Effects of Spontaneous and Streptokinase-inducedRecanalization on Left Ventricular Function

After Myocardial InfarctionPIM J. DE FEYTER, M.D., MACHIEL J. VAN EENIGE, PH.D., ERNST E. VAN DER WALL, M.D.,

PIETER D. BEZEMER, M.D., CEES L. J. VAN ENGELEN, ALBERT J. FUNKE-KUPPER, M.D.,

H. J. JURN KERKKAMP, M.D., FRANS C. VISSER, M.D., AND JAN P. Roos, M.D.

SUMMARY The effect of recanalization of the "infarct vessel" on left ventricular (LV) function was

assessed 6-8 weeks after acute myocardial infarction (MI) in two groups: patients who had streptokinase-induced recanalization during the acute phase and control patients who had spontaneous recanalization.The ejection fraction and severity ofLV wall motion abnormalities in 100 patients with recanalization werecompared with those in 78 patients with persistent occlusion of the infarct vessel. Among patients withinferior MI, LV function was significantly better in those with spontaneous (n = 41, p < 0.05) andstreptokinase-induced recanalization (n = 15, p < 0.02) than in those with persistent occlusion of theinfarct vessel (n = 40) in the control group. The LV function was equally good in patients with spontaneousand streptokinase-induced recanalization. Among anterior MI patients, LV function was significantlybetter in those with streptokinase-induced recanalization (n = 10) than in those with spontaneous recanali-zation (n = 34, p < 0.01) or persistent occlusion in the control group (n = 28, p < 0.001). We conclude thatrecanalization has a beneficial effect on LV function in patients with MI.

AFTER the initial attempt of Boucek et al. in 1960 tolyse the thrombus by application of fibrinoly,sin in theaortic root of patients with acute myocardial infarction(MI), nonsurgical coronary artery reperfusion has at-tracted renewed interest and has recently become afeasible procedure in patients with evolving MI.2-5 In-tracoronary infusion of a thrombolytic agent can rees-tablish antegrade coronary flow in 73-95% of the pa-tients.2-5 To what extent this intervention leads tomyocardial salvage has not been fully evaluated.DeWood et al.6 showed that total coronary occlusion ofthe infarct vessel is frequent during the early hours oftransmural infarction and decreases in frequency dur-ing the initial 24 hours, suggesting subsequent recana-lization in the evolution of infarction. The effects ofthis spontaneous recanalization on LV function areunknown. Documentation of a possible beneficial ef-fect of spontaneous recanalization on infarct sizewould be relevant in evaluating the technique of intra-coronary fibrinolytic therapy.

In this study we assessed the effect of streptokinase-induced recanalization and spontaneous recanalizationon LV function. The left ventriculograms of a consecu-tive series of patients treated with intracoronary strep-tokinase were compared with the ventriculograms of acontrol group, matched for age, history of infarction,site of infarction and site of associated coronary occlu-sion ("infarct vessel"). Ventriculography was per-formed 6-8 weeks after infarction in both groups.

From the Departments of Cardiology and Medical Statistics, FreeUniversity Hospital, Amsterdam, The Netherlands.

Address for correspondence: P.J. De Feyter, M.D., Department ofCardiology, Free University Hospital, De Boelelaan 1117, 1007 MBAmsterdam, The Netherlands.

Received July 22, 1982; revision accepted February 1, 1983.Circulation 67, No. 5, 1983.

MethodsStreptokinase Group

All patients under 65 years of age whose historysuggested acute MI were considered candidates forintracoronary thrombolysis. Further inclusion criteriawere admission within 3 hours from onset of chestpain, ST-segment elevations of at least 0.2 mV and nopathologic Q waves in corresponding leads, no historyof MI and no contraindication for thrombolytic ther-apy.

Between November 1980 and December 1981, 48of 98 consecutive patients admitted with a first MIfulfilled these criteria. Three refused treatment; techni-cal difficulties prevented the procedure in three others.Lysis was attempted in 42 patients; 35 patients wereeligible for this study (table 1). Successfully reper-fused patients were those in whom reestablishment ofantegrade flow was proved angiographically both atthe time of lysis and 6-8 weeks after infarction.Thrombolysis was considered unsuccessful if the pa-tient had no antegrade flow at the time of lysis after 2hours of attempted reperfusion or had early reocclu-sion of the infarct vessel (within 6-8 weeks).

Control GroupThe control group consisted of 143 patients (all

younger than 65 years of age) who survived a firsttransmural MI. As part of a separate research protocol,all survivors had coronary angiography and left ven-triculography 6-8 weeks after the acute event. These143 patients were eligible from a consecutive series of171 patients who were admitted with a transmural MIbetween January 1979 and November 1980, the periodbefore thrombolytic treatment was attempted. Twelveof these 171 patients died during the acute phase and16 refused investigation. Eleven patients died in thehospital, seven with severely impaired LV function

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TABLE 1. Eligibility of Streptokinase-treated PatientsAttem ted lysis

42 pts(LAD:17, RCA:16, Cx:9)

I -~ ~~ ~~~~~~~~~~~~~~~~~

No recanalizationI

I1 pts(LAD:4, RCA:3, Cx:4)

exclusior(obtusus)

-died: 1 pt(LAD)

Recanalization

31 pts(LAD: 13, RCA:13, CX:)

refusal: 2 ptsIn: 2 pts

IReocclusion

within 6 weeks

4 pts

-died: 1 pt(RCA)refusal: I pt(LAD)

Unsuccessful

10 pts(LAD:4, RCA:4, Cx:2)

No reocclusionwithin 6 weeks

I25 pts

SuccessfulI

25 pts(LAD:10, RCA:10, Cx:5)

Abbreviations: LAD = left anterior descending coronary artery; RCA = right coronary artery; Cx = circumflex coronary artery.

and four with rupture of the left ventricle. One patientdied suddenly 1 week after discharge. Excluded weretwo patients with serious other disease and all fivepatients who were referred from other hospitals be-cause of complications of the infarctions. TransmuralMI was diagnosed if all of the following criteria werepresent: typical history, evolution of pathologic Qwave (> 0.04 second) and specific cardiac enzymense.

ProtocolStreptokinase Group

Nonsurgical recanalization was performed on a 24-hour basis. Informed consent was obtained from thepatient and a relative. Before angiography, 600 mg ofaspirin were given orally. Coronary angiography in theacute phase was performed with the Judkins technique.After the infarct vessel was visualized, 10 mg of sub-lingual nifedipine were given to exclude spasm. In nopatient with total occlusion did the vessel show ante-grade flow after nifedipine. The same catheter used forcoronary angiography was used to infuse streptoki-nase. A bolus of streptokinase (10,000-20,000 U) wasinjected into the infarct vessel. Thereafter, streptoki-nase, 2000 U/min, was constantly infused into theinfarct vessel.The effect of streptokinase infusion was checked

angiographically every 20 minutes or after a decreaseof the ST-segment elevation. If occlusions persisted

for more than 1 hour, the streptokinase infusion ratewas increased to 4000 U/min. As a rule, infusion wasnot given for more than 2 hours. After successful re-

perfusion, the streptokinase infusion was continued fora further 10-30 minutes. After the procedure, the cath-eter tip was left in the descending aorta and the patientswere monitored in the coronary care unit. The catheterwas removed 6-12 hours after lysis.

Analgesics and sedation were given as appropriateduring the acute phase. All patients were given aspirin,200 mg/day and nifedipine 30 mg/day. During recov-ery, ,B blockers were added if the patient had anginapectoris. None of the patients were given anti-coagulants.

Control GroupAnalgesics and sedatives were given as necessary.

In the acute phase, no patient received nifedipine, aspi-rin, other vasodilator agents or blockade. From thefirst day of admission all patients received oral antico-agulation (coumarin), which was continued until a fewdays before angiography. After mobilization (48 hoursafter admission), patients were given ,B blockers ifangina pectoris occurred.

InvestigationSix to 8 weeks after acute infarction, all patients

were readmitted for coronary angiography and leftventriculography using the Judkins technique. All

Eligible:

-,,-, .- . , - --. - . 5' -- /

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medication was stopped at least 2 days before ventricu-lography in all patients; digitalis was stopped 14 daysbefore investigation. Left ventriculograms were filmedat 50 frames/sec in the 300 right anterior oblique pro-jection and in the 600 left anterior oblique projection.Left ventriculography was performed before angiog-raphy using 30-40 ml of contrast material (IsopaqueCoronair) injected at a rate of 15 ml/sec. Only theventriculograms of normally conducted beats withoutpreceding extrasystoles were analyzed.

Segmental wall motion of the left ventricle wasqualitatively assessed according to the criteria of theAmerican Heart Association committee.7 Each ven-triculogram was divided into seven segments (fig. 1).Each segment was assigned a score as follows: normal= 0, hypokinesia = 1, akinesia = 2, dyskinesia = 3.For each patient, the scores of the seven segments wereadded to yield a total score, representing the severity ofleft ventricular damage. The range from normal to amaximally damaged ventricle is thus represented by ascore range of 0-21. Ejection fraction was calculatedusing the area-length method.8The coronary arteries were filmed in multiple axial

and hemiaxial views. Only obstructions of left anteriordescending, circumflex and right coronary arterieswere included. Obstructions of diagonal branches ofthe left anterior or descending coronary artery and theobtuse marginal branch of the circumflex coronaryartery were excluded. It was assumed that anteriorinfarction was caused by obstruction of the left anteriordescending and that inferior infarction was caused byobstruction of the circumflex or right coronary artery.If both arteries were obstructed, the more severelyobstructed vessel was selected as the infarct vessel.The angiographic data were analyzed without

knowledge of the clinical details of the patient by twoindependent observers. The ventriculograms were ana-lyzed first without knowledge of the coronary anato-my.

Statistical MethodsEach statistical test was performed at a two-sided

5% level of significance; a result was considered sig-nificant when the two-tailed p value was 5% or less.The ejection fraction in the groups was compared usingthe t test and the total score with the test of Yates.9

ResultsClinical CharacteristicsStreptokinase GroupThe eligible streptokinase-treated group consisted of

14 patients with an acute anterior wall MI and 21patients with an acute inferior wall infarction. In 10 ofthe 14 patients with an anterior MI, successful recana-lization resulted in an open infarct vessel; in four pa-tients streptokinase had no effect and the infarct vesselremained occluded. Fifteen of the 21 patients withinferior MI had a successful recanalization. The timeinterval from onset of symptoms to successful recana-lization was 2-4 hours. The mean total doses of strep-tokinase was 120,000 U (range 60,000-300,000 U).The mean age was 53 years (range 37-64 years).

Mitral / 2 Anterolateral

LAO

RAO5 -GSeptal

Posterobas al

7 Posterolateral4

Apca

Diophroqma ic '

FIGURE 1. Left ventriculograms in the right (RAO) and left(LAO) anterior oblique projections divided into seven seg-ments. Each segment was scored as follows: normal = 0,hypokinesia = 1, akinesia = 2, dyskinesia = 3.

Control GroupThe control group consisted of 62 patients with an

anterior wall infarction and 81 patients with an inferiorwall infarction, mean age 55 years (range 34-65years). Thirty-four of the patients with anterior MI hadan open infarct vessel (spontaneous recanalization)and 28 patients had a persistent occlusion of the infarctvessel. Forty-one of the patients with inferior MI hadan open infarct vessel and 40 patients had an occludedinfarct vessel at the time of investigation.

LV Function in Inferior MIThe ejection fraction and the severity of LV damage

were similar in patients with spontaneous and strepto-kinase-induced recanalization. The ejection fractionwas lower and the LV damage more severe in patientswith persistent occlusion of the infarct vessel (table 2,fig. 2A). The number of patients in whom streptokin-ase treatment was unsuccessful was too small for sta-tistical analysis. The presence of multivessel diseaseand the distribution of circumflex or right coronaryartery infarct vessel were comparable in the groups.

LV Function in Anterior MIThe ejection fraction was higher and LV damage

less in patients with streptokinase-induced recanaliza-tion than in those with spontaneous recanalization orpersistent occlusion of the infarct vessel (table 3, fig.2B). The ejection fraction was higher and LV damageless severe in patients with spontaneous recanalizationthan in those with persistent occlusion of the infarctvessel. These differences were not statistically signifi-cant, at least partly because of the small number ofpatients. The number of patients in whom streptoki-nase treatment was unsuccessful was too small forstatistical analysis. The presence of multivessel dis-ease was comparable in the study groups.

DiscussionFunctional impairment after acute MI is related to

the extent of myocardial ischemic injury. 1012 Massivemyocardial ischemia produces pump failure and seri-ous ventricular arrhythmias"' 13, 14 and is the most com-mon cause of death and morbidity among patients hos-pitalized with acute MI. Both early and late prognosisare worse with larger infarcts.1'3 14 Therefore, methods

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1 CONTROL GROUP

0 STREPTOKINRSE TREATED GlROUP

P < 0.05S P

M.S. F c 0.0. I I

CIRCULATION VOL 67, No 5, MAY 1983

L CONTROL GROUP

I STREPTOKINRSE TREATED GROUP

N.S.

p '0.01 P 0.001-, I

NO41 No 15 N*40 No 6

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N.S. P ' 0.62MS. P -c9.9

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No40 Ne 6

INFRRCT VESSELOCCLUOEO

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INFRRCT ;FSSELB OPEN

FIGURE 2. (A) Ejectionfraction and severity of left ventricular (LV) damage in inferior myocardial infarction.(B) Ejection fraction and severity ofLV damage in anterior infarction.

that reduce left ventricular damage may improve prog-nosis.The presence of a zone of cells with reversible myo-

cardial injury after coronary artery occlusion has beenrecognized. 15 Interventions that either reduce the oxy-gen demand or increase oxygen supply may salvagethis zone. In animals, the amount of reversible ische-mic tissue is largest immediately after coronary occlu-sion and becomes smaller with time until it disappears,6-9 hours after occlusion.'5 Myocardial salvage inter-vention should therefore be instituted as soon as possi-ble, probably within 6 hours. For this reason, onlypatients admitted to the hospital within 3 hours afteronset of symptoms were treated with streptokinase.

Little is known about the natural history of occludedinfarct vessels and the subsequent left ventricular dam-age. Acute MI results from an acute imbalance be-

tween oxygen supply and demand. The severity ofreduction of blood flow during the acute phase of MIhas recently been established by acute angiography.26In the early hours of transmural MI, the prevalence of atotally occluded infarct vessel is 72-95%, all otherlesions being subtotal.21 DeWood et al.6 showed theexistence of spontaneous recanalization during the firsthours of MI. To prove reversal of a total to a subtotalocclusion requires serial studies in a given patient; butcomparison of the studies2- of prevalence of total oc-clusion early after onset of symptoms (72-95%) withthe study of DeWood et al.6 24 hours after the acuteevent (65%) and with those of Bertrand et al.'6 andBetriu et al.'7 2-4 weeks after the acute event (45-53%) and our own study at 6-8 weeks (47%) highlysuggest this to be the case. Therefore, it may be as-sumed that for some time during the acute phase of

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N-28 No 4

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TABLE 2. Ejection Fraction and Severity of Left VentricularDamage in the Streptokinase-treated and Control Patients withInferior Myocardial Infarction

Inferior MI Controls Streptokinase p

Infarct vessel open*No. of patients 41 15Ejection fraction

(%) 54.4 +/- 10.1 57.5 +/- 10.3 NSSeverity of LVdamaget 2.8 +/- 2.3 2.6 +/- 2.3 NS

StatisticsEjection fraction p <0.05 p <0.02Severity of LVdamage p<O.03 p<0.02

Infarct vesseloccludedt

No. of patients 40 6Ejection fraction

(%) 48.9 +/- 12.0 52.8 +1- 10.3Severity of LVdamaget 4.5 +1- 2.5 4.7 +1- 2.3

Values are mean ± SD.*Open = stenosis < 99% 6 weeks after MI (untreated patients:

open = spontaneous recanalization; treated patients: open = strep-tokinase-induced recanalization).

tOccluded = no antegrade flow 6 weeks after MI (untreatedpatients: occluded = persistent occlusion; treated patients: oc-cluded = no effect of streptokinase).

tSeverity = total score (normal = 0, hypokinesia = 1, akinesia= 2, dyskinesia = 3).Abbreviations: LV = left ventricular; MI = myocardial infarc-

tion.

TABLE 3. Ejection Fraction and Severity of Left VentricularDamage in the Streptokinase-treated and Control Patients withAnterior Myocardial InfarctionInfarct vessel

openNo. of patientsEjection frac-

tion (%)Severity ofLV damage

Statistics

Ejectionfraction

Severity ofLV damage

Infarct vesseloccluded

No. of patientsEjection frac-

tion (%)Severity ofLV damage

Values are meantable 2.

34 10

46.1 +/- 13.5 60.3 +/- 10.3p<0.01

6.5 +1- 2.8 3.3 +1-

NS p < 0.001

NS

28

2.7 p<0.005

p<0.002

4

40.0 +/- 13.2 46.8 +/- 13.9

7.3 +/- 3.0 6.8 +/- 1.9

± SD. Definitions and abbreviations are as in

transmural MI, there is a complete absence of ante-grade blood flow in the diseased artery in the majorityof patients. The underlying mechanism is not known,but it appears that in some patients this occlusion per-sists and in others spontaneous recanalization occurs.The same studies suggest that spontaneous recanaliza-tion is an ongoing process, starting in the early hoursafter the onset of symptoms and continuing for wellover 24 hours.

In survivors of MI, angiographic assessment of LVwall motion and ejection fraction is a means of estab-lishing the severity of postinfarction LV damage. Theseverity of asynergy, depicted ventriculographically,and the amount of muscle loss determined histopatho-logically are related.'8 Hypokinetic segments show asmall degree of muscle loss, akinetic segments showmore significant amounts of muscle destruction, anddyskinetic segments show the most extensive muscleloss and subsequent replacement by fibrous tissue. Ourangiographic scoring system takes account of thesedegrees of segmental asynergy and should thereforereflect the severity of LV damage.

Little agreement exists about the natural history ofLV function after acute MI. Some investigators'922have demonstrated no improvement in the LV per-formance 2-6 weeks after the acute event, whereasothers claim improvement in some patients studied 2weeks to 6 months23 and 6-14 months after the acuteevent.24 Studies of coronary occlusion and reperfusionhave shown that a potentially reversible zone may take1-4 weeks to regain normal contractility.25'26 Wetherefore evaluated our patients 6-8 weeks after acuteinfarction.We analyzed the effects of spontaneous recanaliza-

tion and persistent occlusion on LV function and com-pared these with the effect of streptokinase-inducedrecanalization. We found a definite beneficial effect inpatients with inferior MI and spontaneous recanaliza-tion; the same trend was present in patients with anteri-or MI and spontaneous recanalization. Patients whohad an anterior MI and successful recanalization withintracoronary streptokinase had significantly better LVfunction than the control patients with spontaneousrecanalization or persistent occlusion. In patients withinferior MI and successful recanalization, LV functionwas not different from that in patients with spontane-ous recanalization, but was better than that in patientswith persistent occlusion. Although the number of pa-tients with thrombolysis was too small for statisticalanalysis, no worsening of LV function was showncompared with patients who had persistent occlusion.

Experimental and clinical experience suggests thatreperfusion is beneficial only early after the onset ofischemia.2- , " We do not know why and how sponta-neous recanalization has a favorable effect. Reopeningof the artery may increase the flow to the border zonesand thus limit extension of infarction.

Inferior wall MI usually causes a smaller degree ofmyocardial necrosis than anterior MI. 3' 27, 28 This wasalso shown in our study. The potential for a beneficialeffect in inferior wall MI may therefore be smaller.

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Also, in inferior MI, only differences in LV perform-ance were measured, although right ventricular dam-age occurs in 38-50%. 19, 29-31 We may therefore haveseriously underestimated the potential for improve-ment in inferior MI.

All patients treated with intracoronary streptokinasealso received nifedipine and aspirin. We do not knowthe extent to which these drugs affected salvage ofischemic myocardium. Experimental studies of the ef-fect of nifedipine on infarct size are conflicting.15Some showed a reduction, whereas others showed noeffect on infarct size.'5' 32 In dog experiments, a highdose had a deleterious effect and a low dose had abeneficial effect.33 Definite conclusions regarding re-duction of infarct size with intracoronary streptokinaseand subsequent improvement of prognosis for morbid-ity and mortality must be drawn from carefully de-signed randomized studies. At this stage. we do notrecommend widespread use of intracoronary strepto-kinase in acute MI.

AcknowledgmentWe are indebted to A.W. Plu, C.A.M. Hermans, P.J.J. Lutz, P.A.J.

Peters, M. Verspoor and J.A. Zonneveld for technical assistance.

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perfusion of the coronary arteries with fibrinolysin in man follow-ing myocardial infarction. Am J Cardiol 6: 525, 1960

2. Ganz W, Buchbinder N, Marcus H, Mondkar A, Maddahi J, Char-uzi Y, O'Conner L, Shell W, Fischbein MC, Kass R, Miyamoto A,Swann HJC: Intracoronary thrombolysis in evolving myocardialinfarction. Am Heart J 101: 4, 1981

3. Mathey DG, Kuck KH, Tilsner V, Krebber HJ, Bleifeld W: Non-surgical coronary artery recanalization in acute transmural myocar-dial infarction. Circulation 63: 489, 1981

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5. Reduto LA, Smalling RW, Freund GC, Gould KL: Intracoronaryinfusion of streptokinase in patients with acute myocardial infarc-tion: effects of reperfusion on left ventricular performance. Am JCardiol 48: 403, 1981

6. DeWood MA, Spores J, Notske R, Mouser LT, Burroughs R,Golden MS, Lang HT: Prevalence of total coronary occlusionduring the early hours of transmural myocardial infarction. N EnglJ Med 303: 897, 1980

7. AHA Committee Report: A reporting system on patients evaluatedfor coronary artery disease. Report of the Ad Hoc Committee forGrading of Coronary Artery Disease, Council on CardiovascularSurgery, American Heart Association. Circulation 51 (suppl IV):IV-5, 1975

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14. Geltman EM, Ehsani AA, Campbell MK, Schechtman K, RobertsR, Sobel BE: The influence of location and extent of myocardialinfarction on long-term ventricular dysrhythmia and mortality. Cir-culation 60: 805, 1979

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25. Puri PS: Contractile and biochemical effects of coronary reperfu-sion after extended periods of coronary occlusion. Am J Cardiol36: 244, 1975

26. Theroux P, Ross J, Franklin D, Kemper WS, Sasayama S: Coro-nary arterial reperfusion. III. Early and late effects on regionalmyocardial function and dimensions in conscious dogs. Am J Car-diol 38: 599, 1976

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28. Hamby RI, Hoffman I, Hilsenrath J, Aintablian A, Shanies S,Padmanbhan VS: Clinical, hemodynamic and angiographic aspectsof inferior and anterior myocardial infarctions in patients withangina pectoris. Am J Cardiol 34: 513, 1974

29. Rigo P, Murray M, Taylor DR, Weisfeldt ML, Kelly DT, StraussHW, Pitt B: Right ventricular dysfunction detected by gated scinti-photography in patients with acute inferior myocardial infarction.Circulation 52: 268, 1975

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32. Henry PD, Schuchreib R, Borda LJ, Roberts R, Williamson JR,Sobel BE: Effects of nifedipine on myocardial perfusion and ische-mic injury in dogs. Circ Res 43: 372, 1978

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function after myocardial infarction.Effects of spontaneous and streptokinase-induced recanalization on left ventricular

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