Noninvasive tests in the initialmanagement of heart murmurs inchildren. NEngljMed 1983;308:61-4.

9. SmytheJF, Teixeira OHP, Vlad P,Demers PP, Feldman W Initial evaluationof heart murmurs: are laboratory testsnecessary? Pediatrics 1990;86:497-500.

10. HoffmanJ1E, Christianson R.Congenital heart disease in a cohort of19,502 births with long-term follow up.Am3 Cardiol 1978;42:641-7.

11. Danforth DA, Nasir A, Gumbiner C.Cost assessment of the evaluation of heartmurmurs in children. Pediatrics 1993;91:365-8.

12. Rosenthal A. How to distinguishbetween innocent and pathological mur-murs in childhood. Pediatr Clin North Am1984;31 1229-40.

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