gency room, at 10:00 a.m., the physical examination revealed an acutely distressed, pale elderly women with ablood pressure of 131/82 mmHg, a regular heart rate at115 bpm and a mild fever of 100°F.The pulmonaryauscultation demonstrated bibasilar rales. The cardiac cxamination was remarkable only for a 54 gallop and asystolic murmur grade lilY!. The admission electrocardiogram (EKG) showed a sinus rhythm with a ventricularrate of 109, a left anterior hemiblock, left atrial enlargement and ST-segment elevations of 2.0—2.5mm in V2through V6 (Fig. 1). Her initial plain chest radiograph (Fig.2A) revealed an elevated right hemidiaphragm with bibasilar subsegments.! atelectasis. The heart size and pulmonary vessels were normal. The hematologic work upshowed a leukocytosis of 17,200 WBC/mm3 with 77%polymorphonuclears and I 1% lymphocytes. The hematocrit was 40.4% and the erythrocyte sedimentation rate was24 mm/hr. The plateletcount,theprothrombintime andthe partial thromboplastin time were normal. Urinalysiswas slightly positive for occult blood with 5-10 RBCs byhigh power field probably related to an urinary catheterplacement. Blood chemistry revealed hypokalemia of 3.2mmol/liter, hypomagnesemia of 1.4 m&iJliter, SGOT of90 U/liter, LDH of 293 U/liter and CPK of 279 U/literwith a MB isoenzyme fraction of 11.6%. The remainderof the laboratory work up was within normal limits. Thepatient was admitted with a diagnosis of an acute anteriormyocardial infarction and at 11:20 a.m. she was treatedwith intravenous streptokinase. Upon admission to theCoronary Care Unit, the patient was started on heparmn,1000 u/hr (intravenous infusion), enteric-coated aspirin,1 tablet p.o. daily, metoprolol, 100 mg p.o. b.i.d., levothyroxine, 0.1 mg p.o. daily, lithium, 300 mg p.o. daily andintravenous nitroglycerin, which was titrated as needed.She also received two doses of 40 mg of furosemide as anintravenous bolus injection and 5 mg of intravenous metoprolol.

J Nucl Med 1992, 33:1558-1565

75-yr-oldwhite female,with no previoushistoryofcoronary artery disease, presented with severe retrosternalchest pain of 10 hr duration. She was brought to theemergency room where a diagnosis of an acute anteriormyocardial infarction was made and thrombolytic therapywas initiated.

CLINICAL HISTORY

The patient had a history of a congenital heart murmurand rheumatic fever as a child. In 1973, a diagnosis ofbipolar affective disorder was made and lithium therapywas initiated. About 7 yr later, she developed hypothyroidism which was treated with replacement therapy. Thepatient had a 53-pack year history of cigarette smoking,however, she denied history ofdiabetes mellitus, hypertension, coronary artery disease, elevated cholesterol or familyhistory of cardiac disease.

Two days prior to the onset of symptoms she flew fromCalifornia to Boston for a wedding. The day before admission she noted general weakness and mild to moderateshortness of breath. At midnight, the dyspnea becamesevere and she experienced the onset of a left inframammary discomfort radiating to the chest and associated withnausea and dizziness. The patient stayed at home for thefollowing 10 hr with the hope that her symptoms wouldimprove. Due to the persistence of her symptoms, shefinally sought medical advice. Upon arrival to the emer

ReceivedMar.31,1992;revisionacceptedApr.9,1992.For repñntscontact: Irma L Molina-Murphy, MD, Department of Rac@oIogy,

Nuclear Medicine DIVISIOn,Massachusetts General Hospital, Fruit St., Boston,MA 02114.

1558 TheJournalof NuclearMedicine•Vol.33 •No.8 •August1992

Acute Onset of Cardiogenic Shock Associatedwith Normal Coronary Arteries, DiffuseMyocardial Necrosis, and Rapid ClinicalRecoveryGuest Editor: Tsunehiro YasudaCase Presentation: Irma L. Molina-Murphy, Pieter M. Vandervoort, and James F. SouthernCase Discussion: Irma L. Molina-Murphy

From the caserecordsofthe MassachusettsGeneral Hospital, Boston, Massachusettsand Harvard Medical School,Boston,Massachusetts

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FIGURE 1. Initialelectrocardiogramshowsa leftanteriorhemiblock,STelevationsinV2throughV6andleftatrialenlargement.

Within 6 hr of admission, the patient was free of pain,however, the physical examination showed evidence ofcongestive heart failure with rales in the lower one-thirdof the chest and jugular venous distention of 6 cm at 45°.There were a brisk carotid pulse, increased intensity of S2,a 54 gallop and a mid-systolic click followed by a systolicmurmur grade lillY! at the left sternal border and apex.The murmur increased upon standing. No 53 gallop wasaudible. At this time, the radiographic chest evaluation(Fig. 2B) revealed moderate bilateral pleural effusions,mild enlargement of the cardiac silhouette and increasedpulmonary vascular pattern. A pulmonary artery line wasplaced at 8:30 p.m. without any event.

Early the next morning (2:00 a.m.), the patient becamehypotensive (SBP = 95 mmHg, HR = 110 bpm) with noevidence ofleft-to-right shunt as assessed by central venouspressureline, pulmonary arteryand rightatrium blood gasanalysis. The second and third sets of cardiac enzymes,performed every 8 hr, showed a decline in the CPK value.Her EKG evolved to poor R-wave progression and persistent 1—2mm ST-segment elevation in leads Vi throughV3. The right heart hemodynamic evaluation revealed acentral venous pressure of 13 mmHg, a pulmonary arterypressure of 45/16 mmHg, a pulmonary capillary wedgepressure of 20 mmHg and a cardiac index of 1.7 liters!min/m2. An emergency coronary arteriogram was performed to investigatethe possibility ofpotentially treatablelesions. No significant coronary artery narrowings wereseen. The left ventriculogram showed akinesis of the anterolateral and apical segments with diffusely depressedglobal left ventricular function. An echocardiogram excluded the possibility ofcardiac tamponade. At this point,the data indicated cardiogenic shock in the setting ofnormal coronary arteries, without any other specific identifiable causes. The patient was on a combination therapyconsisting of an intra-aortic balloon counterpulsation, dobutamine, 700 sg/min (9.7 @g/kg/min),dopamine, 200

@g/min(2.7 @g/kg/min) and intravenous norepinephrine,14 @ig/min.These were slowly weaned off over the nexttwo days.

Findings of patent coronary arteries and the fact thather left ventricular function was suppressed out of propor

. _

1559Acute Cardiogenic Shock •Molina-Murphy et al

FIGURE 2. Initialchestradiograph(A)essentiallyshowsnormallungswithrighthemidiaphragmeleva@on.Repeatedchestxray(B),lessthan24hr later,demonstratescardiacenlargement,increased pulmonaryvascular pattern and bilateralpleuraleffusions.

tion to the CPK leak resulted in a work-up for myocarditisand cardiomyopathy. A right ventricular endomyocardialbiopsy on the sixth hospital day (Fig. 3, see p. 1563) wasmost consistent with healing ischemic necrosis of themyocardium of about l-wk-old. One of the six fragmentsof endomyocardium submitted for histologic evaluationcontained several foci ofnecrotic myocytes surrounded bya mixed inflammatory inifitrate. The immunoperoxidasestains revealed that macrophages predominated in theinfiltrate, which also contained scarce T-lymphocytes andabsent B-cells. An antimyosin scan (Fig. 4) obtained thesame day as the biopsy, 72 hr after the intravenous administration of 67 MBq of @In-antimyosin,revealed diffusepositive uptake, more intense in the apex. This indicatedthe presence of acute myocyte necrosis. The pattern of

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uptake was not consistent with an acute anterior myocardial infarction. The laboratory work-up for myocarditisshowed normal values for ANA, lyme antibody, rapidplasma reagin test, toxoplasma antibody, heterophile antibody, cold agglutinins and LDH I pattern. She alsounderwent evaluation for a hypercoagulable state, including protein C and protein S determinations, which werenormal, and antithrombin III value, which was minimallydecreased to 70% (normal range 85%—l11%). The patienthad positive rheumathoid factor and cytomegalovirus antibody titers. The thyroid function test revealed a low TSHwith a normal T4 value consistent with her history ofhypothyroidism in hormonal replacement.

The patient was placed on captopril and anticoagulanttherapy. She gradually improved and was transferred fromthe coronary care unit to the regular medical ward in stableclinical condition. A cardiac gated blood-pool scan (Fig.5) performed on the ninth hospital day showed a hypertrophied left ventricle with a discrete area ofapical dyskinesisassociated to hypokinesis of the distal anterolateral wall.There was vigorous contraction ofthe basal portion of theleft ventricle with a normal left ventricular ejection fraction of 67%. The cardiac chambers sizes were withinnormal limits. A second echocardiogram (Fig. 6 A-D)showed mild mitral and tricuspid regurgitation withoutevidence of myocardial hypertrophy. Apical akinesis withwell preserved left ventricular function and an estimatedejection fraction of 60% was demonstrated. Due to theimprovement in her left ventricular function, the ACEinhibitor was discontinued and diltiazem, for the treatment of possible coronary vasospasm, was started.

The patient was discharged to home in stable condition,12 days after the initial event, on calcium channel blockertherapy and Coumadin. The presumptive diagnosis upondischarge was coronary vasoSpasm leading to an anterior

FIGURE 4. Anteriorprojectionoftheantimyosinscanshowingintensemyocardialuptake in the mid to distal left ventricle(twoblackarrows)and less intense uptake inthe base (whitearrow).

myocardial infarction and a discrete apical aneurysm. Herfirst post-hospitalization follow-up visit, 5 days after discharge, was remarkable for the development of bilateral 3plus nonpitting edema of the lower extremities. The patient was started on diuretic therapy. After this examination, she returned to California. Approximately 6 wk afterdischarge, the patient was readmitted to a hospital inCalifornia with substernal discomfort and EKG changesconsisting ofsymmetric T-wave inversions in leads I, AVLand V3 through V6, without ST-segment elevations. Thetotal CPK value was 20 U/liter. A diagnosis of postmyocardial infarction pericarditis (Dressler's syndrome)was presumed on the basis of a small pericardial effusiondemonstrated by echocardiogram. This examination alsorevealed apical hypokinesis to akinesis with compensatoryhypercontractile septum and a left ventricular ejectionfraction of 87%. An exercise test using a modified Bruceprotocol was attempted, but the patient stopped at 1.5 mmdue to severe dyspnea. The test was nondiagnostic. Coumadin was discontinued and upon discharge a regimen ofmoderate physical exercise and a low cholesterol diet wasstarted. She remained clinicallystableon medicaltherapyconsisting ofdiltiazem SR, 90 mg p.o. b.i.d., and nitrates,without any further intervention.

DISCUSSIONThis patient presents a difficult diagnostic dilemma. Her

initial presentation was consistent with coronary arterydisease that caused an anterior wall myocardial infarction

FIGURE5. Diastolicframes(upperpanel)andsystolicframes(lower penal)of the gated bkxxi-pool scan. Left pictures showsanteriorVIeWSand the pk@tureson the right representsLAO 45°views of the heart. The size of the cardiac chambers and theoverall left ventricular contraction are wfthin normal limits. Thereis a suggestion of distal anterolateral wall and apical hypokinesispresent.

/

1560 TheJournalof NuclearMedicine•Vol.33 •No.8 •August1992

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FIGURE6. End-diastolicparasternallong-axisview(A)andschematicdiagram(B)demonstratenormalseptalthickness(11 mm).Diastolic (C) and systolic (D) four chamber apical views show apical akinesis with normal basal contraction. The estimated LVEF is60%. (RV = right ventricle; RA = right atrium; LV = left ventricle; LA = left atrium; IVS = intraventncular septum; Ao = aorta; PW =posterior wall; AV = aortic valve; MV = mitral valve; a segment of the broken line represents approximately 1 cm).

and subsequent cardiogenic shock. Normal coronary angiographic findings and the severe global left ventriculardysfunction were discordant with the magnitude of hercardiac enzyme leak. This necessitated further diagnosticevaluation to elucidate the etiology of her peculiar clinicalcourse. While the right ventricular endomyocardial biopsywas most consistent with ischemic necrosis and failed todemonstrate a significant interstitial inflammatory lymphocytic infiltration, the antimyosin scintigraphic studyrevealed diffuse left ventricular uptake indicating myocardial necrosis in a pattern not compatible with an acuteanterior myocardial infarction. The echocardiographicevaluation showed a normal thickness of the septum andposterior wall without evidence ofa left ventricular outflowtract pressure gradient or abnormal systolic anterior movement ofthe mitral valve, making concentric or asymmetricleft ventricular hypertrophy a less likely diagnosis. Although during the first 48 hr of admission the patient wascritically ill and in cardiogenic shock, a condition whichis fatal in more than 90% of the patients ifassociated withanterior myocardial infarction (1,2), her recovery wasrapid and steady.

It has been estimated that 1%—3%of all myocardialinfarctions occur without demonstrable evidence of significant coronary atherosclerosis (3,4). This number canincrease up to 17% in younger patients less than 36 yr old(5). In the following discussion, we review the differentpossible mechanisms for the development of acute myocardial necrosis with cardiogenic shock in the setting ofnormal coronary arteries.

AcuteCoronaryThrombosisand CoronaryVasospasm

Acute coronary thrombus formation with rapid andspontaneous resolution has been implicated in the etiologyof myocardial infarction in patients with angiographicallynormal coronary arteries (6—9).Thrombosis rarely occurs,however, without pre-existing atherosclerotic coronary disease (10). Acute coronary thrombosis often are single andin the majority of the patients are located in the majorextramural arteries. The initiation of thrombus formationis usuallyassociatedwith plaqueulceration,hemorrhageand rupture (11-16). A coronary thrombus is found to beassociated with a transmural infarction in 60%—90%of

1561AcuteCardiogenicShock•Molina-Murphyet al

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patients compared to 20%—30%in patients with subendocardial injury. In the setting of cardiogenic shock, theprobability of finding a coronary thrombotic event as thecause ofacute infarction is three to four times greater thanin patientswithoutthispostinfarctioncomplication(17—21).

The role of coronary vasospasm in the etiology of acutemyocardial infarction is still unclear (15,22). Coronaryartery spasm is often encountered in patients with concomitant atherosclerotic heart disease. A patent artery supplying the area of necrosis is found in about 35% of patientsstudied within 6 mo of transmural infarction (23,24). Inthose patients, coronary spasm may play an importantrole in the genesis of ischemia. Nevertheless, resolution ofa previously formed thrombus is another considerationthat is a more likely explanation. The incidence of coronary spasm related to acute myocardial injury is higher ininferior wall myocardial infarction when compared toanterior infarction and is often demonstrable in the earlyphase of the ischemic insult (less than 6 hr) (25—27).

Coronary thrombosis and coronary vasospasm are nottwo independent mechanisms for vessel occlusion in theinitiation of an acute myocardial infarction. Although it ispossible to have isolated coronary artery spasm leading tomyocardial necrosis, spasm is usually associated withthrombosis or atherosclerotic disease (15). Coronaryspasm can occur superimposed on a plaque, thus causinginfarction without thrombosis. In some patients it canprecede the onset of thrombus formation and facilitateplatelet aggregation and disruption of an sclerotic plaque.A nonocclusive thrombotic event can also occur first followed by coronary spasm and subsequent occlusion. In allinstances, these mechanisms are modulated by the presence of vasoactive substances that may facilitate the triggering ofvasospasm or the initiation ofplatelet aggregation

(21,28—31).The exact interaction between acute thrombosis, coronary artery spasm, atherosclerotic plaque, platelet function and endothelial mediators for the initiation ofan acute myocardial infarction is a matter for furtherinvestigation (15).

The diffuse uptake of antimyosin antibody in our patient suggests that myocyte necrosis appeared to have takenplace in the entire heart. This also does fit the clinicalfeature of severe left ventricular dysfunction. The suddenness of the illness suggests acute thrombosis or spasm. Itis difficult to imagine that all three vesselswere thrombosed simultaneously. Even when a minimal decrease inthe antithrombin III value was documented in this patient,it probably was not clinically significant to postulate ahypercoagulable state with spontaneous thrombus formation. A spasm, however, is possible.

Diagnosis of Myocarditis: Endomyocardial Biopsy andAntimyosinScan

One of the clinical entities that can resemble acutemyocardial infarction with cardiogenic shock is myocar

ditis (32-34). Patients with myocarditis and normal coronary angiograms can present with left ventricular systolicand diastolic dysfunction, cardiac arrthymias and symptoms of chest discomfort (35,36). According to the mostwidely used histologic criteria for myocarditis, the DallasCriteria (37), the diagnosis requires the presence of an“inflammatoryinfiltrate ofthe myocardium with necrosisand/or degeneration of adjacent myocytes not typical ofthe ischemic damage associated with coronary artery disease.―Once detected, the inflammatory infiltrate is furtherclassified in terms of cell type and the amount and distribution of the infiltrate itself and the associated fibrosis ifpresent.

The sensitivity of the endomyocardial biopsy for thediagnosis ofmyocarditis has been a matter ofgreat controversy (37—41).The reported frequency of endomyocardialbiopsy showing lymphocytic infiltration in patients withthe clinical diagnosis of myocarditis and acute onset ofunexplained heart failure range from 0 to 67% in differentseries (42—44).The great variability in the reported sensitivity of the right ventricular endomyocardial biopsy forthe detection ofmyocarditis is probably related to the focalnature of this disease and the small amount of histologicmaterial available using this diagnostic approach. Despitethe potential for sampling errors, the right ventricularendomyocardial biopsy is still the most accepted standardmethod for the diagnosis of myocarditis.

Indium-l 11-antimyosin antibodies that bind to exposedmyosin which migrates to the extracellular space afterdisruption of the cell membrane integrity has been successfully used in the diagnosis of myocyte damage in acutemyocardial infarction (45,46). Its role in the setting ofacute myocarditis has also been investigated (35,47,48).The sensitivity of the antimyosin scan has been found tobe as high as 83%, while the negative predictive value of anormal scan has been 92% (35). Antimyosin antibodyimaging is probably an appropriate noninvasive procedurefor the selection ofpatients for an endomyocardial biopsies(35,47). Despite a positive antimyosin scan suggestive ofdiffuse myocardial necrosis, endomyocardial biopsy in ourpatient failed to demonstrate the inflammatory responsetypical of myocarditis.

Hypertrophic Cardiomyopathy and lschemiaThe incidence rate of angina pectoris in patients in

whom hypertrophic cardiomyopathy (HCM) has been diagnosed is estimated to be around 76%—83% (49). It isinteresting that the reported incidence of significant coronary artery disease in the same population of patients inonly 15% (49). Necropsy reports indicate that 15% ofpatients with HCM and without significant coronary atherosclerosis had at least one episode of a transmural myocardial infarction (50). The occurrence ofcardiac ischemiain patients with the diagnosis of HCM and normal coronary arteries is probably related to an imbalance between

oxygen supply and demand as a consequence of increased

1562 The Journal of Nuclear Medicine•Vol.33 •No. 8 •August 1992

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Rare Causes of Myocardial Necrosis in the Setting ofNormal Coronary Arteries

Myocardial infarction with reversible ischemia and car. , diogenic shock following excess thyroid administration in

a patient with normal coronary arteries was described byBergeron et al. (69). The thyroid function tests in ourpatient were within normal limits for an individualundergoing thyroid hormone replacement. Moreover, athyrotoxic state was never documented during the hospitalization period.

Sources of coronary emboli include thrombotic endocarditis of infective or nonpyogenic origin, either in relation to native or prosthetic values, cardiac tumors, thromboembolic event during cardiac invasive procedures orsurgery, and atrial or ventricular mural thrombi. None ofthese conditions were detected in our patient.

Myocardial infarction and/or cardiogenic shock havebeen less commonly associated to coronary arteritis as inKawasaki disease (70) and rheumathoid arthritis (71),blunt chest trauma (72), a hypercoagulable state causing athrombotic event (73), acute myocardiotoxicity (74) andto an electrocution event (75). In addition, other reportedcauses of myocardial infarction has been related to inbornerrors of metabolism leading to an accumulation of exogenous substances in the arterial wall with subsequent narrowing of the coronary lumen and congenital anomaliesregarding the origin of the coronary arteries. Recently,Nader et al. (76) described an extremely rare cause of acutefatal myocardial infarction associated with aortic degenerative changes. In that reported case, cystic medial necrosis and elastin fragmentation were documented as promoters of thrombus formation. Nader et al. postulatedthat transient occlusion of the main coronary ostium bythe aortic thrombus was the triggering event in the imtiation of the myocardial ischemia. These unusual circumstances leading to myocardial necrosis were not documented in our patient.

CONCLUSION

This patient's unusual clinical presentation and inconsistent first results make the diagnosis uncertain. Thepathological findings obtained from the right ventricularendomyocardial biopsy were consistent with ischemic necrosis. In addition, a follow-up echocardiogram did notshow improvement ofthe apical “infarction.―The circumstantial evidence, however, suggests that our patient sustamed an ischemic event, regardless of its cause.

ACKNOWLEDGMENT

The authors thank Dr. GeorgeMonasterskyof Laguna Hills,CA for providingthe information relatedto the follow-upstatusof our patient.

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FIGURE 3. RightventricularendomyocardialbiOpSyrevealedscatteredfoci of healingmyocardialischemucnecrosis.Thearrowis pointing to a focus of necrotic myocytes.

myocardial mass (51), septal perforator arterial compression (52), abnormalities of the intramural arteries (53)and disturbance ofleft ventricular relaxation (54,55). Coronary vasospasm and embolic events have also been implicated in the pathogenesis of ischemia in patients withHCM (56). Cardiogenic shock in these patients has beenassociated with fluid depletion causing decreased intracardiac volume and accentuation of the left ventricular outflow tract gradient. This situation can potentially lead tosevere hypotension and decreased coronary perfusion pressure and culminate in myocardial ischemia (56). Functional myocardial impairment in HCM has been evaluatedby 99mTcgated cardiac blood-pool scintigraphy (5 7,58),magnetic resonance imaging (59,60) and 201Tlcardiacimaging (61-63). Assessment ofactive myocardial damagein HCM using antimyosin antibody scintigraphy (64) andpositron emission tomography (65) has been recently reported.

The gated cardiac blood-pool scan in our patient wassuggestive of left ventricular hypertrophy. She presented,however, with normal septal and posterior wall thicknessand no evidence of left ventricular pressure gradient orsystolic anterior movement ofthe mitral valve by echocardiographic evaluation. An apical segmental motion abnormality was detected with both imaging procedures. It is ofinterest that Webb et al. (66) evaluated a group of 26patients with asymmetric myocardial hypertrophy confined to the apex, an entity associated with “giantT-wave―inversion, which was initially described in Japan by Sakamoto et al. (67) and Yamaguchi et al. (68). Webb foundthat the population he studied had a normal septal andposterior wall thickness, none of them presented with leftventricular outflow tract gradient or systolic anteriormovement and one of the patients, with no history ofangina and in whom normal coronary arteries were documented, sustained an apical infarction with the formationof an apical aneurysm and loss of the “giantT-wave―inversion.

Acute Cardiogenic Shock •Molina-Murphyet al 1563

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vascC/inl983;l4:3l.29. Oliva PB. The role ofcoronary arteryspasm in acute myocardial infarction.

CardiovascC/inl983;l4:45.30. Feldman RL Coronary thrombosis, coronary spasm and coronary athero

sclerosis and speculation on the link between unstable angina and acutemyocardial infarction [Editorial]. Am J Cardiol l987;59:ll87.

31. Conti CR, Mehta JL. Thrombosis, platelets, spasm and acute myocardialischemia. Cardiovasc C/in 1987;l8:73.

32. Narula J, Southern iF, Abraham 5, Pieri P, Khaw BA, Yasuda T. Myocarditis simulating myocardial infarction. JNuclMed 1991.32:312.

33. TysonAA,HackshawBT,KutcherMA.AcuteEpstein-Barrvirusmyocarditis simulating myocardial infarction with cardiogenic shock. South MedI l989;82:l184.

34. Constanzo-Nordin MR. O'Connell JB, Subramaman R, Robinson JA,Scalon PJ. Myocarditisconfirmed by biopsy presentingasacute myocardialinfarction. Br Heart J 1985;53:25.

35. Dec WG, Palacios IF, Yasuda T, et al. Antimyosin antibody cardiacimaging; its role in the diagnosis of myocarditis. J Am Coil Cardiol1990;16:97.

36. KeriakesDJ, Parmley WW. Myocarditis and cardiomyopathy. Am HeartJ 1984;l08:l3l8.

37. Aretz HT, Billingham ME, Edwards WD, et al. Myocarditis: a histopathologic definition and classification. Am I Cardiovasc Paihol 1987;l:3.

38. Hauck AJ, Kearney DL, EdwardsWD. Evaluationof postmortem endomyocardial biopsy specimens from 38 patients with lymphocytic myocarditis:implicationfor roleofsamplingerror. MayoC/inPi'ocl989;64:1235.

39. PrzybojewskiJZ. Endomyocardialbiopsy:a reviewoftheliterature. CathetCardiovascDiag1985;l1:287.

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42. Edwards WD. Current problems in establishing quantitative histopathologic criteria for the diagnosis oflymphocytic myocarditis by endomyocardial biopsy. Heart Vessels l985;(suppll):138.

43. Tazelaar HD, BillinghamME. Myocardial lymphocytes:fact, fancy, ormyocarditis? Am J Cardiovasc Pathol l987;l:47.

44. Lie iT. Myocarditis and endomyocardial biopsy in unexplained heartfailure: a diagnosis in search of a disease [Editorial. Ann Intern Medl988;109:525.

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46. Khaw BA, Yasuda T, Gold HK, et al. Acute myocardial infarct imagingwith indium-l 11-labeled monoclonal antimyosin Fab. J NucI Medl987;28: 1671.

47. Yasuda T, PalacioslF, Dec OW, et al. Indium 111 monoclonal antimyosinantibody imaging in the diagnosis of acute myocarditis. Circulationl987;76:306.

48. Carrio I, Berna L, BallesterM, et al. Indium-l li-antimyosin scintigraphyto assess myocardial damage in patients with suspected myocarditis andcardiac rejection. J Nuc/Med l988;29: 1893.

49. WalstonA, Behar VS. Spectrum of coronary artery diseasein idiopathichypertrophic subaortic stenosis. Am I Cardiol 1976;38:l2.

50. Maron BJ, Epstein SE, Roberts WC. Hypertrophiccardiomyopathyandtransmural infarction without significant atherosclerosis of the extramuralcoronary arteries. Am I Cardiol l979;43:1086.

51. Sulton MG, Tajik AJ, Smith HC, Ritman EL Angina in idiopathichypertrophic subaortic stenosis. A clinical corrleation ofregional left yentricular dysfunction: a videometric and echocardiographic study. Circulationl980;6l:561.

52. Pichard AD, Meller J, Teichholz LE, Lipnick S, Grolin R, Herman MV.Septal perforator compression (narrowing) in idiopathic hypertrophic subaortic stenosis. Am J Cardio/ 1977;40:3l0.

53. James TN, Marshall TK. De Subitaneis Mortibus: XII. Asymmetricalhypertrophy ofthe heart. Circulation 1975;5l:l 149.

54. Sanderson JE, Gigson DO, Brown Di, Goodwin JF. Left ventricular fillingin hypertrophic cardiomyopathy. An angiographic study. Br Heart I1977;39:66l.

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1564 The Journal of Nuclear Medicine•Vol.33 •No. 8 •August 1992

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Acute Cardiogenic Shock •Molina-Murphy et al 1565

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1992;33:1558-1565.J Nucl Med.   Irma L. Molina-Murphy, Pieter M. Vandervoort and James F. Southern  Myocardial Necrosis, and Rapid Clinical RecoveryAcute Onset of Cardiogenic Shock Associated with Normal Coronary Arteries, Diffuse

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