Chronic Occlusive Arterial Disease of the...

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Chronic Occlusive Arterial Disease of the Extremities By JOHN L. JUERGENS, M.D. CHRONIC occlusive arterial diseases are the most common and the most disabling of all peripheral vascular disorders. Some of the causes of chronie arterial occlusion are arteriosclerosis obliterans, thromboangiitis ob- literans (Buerger's disease), primary arterial thrombosis, which presumably results froni hypercoagulable blood, embolism, which is almost always associated with heart disease or peripheral arterial aneurysms, trauma, and ergotism.' Of these, arteriosclerosis obliterans is by far the most frequently eiicountered. Although differing clinically and pathologi- cally, all of the diseases are similar in that they cause isehemia of tissues supplied by the occluded arteries. The degree of iseheinia is directly proportional to the rapidity of de- velopment and the extent of occlusion and is inversely proportional to the extent and rapidity of developnient of collateral arterial anastonioses. The isehemia may be increased by arteriolar constriction and decreased by arteriolar dilatation from aiiy cause. When blood flow diminishes to the point where tissue does not receive sufficient oxygen to sustaiii life, or when injury or ilifection inereases the demand for oxygen that the occluded arteries are uiiable to supply, gangrene occurs. It is beyond the scope of this presentation to discuss in detail the distinguishing features of the various chronic occlusive arterial dis- eases. Although much of what follows pertains to all or some of these diseases, most of it deals more specifically with thromboangiitis obliterans (TAO) * and with arteriosclerosis obliterans (ASO) .* Recently the concept of TAO as a diagnostic entity has been vigor- ously challenged and defended on both clini- From the Section of Medicine, Mayo Cliinic and Mayo Foundation, Rochester, MIinnesota. *Hereafter in this discussion thromboangiitis obli- terans will be referred to as TAO and arteriosclerosis obliterans will be referred to as ASO. cal and pathologic grounds. It has been contended that TAO is due in fact to atherosclerosis, arterial embolism, or arterial thrombosis, or to a combination of all three conditions.2 Most experienced students of per- ipheral vascular diseases, however, agree with MeKusick and associates3 that TAO is a dis- tinct clinical and pathologic entity. Recent evidence strongly supports the usefulness of distinguishing between TAO and ASO be- eause of the marked differences in prognosis of patients affected with either disease.4 Some of the distinguishing clinical features of these two diseases are set forth in table 1. Symptoms The symptoms of ehronic occlusive arterial disease result from impairment of blood flow to the extremities. The symptoms may appear gradually as a result of slowly progressive occlusion or suddenly as a result of acute arterial thrombosis or embolism. They may progress episodically or remain relatively static for many years. The outstanding symp- tom of chronic occlusive arterial disease is pain that may take several forms. Intermittent claitdication1 is the commonest and usually the earliest symptom. This is a pain, ache, cramp, or severe fatigue that affects muscles distal to the occluded artery wheni these muscles are exercised. Rest with- out a change of position or cessation of weight bearing promptly relieves the distress. In cases of ASO, intermittent claudication prac- tically always involves one or both lower extreniities, most commonly the calf, but in some patients it is noted in the foot, thigh, or hip alone or in association with the calf. During any stage of the disease intermittent claudication can usually be reproduced con- sistently after a certain distance of walking at a eertain rate. A progressive or sudden decrease in the claudication distance, that is, Circulation, Volume XX VII, May 196? 964 by guest on May 19, 2018 http://circ.ahajournals.org/ Downloaded from

Transcript of Chronic Occlusive Arterial Disease of the...

Chronic Occlusive Arterial Disease of the ExtremitiesBy JOHN L. JUERGENS, M.D.

CHRONIC occlusive arterial diseases arethe most common and the most disabling

of all peripheral vascular disorders. Some ofthe causes of chronie arterial occlusion arearteriosclerosis obliterans, thromboangiitis ob-literans (Buerger's disease), primary arterialthrombosis, which presumably results fronihypercoagulable blood, embolism, which isalmost always associated with heart diseaseor peripheral arterial aneurysms, trauma, andergotism.' Of these, arteriosclerosis obliteransis by far the most frequently eiicountered.Although differing clinically and pathologi-cally, all of the diseases are similar in thatthey cause isehemia of tissues supplied by theoccluded arteries. The degree of iseheinia isdirectly proportional to the rapidity of de-velopment and the extent of occlusion andis inversely proportional to the extent andrapidity of developnient of collateral arterialanastonioses. The isehemia may be increasedby arteriolar constriction and decreased byarteriolar dilatation from aiiy cause. Whenblood flow diminishes to the point where tissuedoes not receive sufficient oxygen to sustaiiilife, or when injury or ilifection inereases thedemand for oxygen that the occluded arteriesare uiiable to supply, gangrene occurs.

It is beyond the scope of this presentationto discuss in detail the distinguishing featuresof the various chronic occlusive arterial dis-eases. Although much of what follows pertainsto all or some of these diseases, most of itdeals more specifically with thromboangiitisobliterans (TAO) * and with arteriosclerosisobliterans (ASO) .* Recently the concept ofTAO as a diagnostic entity has been vigor-ously challenged and defended on both clini-

From the Section of Medicine, Mayo Cliinic andMayo Foundation, Rochester, MIinnesota.

*Hereafter in this discussion thromboangiitis obli-terans will be referred to as TAO and arteriosclerosisobliterans will be referred to as ASO.

cal and pathologic grounds. It has beencontended that TAO is due in fact toatherosclerosis, arterial embolism, or arterialthrombosis, or to a combination of all threeconditions.2 Most experienced students of per-ipheral vascular diseases, however, agree withMeKusick and associates3 that TAO is a dis-tinct clinical and pathologic entity. Recentevidence strongly supports the usefulness ofdistinguishing between TAO and ASO be-eause of the marked differences in prognosisof patients affected with either disease.4Some of the distinguishing clinical featuresof these two diseases are set forth in table 1.

SymptomsThe symptoms of ehronic occlusive arterial

disease result from impairment of blood flowto the extremities. The symptoms may appeargradually as a result of slowly progressiveocclusion or suddenly as a result of acutearterial thrombosis or embolism. They mayprogress episodically or remain relativelystatic for many years. The outstanding symp-tom of chronic occlusive arterial disease ispain that may take several forms.

Intermittent claitdication1 is the commonestand usually the earliest symptom. This isa pain, ache, cramp, or severe fatigue thataffects muscles distal to the occluded arterywheni these muscles are exercised. Rest with-out a change of position or cessation of weightbearing promptly relieves the distress. Incases of ASO, intermittent claudication prac-tically always involves one or both lowerextreniities, most commonly the calf, but insome patients it is noted in the foot, thigh,or hip alone or in association with the calf.During any stage of the disease intermittentclaudication can usually be reproduced con-sistently after a certain distance of walkingat a eertain rate. A progressive or suddendecrease in the claudication distance, that is,

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Table 1Some Distinguishing Clinical Features of Thromboangiitis Obliterans (TAO) andArteriosclerosis Obliterans (ASO)

Factor

Age at onset

Isehemia of one ormore fingers

Superficial thrombophlebitisin nonvaricose veins

Diabetes mellitus

Hypercholesteremia

Calcification ofinvolved arteries

Bruits over abdominalaorta or iliac orfemoral arteries

Decreased or absent pulsations,in one or both poplitealarteries

Sudden occlusion of femoralor iliac arteries

TAO

Usually < 40 yr.

Frequent

Frequent

Rare

Rare

Absent

Absent

Infrequent, particularlyearly in course ofthe disease

Rare

ASO

Usually > 40 yr.

Absent

Absent

Present in approximately20% of cases

Present in approximately50% of patients lessthan 60 yr. of age

Present in approximately85% of cases

Present in approximlately20% of eases

Present in almost allpatients without diabeteswho are less than 60yr. of age

Occurs in approximately20% of cases

the distance that a person affected can walkbefore onset of claudication, indicates an in-crease in the arterial insufficiency of theaffected limb. When intermittent claudicationdevelops for the first time in a patient morethan 40 years old, it is usually due to ASO.

Ischemic rest pain, located in the distalpart of the extremity, may be severe,and isusually worse at night. It indicates a seriousdegree of arterial insufficiency. Numbness andparesthesia of the toes or foot are often pre-cursors of rest pain and indicate moderatelysevere arterial insufficiency. The patient maynotice increased sensitivity of the affectedextremity to cold.The pain of tlceration and gangrene is

similar to ischemic rest pain, although it isusually more localized and probably resultsfrom inflammatory chailges associated withinfarction, secondary infection, and ischemiaof sensory nerve endings.The pain of ischemic neuropathy is usually

due to entensive chronic or sudden occlusion

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of an iliac or femoral artery. The pain ex-tends over a large portion of the extremityand may follow the sensory distribution ofa large nerve trunk. It is paroxysmal, shock-'like, shooting or cutting and may be associ-ated with burning sensations and paresthesia.The pain is frequently severe an'd difficult torelieve.

Physical SignsSignificant occlusive arterial disease of the

extremities may be diagnosed before the onsetof symptoms by routine determination ofpulsations of peripheral arteries at everyexamination. The examination should includecareful and unhurried palpation of the radialand ulnar arteries at the wrists, the abdominalaorta, and the femoral, popliteal, posteriortibial, 'and dorsalis pedis arteries. Absenceor reduction in the amplitude of pulsationin any of these arteries except the dorsalispedis or possibly the posterior tibial arteriesusually indicates occlusive arterial disease.It should be kept in mind, however, that ana-

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tomnic anomalies may account for the sym-mnetrical absence of pulsation in the posteriortibial arteries in as many as 8 per cent andin the dorsalis pedis arteries in as many as15 per cent of normal people.6 The amplitudeof pulsation in each artery may be gradedfrom 0 (absent) to 4 (normal). Such sys-tematic recording of pulsations allows a rela-tively accurate evaluation of the arterial eir-culation at a given time and is of value inassessing progression of the disease process.Elevation and dependency tests allow an

estimation of the cutaneous isehemia. Withthe patient in the supine position, the hipsare flexed and the feet are elevated for ap-proximately 30 to 60 seconds. This emptiesthe visible superficial veins of the foot andcauses varying degrees of pallor of the skinof the ischemic foot. The feet are then madedependent. The time required for normalcolor to return and for refilling of the emptiedveins is noted. In occlusive arterial diseasethe return of color takes longer than 10seconds and refillin-gf of the veins takes longerthan 15 seconds. These observations are in-valid when venous incompetence with retro-grade venous filling is associated. Persistentrubor of the skin of the distal portion of thefoot and toes is usually present when thearterial circulation is greatly impaired. Otherindications of arterial insufficiency are cool-ness and atrophy of the distal portion ofthe affected extremity. Occlusion of a smallerdigital artery may be manifested by a cya-notic, cool digit and occasionally by cutaneousinfarets. In cases of ASO, isehemic ulcerationand gangrene usually are confined to the toesor heel; in cases of TAO, ulceration and gan-grene may affect the finger tips also. Thetypical ischemic ulcer has a grey-black basewith little or no granulation tissue; con-comitant local infection often is present; themost frequent organism is Staphylococcusaureus.

Laboratory and Special StudiesRelatively few laboratory data are needed

to corroborate a clinical diagnosis of chronicocclusive arterial disease of the extremities.

Plethysmography and skin-temperature stud-ies are not necessary to establish a diagnosisor even to determine the best type of treat-ment. Although the oscillometer is still usedby some physicians, it probably gives lessreliable and less consistent information thancareful assessment of the pulses by digitalpalpation.

All patients with occlusive arterial diseaseshould be tested for hyperglycemia, since alarge number of patients with ASO havelatent or frank diabetes. Determinations ofblood lipids may be advisable also, particu-larly for younger patients with occlusive ar-terial disease, since the concentration of cho-lesterol in the blood is elevated in about50 per cent of men and 75 per cent of womenwith ASO who are less than 60 years of age.7Diabetes mellitus or hyperlipidemia or bothare rarely encountered in patients with TAO.Roentgenographic evidence of atheromatouscalcification of the arteries of the pelvis orlower extremities occasionally may be usefulin distinguishing ASO from TAO. Electro-cardiograms are advisable in patients withASO, whether or not symptoms of coronaryheart disease exist, because of the frequencywith which coronary sclerosis is associatedwith arteriosclerosis of the arteries of theextremities.

Arteriograms are almost never necessaryin making a diagnosis of occlusive arterialdisease of the extremities. Although arterio-graphic distinctions between ASO and TAOexist,3 the exact nature of the obstruetinglesions cannot always be determined by thismeans. Arteriograms are frequently neces-sary, however, to determine the exact siteand extent of the obstructing arterial lesionsif arterial surgery is contemplated. Arteriog-raphy is rarely justifiable when the clinicalfindings indicate that the obstructing lesionsare entirely distal to the popliteal arteries orwhen it is certain for other reasons that adirect surgical attack will not be made. Inthe absence of clinical evidence of involvementof the adbominal aorta or iliac arteries, thefemoropopliteal system may be better visual-ized by percutaneous injection of contrast

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SYM1POSIUM-PERIPHERAL VASCULAR DISORDERS

medium into the common femoral artery onthe affected side; otherwise an aortogramshould be made. Both femoral arteriographyand aortography carry a small but definiterisk of serious local and systemic complica-tions.

PrognosisA recent study4 of patients who were 45

years of age or less when a diagnosis of chron-ic occlusive arterial disease of the extremi-ties was first made indicated a practicallynormal life expectancy for thos.e with TAOand a decreased life expectancy for thosewith ASO (fig. 1). Patients with ASO donot die because of the occlusive lesions intheir peripheral arteries but rather becauseof the frequently associated arterioscleroticlesions in their coronary and cerebral arteries.Since these patients do not die of ASO perse, surgical restoration of arterial blood flowto the extremities cannot be expected to altertheir life expectancy.

The same study showed that the incidenceof ulceration and the necessity for amputationof a lower extremity before or at the timeof diagnosis and for 10 years thereafter wassignificantly lower among patients with ASOthan among patients with TAO. None of thepatients with ASO required an amputationof a finger, whereas 6.3 per cent of the pa-tients with TAO required amputation of oneor more fingers within the 10-year follow-upperiod. In another study7 on nondiabetic pa-tients with ASO who were less than 60 yearsof age at the time of diagnosis, only 4 percent required amputation of a leg shortlyafter the original examination and an addi-tional 5 per cent required similar amputationduring the follow-up period, which was aminimum of 5 years. If the patient discon-tinued smoking, the subsequent amputationrate was much lower than when use of tobaccowas continued. The subsequent amputationrate among diabetic patients with ASO in-volving the femoral artery was approximatelyfour to five times that of nondiabetic patients,and the diabetic patient who has isehemiegangrene has only about a 50 per cent ehaniceof avoiding amputation of the involved leg.8

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90

> 80

"0t-

Nom lpopulation~~~~~9B85 97.7 IG; p p u u

,K-on

93.6

850\

756

660

"0 2 3 4 5 6 7 8 9 10

Yeors after diagnosis

Figure 1Survival curves for patients with thronbohangiitisobliterans (TAO) and arteriosclerosis obliterans(ASO) compared with that of a normal p,opu-lation (Aclapted from McPherson, Juergens, andGifford).4

TreatmentMedical Measures

The general principles of medical treat-ment are the same for all types of chronicocclusive peripheral arterial disease, but treat-ment of the patient with a specific occlusivedisease must be individualized. Control ofassociated conditions such as diabetes melli-tus or polycythemia vera should not be ne-glected. Although there is no definite proofthat the course of ASO is altered by decreas-ing elevated concentrations of lipids in theblood, an attempt should be made to controlhyperlipidemia, preferably by dietary means.9The precipitating cause of many of the

ulcerative or gangrenous lesions is traumafrom mechanical, chemical, or thermal sources.All patients, therefore, should be given de-tailed instructions concerning the care ofextremities and the avoidance of trauma.Minor wounds, contusions, scratches, appli-cation of heat, fungous infections, or surgicalprocedures around the nails may lead tolocal necrosis and secondary pyogenic infec-tion. Strong antiseptic solutions or ointmentsshould not be applied to the skin of isehemicextremities. Sloughs and crusts may bedrained or loosened with soaks or warm wetdressings of normal saline or boric acid,solution. Since most ulcerative or gangrenous

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lesions are secondarily infected, appropriatesystemic antibiotic therapy may be helpfulin healifig the lesions. Occasionally, carefulsurgical debrideinent of gangrenous tissuewill facilitate healing, but this should be doneonly after conservative local and antibiotictreatment.

Repeated use of analgesics may be necessaryfor temporary relief of ischeniie rest painor the pain of isehemic neuropathy. Salicy-lates, d-propoxyphene hydrochloride (Dar-von), or one of the narcotic alkaloids such aslevorphanol tartrate (Levo-Dromoran) nmaybe needed to control the pain, which is oftensevere. Oiie of the phenothiazine tranquilizersmay be helpful in alleviating anxiety oftenassociated with severe pain. Narcotics shouldbe used with caution because the chronicityof ischemic pain mnay lead to addiction.

Long-ternm anticoagulant treatment withone of the coumarin compounds is usuallyindicated for patients who have had morethan one episode of sudden arterial occlusioiiwhether this be due to embolism froin chronicatrial fibrillation, primary arterial thrombosis,or thrombosis associated with ASO. Thesedrugs should not be used, however, ulilessthe patient is cooperative and facilities areavailable for accurate prothrombin-time de-terniinations.

Tobacco snmoking is very likely an impor-tant factor in the etiology of TAO and maybe an important etiologic factor in ASO.Amputation is much less frequent amongpatients with either disease who discontinuesmoking than among those who continue tosmoke. In addition, smoking causes peripheralvasoconstriction in almost all persons. Forthese reasons the physician should urge coni-plete and permanent abstinence from tobaccofor all patients with chronic occlusive periph-eral arterial disease.

In addition to abstaining fromn tobacco,patients with occlusive arterial disease shouldavoid vasoconstricting drugs and exposure tocold. A warm enviroinnental teniperature maybe of value in producing reflex vasodilatationl.An ounce of whiskey or brandy given threeor four times daily is a simple and relativelv

effective type of medication when ischemicrest pain is present and the need for vaso-dilatation is critical. Although there is physio-logic evidenee that the nunierous vasodilatingdrugs currently available cause vasodilatationin, normal extremnities, the evidence for sig-nifieant vasodilatation in extremities affectedby occlusive arterial disease is not impressive.Papaverine hydrochloride and tolazoline hy-drochloride (Priseoline) may be of value whengivenl intravenously or intra-arterially in thetreatnment of an acute arterial occlusion, butthese and other drugs appear to be of littlevalue in chroniie oeelusive arterial disease.Surgical Measures

Regional symnpathetic ganglionectomy isprobably the imost effective method of pro-ducing mnaximal and persistent vasodilatation.This procedure is indicated when an increaseof the circulation to aii ischemic band orfoot is needed, in the latter case particularlyif a direct surgical attack on the arteries istechnically impossible or contraindicated. Itdoes not cure the basic disease process andafter such operatioiis there is still need foravoidance of trauma and tobacco. It is doubt-ful that intermittenit claudication is evermuch improved by sympathectomy but thepersistent vasodilatation probably offers someprotection against further isehemic skin com-plications. Svmpathectomy gives the best re-sults in patients with nioderate isehlemia ofthe feet or hands with minimal or no skinlesions, or with only minor degrees of isehemicneuropathy. In some patients with extremelysevere ischeniia, sympatbectomy may precipi-tate gangrene, the so-called paradoxical effect.Destruction of the sympathetic ganglia bypereutaneous injection of absolute alcoholmay be of value when ganglionectomy seemsindicated but the risks of such a procedureare deemed prohibitive. An alcohol block isless permanent than surgical ganglionectomy;it should not be attempted bv anyone whois not skilled in this type of therapy.

Surgical restoration of arterial contiiiuitymay be accomplished by resection of a chron-ically obstructed segment and insertion of

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a graft, insertion of a prosthetic tube tobypass an occluded segment, or thronmboen-darterectomy.1 The last procedure is being usedwith increasing frequency and occasionallya patch graft of plastic material or autog-enous vein is sutured in at the same timeto enlarge the lumen. Bypassing proceduresare used when the occlusive lesion is too ex-tensive for thromboendarterectomy. Recon-structive arterial surgery is applicable forocclusions that are proximal to the trifurea-tion of the popliteal artery, and operabilitydepends on the occlusion being segmental,that is, there must be an adequate arteriallumen above and below the occlusion. Recon-structive arterial surgery for chronic occlu-sive peripheral arterial disease is practicallylimited to ASO involving the abdominal aorta,iliac, and femoral arteries. Arteriosclerotic oc-clusion of the subelavian or brachial arteriesrarely produces severe ischemic symptoms andTAO almost always involves the smaller dis-tal arteries, which are inoperable for technicalreasons.

Direct arterial operation in nondiabeticpatients is chiefly indicated for disabling in-termittent claudication. As mentioned previ-ously, this type of surgical procedure is notlifesaving because patients rarely die as aresult of ischemia of tissue distal to thearterial obstruction. If the disease is progres-sing rapidly or if amputation seems inevitable,an arterial operation is justified in the hopethat amputation can be avoided or can bemade at a lower level. This type of procedureshould not be employed merely because anarterial lesion is present, and it cannot berecommended as a routine prophylactic meas-ure for preservation of an affected limb, sincethe incidence of gangrene is relatively lowin the usual uncomplicated case of ASO. Inselecting patients for arterial reconstructivesurgical procedures, consideration must begiven to the fact that postoperative occlusionof an inserted graft or an endarterectomizedsegment, particularly in the femoropopliteal

region, may occur even if the surgery has beenperformed by experienced vascular surgeons.

Unfortunately, amputation of a finger issometimes necessary in cases of TAO andamputation of a lower extremity is sometimesnecessary in cases to TAO and of ASO. If gan-grene is extensive and there is evidence oftoxeinia, amputation should not be delayed.When there is severe and intractable isehemicrest pain without gangrene, amputation maybe necessary if a thorough trial (at least6 weeks) of medical or of other surgicaltreatment fails to control the pain. It isfrequently advisable to administer antibioticsbefore and after the amputation.

References1. ALLEN, E. V., BARKER, N. W., AND HINES, E. A.,

JR.: Peripheral Vascular Diseases. Ed. 3.Philadelphia, W. B. Saunders Company, 1962,1044 pp.

2. WESSLER, S., MING, S., GUREWICH, V., ANDFREIMAN, D. G.: A critical evaluation ofthromboangiitis obliterans: The case againstBuerger's disease. New England J. Med. 262:1149, 1960.

3. McCKUSICK, V. A., HARRIS, W. S., OTTESEN, 0. E..GOODMAN, R. M., SHELLEY, W. M., AND BLOOD-WELL, R. D.: Buerger 's disease: A distinetclinical and pathologic entity. J.A.M.A. 181:5, 1962.

4. MCPHERSON, J. R., JUERGENS, J. L., AND GIFFORD,R. W., JR.: Thromboangiitis obliterans andarteriosclerosis obliterans: Clinical and prog-nostic differences. Unpublished data.

5. JUERGENS, J. L.: Intermittent claudication. M.Clin. North America 42: 981, 1958.

6. SILVERMAN, J. J.: The incidence of palpable dor-salis pedis and posterior tibial pulsations insoldiers: An analysis of over 1,000 infantrysoldiers. Am. Heart J. 32: 82, 1946.

7. JUERGENS, J. L., BARKER, N. W., AND HINES,E. A., JR.: Arteriosclerosis obliterans: Reviewof 520 cases with special reference to patho-genic and prognostic factors. Circulation 21:188, 1960.

8. SCHADT, D. C., HINES, E. A., JR., JUERGENS,J. L., AND BARKER, N. W.: Chronic athero-sclerotic occlusion of the femnoral artery.J.A.M.A. 175: 937, 1961.

9. Council on Foods and Nutrition: The regulationof dietary fat: A report of the council.J.A.M.A. 181: 411, 1962.

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JOHN L. JUERGENSChronic Occlusive Arterial Disease of the Extremities

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1963 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Circulation doi: 10.1161/01.CIR.27.5.964

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