jurnal metoprolol 1

7222019 Jurnal Metoprolol 1

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Open Access Research Journal Medical and Health Science Journal MHSJ

wwwacademicpublishingplatformscom ISSN 1804-1884 (Print) 1805-5014 (Online) Volume 7 2011 pp 119-124

- 119 - copy 2011 Prague Development Center

THE EFFECT OF BETA-BLOCKERS METOPROLOL AND ATENOLOL ON LEFT

VENTRICULAR EARLY REMODELING IN PATIENTS WITH ST SEGMENT

ELEVATION ACUTE CORONARY SYNDROME

Effect of metoprolol and atenolol on early remodeling of the left ventricle in patients with acute coronary syndrome with STsegment elevation The purpose of the work was to study theeffect of cardio selective beta-blockers on the overall and regionalcontractility of the left ventricle in patients with acute coronarysyndrome with ST segment elevation Seventy patients aged 38-65years were observed The conventional treatment includedanticoagulants antiagregants statins beta-blockers nitrates ACEinhibitors The patients were randomly divided into 2 groups 35each on atenolol and metoprolol therapies respectively

Echocardiography was performed on the first day afterrevascularization with assessment of cardiac volumes andhemodynamic indices After stabilization of the patients a stress-echocardiography with dobutamine was performed Disorders oflocal contractility were differentiated by 4 grade scalehyperkinesis - 0 normokinesis - 1 hypokinesis - 2 akinesis - 3dyskinesis - 4 Early use of metoprolol or atenolol beta-blockersallowed the decrease of reperfusion impairment of themyocardium and prevented left ventricle remodeling due topreservation of viable myocardial zones Metoprolol assuperior to atenolol in preventing left ventricle remodeling

K HASAN M AMATKULOV

ANIS ALAVI

M UZAFFAR U SAROV

Tashkent Medical AcademyRepublican Scientific Centre of

Emergency Medicine Uzbekistan

Keywords Acute coronary syndrome metoprolol atenolol left ventricular remodeling dobutamine

UDC 616127-0058

Introduction

Wide use of beta-adrenoceptor blockers in clinical practice started after (Prichard et al1964) publication devoted to рropranolol use in treatment of patients with arterialhypertension Further this group preparation was used in chronical ischemic disease acutemyocardial infarction (AMI) and heart failure (Smart et al 1993) The increase ofcirculating catecholamine concentration and product of their partial oxidation in AMIappearing in mental pain stress due to myocardial ischemia takes additional damage tocardiomyocites resulting in amplification of electronic myocardium instability spreading

of necrosis and impairment of disease prognosis This is a theoretical justification of earlyuse of beta-adrenoceptor blockers for AMI (Zaret et al 1993 Horak et al 1983) Thefindings of different international multi-centered follow-ups (MIAMI ISIS-1 ISIS-4

TIMI-II ВНАТ) are evidence of high efficiency of beta-adrenoceptor blockers in AMIthis group preparation is able to limit zone of myocardium damage not only in theexperimental models but in clinical practice as well (Horak et al 1983) Lethality decreasehas been registered in one of the recent studies using beta-adrenoceptor blockers inpatients with AMI (CAPRICORN) (Darcie 2001) Despite advances in reperfusiontherapy for AMI a significant proportion of patients still develop recurrent ischemiareinfarction and malignant ventricular arrhythmias andor they die Whether prophylacticbeta-adrenergic blocker therapy before reperfusion improves survival is undetermined

Historically several studies demonstrated

reduced mortality in patients treated withintravenous beta-blockers in AMI without reperfusion therapy (Roberts et al 1991)Conversely trials of intravenous beta-blockers in patients treated with thrombolytictherapy while demonstrating reductions in recurrent ischemia have reported either no



983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081


survival benefit (Freemantle et al 1999 Pfisterer et al 1998) or increased mortality(Harjai et al 2003) A recent report from the Primary Angioplasty in MyocardialInfarction (PAMI) trials found intravenous beta-blocker administration beforepercutaneous coronary intervention (PCI) to be associated with improved in-hospitalsurvival and reductions in procedural complications including serious arrhythmias and theneed for intra-aortic balloon counterpulsation (Smart et al 1993 Pfisterer et al 1998Grines et al 1991) The aim of the present study was to study the effect of cardioselective

beta-adrenoceptor blockers of metoprolol and atenolol on global and regional myocardialcontractility of left ventricle (LV) for patients with STEACS

Methods

70 patients with ST elevation acute coronary syndrome (STEACS) between 38 to 65 yearsold were examined admitted in cardio-resuscitation department of Republic ScientificCentre of Emergency Medicine at first 6 hours since the occurrence of MI clinicalsymptoms

In all cases elevation of ST segment in the leads I AVL V1-V6 from 2 to 12 mm of

isoline was followed Standard therapy included anticoagulants antiaggregants statinsbeta-adrenoceptor blockers nitrates ACE inhibitors Patients were randomized into twogroups (35 patients in each one) I group of patients received atenolol (50-100 mg) and inII group of patients - metoprolol (50-100 mg) Myocardium revascularization byimmediate PCI was made successfully in all patients Time a door-balloon has averaged88plusmn76 minutes

Echocardiography (EchoCG) with definition of end diastolic and end systolic sizes and volumes ( LV EDS LV EDV LV ESS and LV ESV) LV ejection fraction (EF) LVfraction of shortening (FS) systolic thickening of interventricular septum (TIVS) andsystolic thickening of posterior wall LV was made after PCI

Dobutamine Stress EchoCG (DSE) was carried out after stabilization of condition on 8-

10 day there determined increase of LV wall systolic thickening in zones of dissynergy oflow-dosed (5-10 mkgkgmin) or increase of systolic thickening rise with its followingdecrease andor appearance of new disorders of regional contractility in high doses(more25 mkgkgmin) Dobutamine individual doses were calculated considering body mass ofa patient submaximal heart rate (HR) Criteria of test stopping were the use of maximalpossible dose of dobutamine getting of submaximal HR angina pectoris progressingischemic (more than 1 mm) decrease or ST segment elevation on ECG andorappearance or depression of dissynergy on EchoCG systolic BP rise (SBP) more than 200mm Hg or SBP fall more than 20 mm Hg from initial pressure high-grade arrhythmia(frequent ventricular premature beats ventricular and supraventricular paroxysmaltachycardia) Impairments of LV local myocardium contractility in 16 segments before

and within test process were differentiated by 4-ball scale hyperkinesis - 0 normokinesis- 1 hypokinesis - 2 akinesis - 3 diskinesis - 4 (Belenkov et al 1997) Wall motion scoreindex (WMSI) was considered as ratio of analyzed segments score to their total amountCriteria of myocardium vitality (reversible dysfunction) by stress-EchoCG data wereappearance of two-phase response of myocardium contractility in the zone of formingscar (the increase of its contractility on 1 ball and more and augmentation of systolicthickening more than 3 mm in low doses of dobutamine with following impairment ofcontractility on high doses) or constant increase of local contractility at the same placeover all pharmacological test time

Statistics

Statistical data manipulation were made using STATISTICA 50 (StatSoft) programme There calculated mean values standards errors and confidence 95 interval Hypothesisof equality of mean values was assessed by Student t- criterion Statistical differences of



983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081


sample selection were established at рlt005

Results

EchoCG data at rest after reperfusion therapy in both groups it was been registeredmoderate augmentation of LV lined sizes (Table 1) No significant differences between

groups by TIVS index was revealed though it was lowered in all patients According toEchoCG initial data no valuable differences were found LV EF in Ist group of patients was 430plusmn18 in II-nd group of patients - 422plusmn20

TABLE 1 OUTCOMES OF ECHOCG AT REST IN 1 (NUMERAL) AND ON THE 10 (DENOMINATOR) DAYS OF DISEASE

Index Groups

1-st 2-nd

LV ESS cmLV EDS cmLV ESV mlLV EDVmlTIVS TPWLV LV SF LV EF

45plusmn0149plusmn0160plusmn0556plusmn03

955plusmn41694plusmn21 1658plusmn431458plusmn45243plusmn12283plusmn14349plusmn11366plusmn10225plusmn06252plusmn08431plusmn09527plusmn08

43plusmn01^41plusmn01^59plusmn0455plusmn04

901plusmn31^ 589plusmn31^1595plusmn591315plusmn50^255plusmn19^310plusmn13372plusmn15382plusmn15

245plusmn05^275plusmn04422plusmn10552plusmn 10^

Note рlt005 - in comparison with analogical indices on 1st day of revascularization ^- with

indices in Ist group

After revascularization segmental EF was depressed in all patients EF on anterior and

septum segments was lower than on lateral and inferior EF on all walls at apical level waslower on middle and basal LV segmental contractility in II group of patients was higherthan in Ist group of patients Segmental contractile ability of LV was considerably lowerthan in I group Segmental EF was higher in II group of patients IM segmentalcontractility out of zone was depressed (Table 2) particularly in Ist group of patients LVlocal myocardium contractility was studied in 1120 segments of them in 280 (25)normokinesis was determined in 806 (72) - hypokinesis in 34 (30) - akinesis WMSImakes up 22plusmn0037

Thus moderate dilatation of LV depression of systolic wall thickening short-cuttingfraction and LV EF in patients with STEACS after revascularization was establishedImpairment of LV local contractility takes place not only in zone of myocardium

infarction but also out of itDuring DSE in 38 patients (in 30 from II and in 8 from I groups of patients) wasestablished complete and in 32 (in 27 from I group of patients and in 5 of II one) partialrestoration of all asynergic segments As detected in studying of LV myocardiumfunctional condition to reveal reverse dysfunction hibernation and presence of viablemyocardium in the area of ischemic damage Normokinesis of segment was noted morerarely in I group of patients than in II group of patients Hypo- and akinesis werefollowed more frequently in I group of patients WMSI in I group are authentically higherthan in II group of patients (Table 3)

In low-dosed dobutamine administration for II group of patients TIVS increased in653plusmn37 TPWLV - till 611plusmn38 (Рlt001) SF up to 428plusmn20 (Рlt001) Inotropicstimulation resulted in decrease of ESS in 23 ESV- in 18 (Рlt001) End diastolicindices had no significant changes (Рgt005) LV EF was higher from 422plusmn20 to550plusmn14 (Рlt005) LV segmental EF increased authentically in all sections and moreintensive on posterior and septum segments (Table 2) After treatment normokinesis of



983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081


segments with asynergy was noted There revealed 448 (80) segments with reversedysfunction WMSI decreased in 10plusmn01 (рlt001)

TABLE 2 SEGMENTAL EF () LV IN 1ST AND 2ND GROUP

BASELINE AND DURING DOBUTAMINE TEST

Segments Afterrevascularization Low doses High dosesANTERIOR SEPTAL basic 431plusmn12443plusmn13 622plusmn14642plusmn17 402plusmn23412plusmn20 middle 433plusmn13442plusmn17 692plusmn15703plusmn19 414plusmn18437plusmn19apical 333plusmn18363plusmn17 506plusmn14546plusmn16 383plusmn14407plusmn16ANTERIOR basic 464plusmn09462plusmn17 636plusmn13676plusmn13 450plusmn16470plusmn14 middle 467plusmn11486plusmn15 647plusmn14697plusmn17 482plusmn15489plusmn12apical 350plusmn17420plusmn17 483plusmn11525plusmn10 443plusmn16440plusmn15POSTERIOR SEPTUM basic 437plusmn11468plusmn12 633plusmn15643plusmn15 390plusmn23420plusmn20 middle 438plusmn12498plusmn17 641 plusmn 18691 plusmn 18 443plusmn14443plusmn16 ANTERIOR LATERALbasic 490plusmn09520plusmn11 642plusmn10666plusmn15 483plusmn21483plusmn21 middle 504plusmn11548plusmn17 654plusmn13694plusmn16 534plusmn17544plusmn17 apical 399plusmn18479plusmn17 444plusmn16464plusmn16 396plusmn10420plusmn10 POSTERIORbasic 467plusmn09523plusmn10 608plusmn13651plusmn14 434plusmn18454plusmn18 middle 480plusmn11530plusmn11 634plusmn16694plusmn15 423plusmn16493plusmn16 apical 386plusmn16462plusmn17 535plusmn13565plusmn15 408plusmn19448plusmn19 POSTERIOR LATERALbasic 491plusmn09532plusmn11 655plusmn10675plusmn09 489plusmn21489plusmn21 middle 507plusmn11531plusmn11 643plusmn15693plusmn16 532plusmn17532plusmn17 Note- рlt 001 - in comparison with analogical indices after revascularization

TABLE 3 DISTRIBUTION OF LV SEGMENTS DEPENDING ON TYPES WMA IN PATIENTS

OF IST (NUMERAL) AND IIND (DENOMINATOR) GROUPS

WMA Baseline Low dose DSE High dose DSE

Normokinesis

Hypokinesis

Akinesis

WMSI

57(119)98(204) ^

389 (808)362 (754)

35 (73)20 (42)

195plusmn004187plusmn01

326 (68)480 (100)

154(32)-

--


53(11)120(25) ^

384(80)341 (71)

43(90)19(4) ^

198plusmn0119plusmn004Note рlt005 - in the dependence on analogical indices at rest ^ - with indices in I group of patients

WMSI - wall motion score index WMA - wall motion abnormalities DSE - dobutamine stress echocardiography

TIVS was augmented to 562plusmn60 in patients of I group with partially LV reversedysfunction in dobutamine low doses TPWLV to 575plusmn43 (рlt001) SF to 353plusmn19(рlt001) Inotropic stimulation with dobutamine led to decrease ESS (рlt0001) but ESVin contrast to that in II group was unauthentically decreased End diastolic indices did notchange considerably (рgt005) EF became higher from 430plusmn18 to 501 plusmn16(рlt0001) Degree of changes of LV sizes within maximal contractility improvement ininotropic stimulation was lesser than in II group of patients

In Ist group of patients in dobutamine low doses 180 (396) segments were asynergic iedysfunction was irreversible asynergy It was detected 274 (604) segments with



983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081


reversible dysfunction WMSI was lower up to 132plusmn01 (рlt0001)

There was improvement of systolic indices on 10 day of disease in both groups (Table1) The more authentical improvement of systolic LV function comparing with the sameone after revascularization was observed in patients who received metoprolol Therenoted authentical diminishing of LV EDS and LV ESS on 39 and 67correspondingly authentical elevation of LV EF from 422plusmn20 to 472plusmn10 Thepatients who received atenolol improvement of LV myocardium remodeling indices werenoted as well but authentical changes as in those who received metoprolol were notregistered

Discussion

In the PAMI trials beta-blocker use preceding primary PCI was associated with improvedin-hospital survival (Freemantle et al 1999) Similarly in the present study pre-procedural administration of intravenous beta-blockers was associated with reducedmortality at 30 days a reduction that first became significant during the indexhospitalization By multivariate analysis pre-procedural intravenous beta-blocker use in

patients not previously maintained

on oral beta-blockers was an independent predictor ofsurvival suggesting a possible causative relationship

Thus patients with LV dysfunction conditioned with the presence of macro focalmyocardial changes in anterior septum its viability according to data of low-doseddobutamine test was established This indicates to the effect of enteral using metoprololbefore PCI in infarct related artery

The main findings of the present study are as follows 1) oral administration of beta-blockers in patients with STEACS before primary PCI resulted in improved of left

ventricular systolic function 2) In early administration of beta-adrenoceptor blockers toSTEACS patients who were subjected to myocardial revascularization positive changes ofLV early remodeling had been noted 3) In patients STEACS metoprolol or atenolol

administration provides LV remodeling prevention but first beta-adrenoceptor blockergives more marked effect Owing to impairment of dilatation development LV end-diastolic and end systolic indicesare not changed within 10 days of follow-up time LV EF increases in both groups butits more valuable increase on 10 day after revascularization has been reported in II groupof patients

Possible alternative mechanism might be a reduction in infarct size with beta-blockeradministration Some studies but not all have found that oral or intracoronary beta-blocker use before elective PCI attenuates procedure-related myonecrosis The greaterextent of myocardial recovery occurring in patients pre-treated with intravenous beta-blockers in the present study supports this possibility Less obvious is why such an effect

would be confined to patients not recently exposed to beta-blockers though alterations inmyocardial expression of beta-adrenoreceptors might be a possible explanation

Conclusion

Early administration of metoprolol or atenolol as beta-adrenoceptor blocker allowsreducing of reperfusion myocardium damage in revascularization and due to preservationof myocardium vital zones to prevent LV remodeling In patients STEACS metoprolol oratenolol administration provides LV remodeling prevention but first beta-adrenoceptorblocker gives effect that is more marked



983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081


References

Dargie H 2001 ldquoEffect of carvedilol on outcome after myocardial infarction in patients with left-ventriculardysfunction The Capricorn randomised trialrdquo Lancet Vol 357 pp1385-390

Freemantle N Cleland J Young P Mason J Harrison J 1999 ldquoBeta blockade after myocardialinfarction Systematic review and meta regression analysisrdquo BMJ Vol318 pp1730-737

Grines L Booth C Nissen E Gurley C Bennett A DeMaria N 1991 ldquoAcute effects of parenteral

beta-blockade on regional ventricular function of infarct and noninfarct zones after reperfusion therapy inhumansrdquo J Am Coll Cardiol Vol17 pp1382-387

Harjai J Stone W Boura J et al 2003 ldquoEffects of prior beta-blocker therapy on clinical outcomes afterprimary coronary angioplasty for acute myocardial infarctionrdquo Am J Cardiol Vol91 pp655-60

Hjalmarson A Elmfeldt D Herlitz J et al 1981 ldquoEffect on mortality of metoprolol in acute myocardialinfarction A double-blind randomised trialrdquo Lancet Vol2 pp823-27

Horak A Opie L 1983 ldquoEnergy metabolism of the heart in catecholamine-induced myocardial injuryConcentration-dependent effect of epinephrine on enzyme release mechanical function and ldquooxygen-

wastagerdquo In Chazov E Saks V Rona G (Eds) Advances in Myocardiology Vol4 PlenumPublishing New York pp23-43

Pfisterer M Cox L Granger B et al 1998 ldquoAtenolol use and clinical outcomes after thrombolysis foracute myocardial infarction The GUSTO-I experience global utilization of streptokinase and tpa

(alteplase) for occluded coronary arteriesrdquo J Am Coll Cardiol Vol32 pp634-40

Roberts R Rogers W Mueller S et al 1991 ldquoImmediate versus deferred beta-blockade followingthrombolytic therapy in patients with acute myocardial infarction Results of the thrombolysis inmyocardial infarction (TIMI) II-b studyrdquo Circulation Vol83 pp422-37

Smart S Sawada S Ryan T et al 1993 ldquoLow-dose dobutamine echocardiography detects reversibledysfunction after thrombolytic therapy of acute myocardial infarctionrdquo Circulation Vol88 pp405-15

Zaret B Wackers F Terrin M et al 1995 ldquoValue of radionuclide rest and exercise left ventricular ejectionfraction in assessing survival of patients after thrombolytic therapy for acute myocardial infarction Resultsof Thromobolysis in Myocardial Infarction (TIMI) phase II studyrdquo J Am Coll Cardiol Vol26 pp73-79



983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081


survival benefit (Freemantle et al 1999 Pfisterer et al 1998) or increased mortality(Harjai et al 2003) A recent report from the Primary Angioplasty in MyocardialInfarction (PAMI) trials found intravenous beta-blocker administration beforepercutaneous coronary intervention (PCI) to be associated with improved in-hospitalsurvival and reductions in procedural complications including serious arrhythmias and theneed for intra-aortic balloon counterpulsation (Smart et al 1993 Pfisterer et al 1998Grines et al 1991) The aim of the present study was to study the effect of cardioselective

beta-adrenoceptor blockers of metoprolol and atenolol on global and regional myocardialcontractility of left ventricle (LV) for patients with STEACS

Methods

70 patients with ST elevation acute coronary syndrome (STEACS) between 38 to 65 yearsold were examined admitted in cardio-resuscitation department of Republic ScientificCentre of Emergency Medicine at first 6 hours since the occurrence of MI clinicalsymptoms

In all cases elevation of ST segment in the leads I AVL V1-V6 from 2 to 12 mm of

isoline was followed Standard therapy included anticoagulants antiaggregants statinsbeta-adrenoceptor blockers nitrates ACE inhibitors Patients were randomized into twogroups (35 patients in each one) I group of patients received atenolol (50-100 mg) and inII group of patients - metoprolol (50-100 mg) Myocardium revascularization byimmediate PCI was made successfully in all patients Time a door-balloon has averaged88plusmn76 minutes

Echocardiography (EchoCG) with definition of end diastolic and end systolic sizes and volumes ( LV EDS LV EDV LV ESS and LV ESV) LV ejection fraction (EF) LVfraction of shortening (FS) systolic thickening of interventricular septum (TIVS) andsystolic thickening of posterior wall LV was made after PCI

Dobutamine Stress EchoCG (DSE) was carried out after stabilization of condition on 8-

10 day there determined increase of LV wall systolic thickening in zones of dissynergy oflow-dosed (5-10 mkgkgmin) or increase of systolic thickening rise with its followingdecrease andor appearance of new disorders of regional contractility in high doses(more25 mkgkgmin) Dobutamine individual doses were calculated considering body mass ofa patient submaximal heart rate (HR) Criteria of test stopping were the use of maximalpossible dose of dobutamine getting of submaximal HR angina pectoris progressingischemic (more than 1 mm) decrease or ST segment elevation on ECG andorappearance or depression of dissynergy on EchoCG systolic BP rise (SBP) more than 200mm Hg or SBP fall more than 20 mm Hg from initial pressure high-grade arrhythmia(frequent ventricular premature beats ventricular and supraventricular paroxysmaltachycardia) Impairments of LV local myocardium contractility in 16 segments before

and within test process were differentiated by 4-ball scale hyperkinesis - 0 normokinesis- 1 hypokinesis - 2 akinesis - 3 diskinesis - 4 (Belenkov et al 1997) Wall motion scoreindex (WMSI) was considered as ratio of analyzed segments score to their total amountCriteria of myocardium vitality (reversible dysfunction) by stress-EchoCG data wereappearance of two-phase response of myocardium contractility in the zone of formingscar (the increase of its contractility on 1 ball and more and augmentation of systolicthickening more than 3 mm in low doses of dobutamine with following impairment ofcontractility on high doses) or constant increase of local contractility at the same placeover all pharmacological test time

Statistics

Statistical data manipulation were made using STATISTICA 50 (StatSoft) programme There calculated mean values standards errors and confidence 95 interval Hypothesisof equality of mean values was assessed by Student t- criterion Statistical differences of



983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081



Results




Index Groups

1-st 2-nd
















983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081









Normokinesis

Hypokinesis

Akinesis

WMSI

57(119)98(204) ^

389 (808)362 (754)

35 (73)20 (42)


326 (68)480 (100)

154(32)-

--


53(11)120(25) ^

384(80)341 (71)

43(90)19(4) ^







983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081




Discussion










Conclusion




983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081


References
















983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081



Results




Index Groups

1-st 2-nd
















983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081









Normokinesis

Hypokinesis

Akinesis

WMSI

57(119)98(204) ^

389 (808)362 (754)

35 (73)20 (42)


326 (68)480 (100)

154(32)-

--


53(11)120(25) ^

384(80)341 (71)

43(90)19(4) ^







983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081




Discussion










Conclusion




983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081


References
















983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081









Normokinesis

Hypokinesis

Akinesis

WMSI

57(119)98(204) ^

389 (808)362 (754)

35 (73)20 (42)


326 (68)480 (100)

154(32)-

--


53(11)120(25) ^

384(80)341 (71)

43(90)19(4) ^







983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081




Discussion










Conclusion




983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081


References
















983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081




Discussion










Conclusion




983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081


References
















983117983141983140983145983139983137983148 983137983150983140 983112983141983137983148983156983144 983123983139983145983141983150983139983141 983114983151983157983154983150983137983148 983087 983117983112983123983114 983087 983113983123983123983118983098 983089983096983088983092983085983089983096983096983092 983080983120983154983145983150983156983081 983089983096983088983093983085983093983088983089983092 983080983119983150983148983145983150983141983081


References














jurnal metoprolol 1

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