Heart 1996;75:582-587

Prognostic significance of ST-T segmentalterations in patients with non-Q wave myocardialinfarction

Jose Antonio F Ramires, Carlos V Serrano, Maria C Solimene, Paulo J Moffa,Bruno Caramelli, Fuilvio Pileggi

Heart Institute,University ofSaoPaulo, School ofMedicine, Sao Paulo,SP, BrazilJ A F RamiresC V SerranoM C SolimeneP J MoffaB CaramelliF PileggiCorrespondence to:Dr J A F Ramires, HeartInstitute, University of SaoPaulo School of Medicine,Clinical Division, Av DrEneas C Aguiar 44, SaoPaulo, SP 05403-000, Brazil.

Accepted for publication15 June 1995

AbstractObjective-To determine whether, among

patients with non-Q wave myocardialinfarction, the characteristics of the seg-

ment ST-T shifts at presentation in thediagnostic electrocardiogram can identifythose with more severe coronary arterydisease and predict a poor clinical out-come.Design-Prospective controlled clinicaltrial.Setting- Primary referral medical centre.Patients-93 patients (mean (SD) 62-0(7.5) years) were studied: 41 with non-Qwave myocardial infarction and T wave

inversion and 52 with ST segment depres-sion. Cardiac events and mortality rateswere assessed over 42 months. Age, sex,risk factors, creatine kinase MB isoenzymepeak, and left ventricular function were

comparable.Results-31 patients with T wave inversionmyocardial infarction (94.6%) had totalocclusion of the infarct related artery,compared with 12 patients with ST seg-ment depression myocardial infarction(26-7%) (P < 0.05). When compared withpatients with T wave inversion, patientswith ST segment depression had a higherincidence of cardiac events during the firstmonth and in the 41 subsequent months:9-6% and 30*8% v 0% (P < 0-01) and 9-8%(P < 0.02), respectively. For the same

observation periods, the mortality rates inpatients with T wave inversion were 4 9%and 7 3%, and in patients with ST segmentdepression they were 5-8% and 9-6%,respectively.Conclusion-These data suggest that dur-ing a non-Q wave myocardial infarctionthe presence of ST segment depression isrelated to higher rates of short and longterm cardiac events when compared withT wave inversion-possibly because of a

higher incidence of residual stenosis of theinfarct related artery.

(Heart 1996;75:582-587)

Keywords: acute myocardial infarction; non-Q wave

myocardial infarction; reinfarction; prognosis

Prognosis after an acute myocardial infarctiondepends largely on infarct size, left ventricularfunction, residual myocardium in jeopardy,state of coronary circulation, and the presenceof complex ventricular arrhythmias at hospital

discharge. 1-6 Recently, several studies haveemphasised important clinical differencesbetween patients with non-Q wave and Q wavemyocardial infarction that may have prognosticand therapeutic implications. It is known thatpatients with non-Q wave infarction havesmaller infarct size and greater residualmyocardium at risk than patients with Q waveinfarction.78 These findings are based on stud-ies that have shown that subtotal occlusion ofthe infarct related artery is more frequentamong patients with non-Q wave myocardialinfarction.9 10 This angiographic picture proba-bly explains the higher incidence of recurrentischaemic events in patients with non-Q waveinfarction than in those with Q wave infarc-tion.9-12

However, little is known about the prognos-tic significance of early ST-T segment shiftspresent in patients during the evolution of anon-Q wave myocardial infarct. Since mostmyocardial infarcts (within the first severalhours) begin without Q waves, it is importantto establish whether the early electrocardio-graphic (ECG) findings differ appreciably fromthose normally encountered in Q wave myocar-dial infarction and whether ST-T segmentshifts provide any meaningful informationabout short and long term outcomes.The objective of our study was therefore to

determine whether, among patients with non-Qwave myocardial infarction, ST-T segmentshifts would identify those with a more severecoronary artery disease and predict a poor clini-cal outcome.

MethodsThis study was part of a population basedinvestigation of temporal trends in the inci-dence and case fatality rates of patients admit-ted to hospital with acute myocardial infarctionin the Heart Institute (Sao Paulo, Brazil). Allpatients were admitted with predefined diag-nostic criteria for acute myocardial infarction.

STUDY POPULATIONFrom a total of 1287 patients with acutemyocardial infarction admitted in our hospital,93 (82 men; mean (SD) age 62-0 (7-5)) pre-sented with a non-Q wave myocardial infarc-tion and were studied prospectively for 42months. Patients with any of the following con-ditions were excluded from the study: refusedto participate; more than 24 h from onset ofsymptoms; use of thrombolytics; past history ofmyocardial infarction or congestive heart fail-ure; left ventricular hypertrophy. Patients were

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Prognostic significance ofST-T segment alterations in patients with non-Q wave myocardial infarction

Table 1 Medical treatment, distribution of baseline characteristics, and angiographicaspects of the patients with non-Q wave myocardial infarction. Values are mean (%) ormean (SD)

T wave inversion(n = 41)

Medical treatmentIntravenous glyceryl trinitrateOral nitratesP blockersCalcium channel blockersAspirinLignocaine

Distribution of baseline characteristicsAge (years)MaleRisk factorsDislipidaemiaSmokerDiabetes mellitusArterial hypertensionPain duration (h)CKMB peak (IU/litre)Site of qualifying infarct

Anterior wallInferior wallLateral wall

Angiographic aspectsCineangiograms performedInfarct related artery

Right coronaryLeft anterior descending**Left circumflex

Occlusion of infarcted related arteryNumber of coronary arteries with lesiontOneTwoThree

Left ventricular ejection fraction

30 (73-2%)40 (97-6%)31 (75 6%)33 (80 5%)40 (97.6%)*5 (12-2%)

63 (5)38 (93%)

14 (34-1%)11 (26.8%)5 (12-2%)

17 (41-5%)7-2 (5-1)

55 (8)

23 (56-1%)6 (14-6%)

12 (29-3%)

37 (90%)

5 (13-5%)25 (67-6%)7 (18-9%)

35 (94-6%)t

16 (43 2%)10 (27 0%)11 (29-7%)0-65 (0-12)

ST segment depression(n = 52)

47 (90 4%)50 (96 2%)39 (75 0%)42 (80 8%)52 (100%)11 (21-2%)

61 (8)44 (84 6%)

14 (26 9%)11 (21-2%)5 (9 6%)

17 (32 7%)8-4 (6-5)

49 (10)

31 (59 6%)6 (11-6%)

15 (28 8%)

45 (87%)

4 (8 9%)35 (77 8%)6 (13-3%)

12 (26-7%)t

13 (28 9%)19 (42-2%)13 (28-9%)0-58 (0 09)

CKMB, creatine kinase MB isoenzyme.*One patient had aspirin stopped because of peptic ulcer.**Overall incidence 73-2%.tIntergroup: P < 0.05.t> 70% obstruction.

also excluded if they developed either ST seg-ment elevation or ST segment depression asso-ciated with tall R waves. This represents a Qwave equivalent posterior myocardial infarc-tion. Fifty four patients with non-Q wavemyocardial infarction were excluded from thestudy since they arrived at the hospital withsymptoms for more than 24 h (range 1-3-8-6 d).The patients were divided according to ST-

T segment alterations in their diagnostic ECG:there were 41 patients (44-1%) with T waveinversion and 52 patients (55 9%) with ST seg-ment depression.

DIAGNOSIS OF NON-Q WAVE ACUTEMYOCARDIAL INFARCTIONCriteria for inclusion of patients in the studywere based on the diagnosis of non-Q wave

acute myocardial infarction, which needed thepresence of two of the following: (1) Chest pain:history of precordial pain was defined as thepresence of typical cardiac chest pain lastingmore than 20 min. (2) ECG coding: 12-leadresting ECG on admission showing sustained Twave inversion or ST segment depression (> 2mm), and absence of Q waves > 1 mm indepth and 0-02 s in duration. The ECG was

obtained every 3 h during the first 24-48 h ofmyocardial infarction. Patients who initiallyhad ST segment depression on their admissionECG and later evolved to combined T wave

inversion were considered to be in the ST seg-ment depression group. The diagnostic ECGsof all study patients were reviewed by twoinvestigators to reach agreement on the magni-tude of T wave inversion and ST segmentdepression. ST-T changes were considered to

be transient if, on resolution of the pain, the Twaves and ST segments returned to the leveland configuration obtaining before the painoccurred. (3) Cardiac enzymes: elevation ofserum creatine kinase-MB (CKMB) levelsabove 20 IU/litre sampled every 6 h within 48 hafter the onset of precordial pain.

CARDIAC CATHETERISATION TECHNIQUETwo to 12 days following the myocardialinfarct, coronary arteriography and left ven-triculograms were performed by the Shirey-Sones technique. The angiograms werereviewed for the presence of significant coro-nary artery narrowing, defined as a diameterreduction of > 70%. The coronary arterylesions were further evaluated for the locationof the narrowing or obstruction in each vessel,and the presence and origin of collateral bloodflow. Global left ventricular ejection fractionswere calculated using an area-length tech-nique.'3

CLINICAL PROTOCOLThe subjects were admitted to coronary careunits and treated with analgesia (morphine),adequate oxygenation, bed rest, anxiety reduc-tion (diazepam 5 mg orally four times a day),and correction of disturbances of acid-base bal-ance and electrolytes.

During the early phase of myocardial infarc-tion, patients with evolving congestive heartfailure underwent specific haemodynamic andpharmacological management, including ino-tropic support. Other complications such asventricular tachyarrhythmias were treated simi-larly.

CLINICAL AND LABORATORY EVALUATIONAfter admission the following evaluations wereperformed: (1) daily clinical examination by theinvestigator; (2) 12-lead ECG, daily for the first4 d, then on alternate days until 10 d or hospitaldischarge; (3) ECG at the time of recurrentpain and for a minimum of three consecutivedays if reinfarction was suspected; and (4) serialblood samples for analysis of CKMB activity.Sampling times consisted of an initial sample atthe time of admission, followed by samplesdrawn every 6 h thereafter throughout 2 d.Additional samples were collected at least every8 h for the subsequent 72 h in patients in whomreinfarction was suspected. The subsequentclinical course was evaluated weekly in the restof the first month, monthly during the followingthree months, quarterly during the first year,and then intermittently until the 42nd monthafter the infarction.

TREATMENT REGIMENAs seen in table 1, all patients received standardmedical treatment in accordance with conven-tional guidelines, and there were no significantdifferences among the two groups of patients.Use of glyceryl trinitrate, ,B blocking drugs, cal-cium channel blocking agents, salicylates, andlow dose heparin was permitted when indi-cated. Initial treatment for angina includedsublingual glyceryl trinitrate or morphine. Theapproach to angina refractory to medical treat-

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Ramires, Serrano, Solimene, Moffa, Caramelli, Pileggi

ment (long acting nitrates, intravenous glyceryltrinitrate, ,B blocking drugs, and calcium chan-nel blocking agents) was individualised andpatients had coronary angioplasty or surgery ifnecessary.

DEFINITION OF ENDPOINTSThe primary endpoint of the study was a car-

diac event within two periods: in the firstmonth after the infarction, defined as shortterm follow up, and in the 41 subsequentmonths, defined as long term follow up. A"cardiac event" was defined as follows: (1)unstable angina, defined as a new occurrence oftypical ischaemic chest pain that developed atrest or with minimal effort, and was associatedwith transient ECG alterations and without a

new rise in plasma CKMB activity; (2) reinfarc-tion, defined as the presence of at least two ofthe following: (a) recurrent and persistentischaemic pain while in hospital more than 24 hafter admission, (b) increase in CKMB level ofat least 20% over the last abnormal value, and(c) new persistent ECG changes; (3) congestiveheartfailure, New York Heart Association classi-fication class II to IV during the late evolutionperiod, and Killip-Kimbal class II to IV classifi-cation during in-hospital evaluation; (4) percu-taneous transluminal coronary angioplasty or

coronary artery bypass graft surgery-treatmentsindicated at any time during the study becauseof critical stenosis (. 95%).The other endpoint of the study was death

secondary to cardiac causes, also within thesame observation periods.

STATISTICAL ANALYSISMeans (SD) (range) were calculated for contin-uous variables, and absolute and relative fre-quencies were measured for discrete variables.Comparisons between groups were carried outby Student's t test in the case of continuousvariables and by the X2 test. The independenteffect of selected clinical variables on short termmortality was assessed and estimated as relativerisks with corresponding 95% confidence inter-vals. The following variables were included inthis multivariate analysis: age, sex, coronary riskfactors (hypercholesterolaemia, smoking, dia-betes mellitus, and systemic arterial hyperten-sion), duration of chest pain, site of qualifyinginfarct (anterior, inferior, or lateral wall), andserum CKMB findings. For long term analysis,survival rates were calculated by the Haenszel-Mantel method. All tests were two tailed, and a

P value of < 0 05 was considered to indicatestatistical significance.

ResultsCONTRIBUTION OF BASELINE CHARACTERISTICS

Patients with both T wave inversion and STsegment depression non-Q wave myocardialinfarction had a similar distribution of baselinecharacteristics relating to age, sex, pain dura-tion, maximum CKMB values, coronary riskfactors, site of qualifying infarct (table 1), andconcurrent treatment with blocking drugs,nitrates, calcium channel antagonists, andantiplatelet agents.

ANGIOGRAPHIC DATA

Coronary arteriography and left ventriculo-grams were performed in 37 of the patients(90 2%) with T wave inversion, and in 45 ofthe patients (86 5%) with ST segment depres-sion. We found no angiographic differencesbetween these two sets of patients concerningthe infarct related coronary artery, the numberof coronary arteries with disease () 70%obstruction), and left ventricular ejection frac-tion. The left anterior descending coronaryartery was the vessel most affected by obstruc-tive disease in the study (67 6%), indepen-dently of ST-T alterations (table 1).

Only 26-7% of the patients with ST segmentdepression had total occlusion of the infarctrelated artery in their coronary arteriograms,while 94-6% of the T wave inversion patientshad total occlusion (P < 0 05).

IN-HOSPITAL CLINICAL COURSEIndependent of the type of non-Q myocardialinfarction (T wave inversion or ST segmentdepression), more than 95% of the patientsstudied showed no or mild clinical manifesta-tions of left ventricular failure during their in-hospital clinical course as they evolved in Killipclasses I-II (table 2).

In addition, two patients (4%) with ST seg-ment infarction developed ventricular tachy-arrhythmias, while none of the patients with Twave inversion myocardial infarction had sucharrhythmias in the postinfarction period (table2).

CARDIAC EVENTSDuring the 42 month follow up period, 26(27 9%) of the original 93 patients had a car-diac event. Compared with patients with Twave inversion, patients with ST segmentdepression showed a higher incidence of car-diac events during the first month and duringthe 41 subsequent months postinfarction: 9-6%and 30-8% v 0% (P < 0-01) and 9-8% (P <0-02), respectively (table 3).

Overall, the cardiac event encountered mostfrequently was the need for coronary angio-plasty or a surgical bypass treatment (52 0%).These procedures were indicated becauseangiography showed critical stenosis in theinfarct related artery or in other coronary arter-ies. The cardiac catheterisations were per-formed between two and 12 dayspostinfarction. Another interesting observationis that none of the patients with T wave inver-sion in their diagnostic ECG had a cardiacevent during the first postinfarction month andonly four had an event during the 41 subse-

Table 2 Incidence of congestive heart failure (CHF) andventricular arrhythmia according to the type ofnon-Qwave myocardial infarction during the 42 month studyperiod. Data are expressed as number ofpatients or asincidence (%) to related variable

T wave inversion ST segment depressionCHF (Killip class) (n = 41) (n = 52)

I-II 40 (98%)* 50 (96%)tIllI-IV 1 (2%)* 2 (4%tVT/VF 0 (0%) 2 (4%)

VT/VF, ventricular tachycardia/ventricular fibrillation.*, tIntragroup: P < 0-05.

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Table 3 Incidence of cardiac events (deaths excluded) according to the type ofnon-Qwave myocardial infarction during the first month and 41 subsequent months aftermyocardial infarction. Data are expressed as number ofpatients or as incidence (%) torelated variable

T wave inversion ST segment depression(n = 41) (n = 52)< 1 month 1-42 months < 1 month 1-42 months

Unstable angina 0 1 1 4Reinfarction 0 1 1 3Congestive heart failure 0 0 0 1PTCA/CABG 0 2 3 8Total 0 (0%)* 4 (9-8%)t 5 (9-6%)* 16 (30-8%)t

CABC, coronary artery bypass graft surgery; PTCA, percutaneous transluminal coronary angio-plasty.Intergroup: P * 0-01, t < 0-02.

Table 4 Causes of deaths according to the type ofnon-Q wave myocardial infarctionduring the first month and 41 subsequent months after myocardial infarction. Data areexpressed as number ofpatients or as incidence (%) to related variable

T wave inversion ST segment depression(n = 41) (n = 52)

< 1 month 1-42 months < 1 month 1-42 months

Reinfarction 1 0 2 2Congestive heart failure 0 1 0 0Sudden death 1 1 0 2Post-PTCA/CABG* 0 0 1 1Unidentified 0 1 0 0Total 2 (4 9%) 3 (7 3%) 3 (5 8%) 5 (9-6%)

PTCA, percutaneous transluminal coronary angioplasty; CABC, coronary artery bypass graftsurgery.*During the first week of treatment.

quent months (two cases of invasive treatmentand one case each of unstable angina and rein-farction). On the other hand, in patients withST segment depression there was one case ofangina, one of reinfarction, and three casesneeding invasive treatment in the first monthpostinfarction, while in the 41 subsequentmonths, there were four cases of angina, threecases of reinfarction, one congestive heart fail-ure, and eight cases needing invasive treatment.

MORTAITYDuring the study, 13 (14-0%) of the original 93patients died of cardiac causes (table 4). Nosignificant differences were observed during thefirst month or during the 41 subsequentmonths between patients with T wave inversionand those with ST segment depression whenthe mortality was analysed: 4-9% and 7-3% v5-8% and 9-6%, respectively. There were nodifferences between the groups in the cause ofdeath.To clarify the interpretation of the cardiac

events and mortality in relation to ST-T seg-ment variability, rate curves were calculatedand are shown in figs 1 and 2.

Figure I Cumulativeprobabilities (%) ofcardiac events at selectedtimes in patients with Twave inversion (P) andST segment depressionnon-Q wave myocardialinfarction (0). *P < 0-02at one month (broken line)and at 41 months.

50

40

> 30._

n 200

a-

10

3 24 30 36 42Month

100l

80

_60-

U

2 402n

20

L

L_!

l

v0 6 12 18 24 30 36 42

Month

Figure 2 Cumulative survival (%) at selected times inpatients with T wave inversion (a) and ST segmentdepression (0) non-Q wave myocardial infarction.Broken line indicates the one month follow up.

DiscussionQ WAVE AND NON-Q WAVE MYOCARDIALINFARCTIONThe terms "transmural" and "non-transmural"myocardial infarction, as detected by an ECG,imply a pathological counterpart, but correla-tion with the anatomical definition of trans-mural/non-transmural myocardial infarction atnecropsy is poor. Consequently, the moreappropriate ECG terms of Q wave and non-Qwave myocardial infarction have become widelyaccepted in medical writing and practice.'4Non-Q wave myocardial infarction is not associ-ated with a specific ECG pattern, and patientsmay present with ST segment depression or Twave abnormalities or both without the evolu-tion of Q waves. However, confirmation ofmyocardial necrosis through raised plasmaCKMB activity is required.

Prolonged chest pain and ST segment eleva-tion on the admission ECG are now used as theprincipal criteria for prescribing thrombolytictreatment in patients with evolving acutemyocardial infarction,'5 the justification beingthat acute ST segment elevation representstransmural ischaemia resulting from totalocclusion of a coronary artery and is a precur-sor of transmural (Q wave) myocardial infarc-tion.'6 Therefore, the importance of earlyhospital admission for thrombolytic treatment(the success of which is critically time depen-dent) make it both relevant and feasible toexamine the significance of acute ST-T seg-ment shifts during the early course of an evolvingmyocardial infarct.'7-'9

CARDIAC ISOENZYME ANALYSISOur data accord with other studies5202' whichhave shown that non-Q wave myocardialinfarction is associated with low CKMB releaseand a reduced incidence of congestive heartfailure postinfarction-probably because of thesmall extent of myocardial necrosis.

PROGNOSIS AFTER A NON-Q WAVE MYOCARDIALINFARCTIONThe prognosis of patients who develop non-Qwave acute myocardial infarction is uncertain.Only a few studies have reported a favourableoutlook in patients with a first non-Q waveinfarct. Mahony and associates22 reported anexcellent in-hospital and one year survival rate

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in 24 patients; however, data about recurrentischaemic events were not reported. Similarly,Coll and associates23 reported good long termsurvival in 28 patients after a first non-Q waveinfarct, though subsequent coronary eventswere not clearly identified. Krone and associ-ates20 reported a favourable outcome in 41patients less than 60 years of age who presentedwith non-Q wave infarction. In that study, thecauses of death were not reported.

In examining the prognosis of dischargedpatients, the majority of published studies haveeither found the long term survival rates to besimilar21 24-26 or worse27 28 for patients with non-Qwave infarction compared with patients with Qwave infarction.

ST-T SHIFT IN NON-Q WAVE MYOCARDIALINFARCTIONOur study extends the findings of these previ-ous reports in defining better the clinical impli-cations and prognosis of patients after a non-Qwave infarction. We considered the ST-T shiftto be a possible prognostic factor for stratifica-tion. There have been few studies of the signifi-cance of ECG findings in non-Q wavemyocardial infarction,'229 and this is importantbecause most myocardial infarctions (withinthe first several hours) begin without Q waves.Hence, we emphasise the distinction of thesetypes of non-Q wave infarction since differenttypes of treatment may be chosen in the initialhours after the onset of an acute myocardialinfarct.

ANGIOGRAPHIC CRITERIA FOR PROGNOSTICEVALUATIONPrevious postinfarction angiographic studieshave shown that patency of the infarct relatedcoronary artery is a frequent finding amongpatients with non-Q wave myocardial infarc-tion,9303' possibly related to spontaneous earlyreperfusion.'4 In the present study, this angio-graphic picture was much more frequent inpatients with ST segment depression (76 9%)than those with T wave inversion (14-6%). It isknown that patients with patent infarct vesselsare subjected to a higher incidence of subse-quent ischaemic cardiac events than those withtotal occlusion of the infarct related artery sincegreater residual myocardium is at risk.89Consequently, a poor outcome is more likely inthe former set of patients.

With respect to left ventricular dysfunction,we found that both the patients with T waveinversion and the patients with ST segmentdepression had similar and normal left ventricu-lar ejection fractions. This is a usual findingamong patients with non-Q wave myocardialinfarction.37

CLINICAL IMPLICATIONSIt is clear that other clinical variables and stan-dard risk factors have an important predictivevalue in risk stratification after myocardialinfarction. Several other studies have identifiedsubgroups of patients with non-Q wavemyocardial infarction with increased case fatalityrates. Scheinman and Abbot* reported highermortality rates for patients with non-Q wave

infarction accompanied by raised cardiacenzyme peaks than for patients with Q waveinfarction and low enzyme release. Rigo andassociates9 found a significantly higher inci-dence of abnormal QRS complexes in patientswith non-Q wave infarction than in patientswith Q wave infarction. Furthermore, otherstudies2432 33 have reported low survival rates forpatients with non-Q wave infarction compli-cated by an infarct extension during their hospi-tal admission.We believe that one of the mechanisms

accounting for the poor outcome of patientswith ST segment depression is that thesepatients suffered "incomplete infarctions", thatis, they had potentially jeopardised myo-cardium within the perfusion zone of the patentinfarct related vessel. Therefore, they wereexposed to repetitive ischaemic events. Weobserved that patients with ST segment depres-sion had a fivefold higher incidence of cardiacevents during the total follow up period com-pared with patients with T wave inversion.However, it must be pointed out that the needfor coronary angioplasty or bypass surgerycould have been influenced by subjective criteriaas well as by the angiographic findings. Anotherpossible mechanism is the existence of impairedor threatened collateral circulation34; unfortu-nately, the functional significance of collateralvessels in our patients was unclear.

Finally, our interpretation of the dataobtained in this study is that the ST-T shift pre-sent in the diagnostic ECG is capable of outlin-ing two subgroups of patients with non-Q wavemyocardial infarction with distinct outcomesand angiographic characteristics: patients withT wave inversion, who have a favourable out-come, and patients with ST segment depres-sion, who have a poor prognosis, possiblybecause of a higher incidence of residual steno-sis of the infarct related artery. However, persis-tent ST depression was not an independent riskfactor for mortality. Therefore, ST segmentdepression is a potential predictor of adverseshort and long term cardiac events for patientswith non-Q wave myocardial infarction. Thesedata may provide a guide to therapeutic deci-sion making. Nevertheless, the role of throm-bolytic treatment in patients with evolvingmyocardial infarction characterised chiefly byST segment depression remains to be eluci-dated.

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