Echocardiographic Prediction of Left Vent~i~uiar Volume After Myocardial Infarction MALCOLM HEATHER Aactbnd.
ABERNETHY. SMITH.
MBCHB.
NORMAN
DMU. GREG GAMBLE.
SHARI%.
MD. FRACP.
FACC,
MS
nRer mycordial infarction would prwlict later loft ventricular dilation. Forty4ght patientswith unrompliratedtransmuralmywardis, infarctionhad echocardiography 5 II 10 daysnflrr m)axxardisl inFaWionand ~fyllment of clinics,variablesincludingpeak orestine kinase and sum of electrowdiagraphic ST segment elrvntion.L% ventriculardimension;were measuredirom the echocardiogram in theparaarnsl YEWandalsoin theapicalfour andtwochamberviewsat the kvctof the mitral lestlee. papillary mu~~lwand apex. A cardiacwslt notian scorewas abtsiwd by sqmentat anslysir aT the apical V,WS. Ech-rdigraphic IdR ventricularvolumewps measuredshrr the apical
L~PHSwith we al a Simapron’r rule method.Initial e,iniQ, a,,., whaeardiographie variat& werecorre,aledwith the Mt rentrieu,ar wtume a, I year. There HBS a &i&ant relation hetwen the initial four ood twu chamberend-diastolic dimemiansand the Id wntricular
apicaltewt ti.ur chamberR’l; 0.66. p = 0.&4Bt.tso chamber R’ = 0.61. p = O.Wtt,l. Other clinicalrariabb. pansternalletI ventriculardimendoasand cardiac~a,, motionMT~ were rot rigniticantl~relatedto ,eR ventricukwwbme. A pawerR!,three wiable mode,obtnillPdby multipleqresSw and includingthe inttiat tw chamberapicaldimension.cardiacsat, motionwore and bodysurfatpa~1 accounted lor 82% otthe variationin ,eR
I )ewfrom
After transmural myocardial infarction. early iofarcr e~~ansion and regional dilation may be followed by progresrive global ventricular dilation and dysfunrtn 1-S). Left yenwicular volume is the strongestpredictor of survival after myocardial infarclion. more powerful than the extent of coronary aneiy disease 16.71. Experimental animal and clinical studieshave show that ilnpiotenSin.cvnverIinaenzyme inhibition can modify ventricular dilation after myocardial infarction (8.9). Rarher than Irea all patients in thas fashion, it might he possible to wxat patent\ velecuvely if those most likely to develop lefr ven~ncular dilation after myocardial infarction could be identified. Left ventricular volume is not easily measured. requinng time-consuming laboratory techniques for accurate a~essment. The aim uf this study was to determine which practxal clinical or echocardiographic criteria would predict left ventricular dilation during the year oiler rransmur;ll myocardial mfarclion.
t
Methods Patient utwlmn. ConsiderLd for thi\ stud, were patients ;4mslcd IO the Auckland coronary care units with detinile tnmmuml myucardial infarction who had not received rhmmbolytic treatment. Patients who were clinically stable wthoul evidence al myocardial ircheniv or requirement for trcalment for arrhythrnna or heart failure undenvent echacardiognphy 5 to IO day\ after myocardial infarction. Those with adequate image quabty and cchocardiogmphic left ventricula ejection faction , >,
A more powerfoul lhrrc variable model predicting 82% of the wn.moo in left ventricular end-diastolic volume at (R’ = 0.82. p i 0.01) and in&ding the apical diastolic dimcnwn from the two chamber view (?A-EDD). the cardnc wall motion score (WMS) and body sulfate orea (BSAI ulil*:
I year
LYEDV
- 3 7 l?A-EDD,\,
,, ,J
8.8 Icardiac WMS,,,
,,J
4612 ms.4,,,,,J- Y&L l”, Baseline ventricolar volume was strongly predictive of volume, a, I vea, (RI = 0.85. p < 0.01,. A single variable model predict& 85% of the variation in end-diastolic vol. ume \,‘.I>
Discussion Echoeardiogrsphic prediction of ventricular volume 1 year after myorardiat infarction. This study has shown that simple linear echocardiographic measurements week after myocardial infarction correlate wth lefr venlricular enddiastolic volume at I year. The apical diastolic dimensions yield the \troqest correlalions of the single baseline variables with left ventricular end-diastolic volume. Furthermore. mulllple regression has prodw J a powerful three variable model predicling 82X of the variaion in left ventricular end-diastolic volomc at I year. This model used the two chamber apical diastolic dimension that, like Ihe other dimensions. can be dotined readily by m aimizing the endocardial echocardiogram and freezing the image in diaslole. Although the simple cardiac wall motion score obtained corrclatcd poorly by i&elf wilh lefl venlricular volume because of intercorrelation wilh the other two variables. it provided imponant additional information for the model. 11 is not unusual to encoonter a variahk that individually has poor correlation but has a synergistic effect with other variables because information from this variable may be unique and directly additive to the model. This ha5 been recognized by previous studies 11.13) that have shown that cardiac wall motion is an imponant predictor of left vc~~~r&dx volume alad prognosis after myocardial infarction. More sophisticated asseaament of wall motion might have yielded a better correlation with left ventricular volume. but our aim was to assess a simple method that coulo be easily applied. The contribution of body surface area in our model is unlikely 10 be a type I error because body surface area consistently appeared in mw of the multivariable models and was an importam indcpendeot variable. Although a so& estimated value for peak creatine kinase did not correlate with left ventricular volume. more
I
frequent crcatine kinase measurements and integration of the creatine kinale time curve as an estimate of infarct size might have correlated better. Similarly, multiple precordial ST segmem mapping (14) would have provided more exact ECC asseswwd of infarct size than was provided by a single I2 lead ECG. Pathagenosis of left ventricular dilation after myoeardtul infarction. Left ventricular dilation after myochrdial infarction signifies a poor prognosis. Early dilation within the 1st 2 to 3 days after myocardial infarction is attributed to infarct scgmem expansion 13) lhat begins within minutes of the onset of ischemia (4). This may be a consequence of reduced systolic ejection and increased left ventricular end-diastolic volume and pressure. causing increased wall stress (51. Increased wall stress causes myotibril stretching and thinning and compression of the inlercellular space resulting in infarct exoansion (15) and it is irreversible at 3 h (41. This early in& expansion may increase the length of the inimct ~eement bv as much as 65% (2). The result of earlv infarct expansion is an increased left v&tricolar volume that allows cardiac output to be maintained at a lower left ventricular tilling prcsswc (5). Patients who do not develop early infarct expansion are unlikely to develop left ventricular dilation subsequently and in some cases the infarct segment may shrink as .hcaling occon 13). Conversely, patients with early infarct segment expansion commonly develop later global venlricular dilation over subsequent months (2). Latr left ventricular dilation occurs in both the infarcted and noninfarcted segments 12). lo response to left ventricular dilation and incrcaed wall stress. compensatory hypertw phy may follow in the noninfarcted segment (5). Thus. ventricular dilation ailer myocardial infarction is due to early stretching of the infarct segment and later generalized ventricular enlargement. Although this adaptation allows initial maintenance of cardiac output, the increase in muscle mass and wall tension promores further hytxrtrophy and eventual myocardial failure 116). In this study much of the early infarct segment expansion md regional left ventricular dilation would have occurred by the time of the baseline echofardiogram. However. further significant left ventricular dilation continued over the followine. war. esoeciallv durina thr 1st 3 months (9). This study de&nsl&s that simple fncar crhocardiogmphic measure ment~ are sensitive enough to detect early changes in left veo!i.icular size that correlate with left ventricular volume at 1 year. Prediction of left ventricular volume at I year can be achieved by using a combination of simple measurements obtained early after myocardial infarction. Prognostic importance of lelt ventridar dllatlon. A study (7) of 733 patients after myocardial infarction showed that ejection fraction was the most important indicator of sorviva1 aftcr myocardial infarcrion. f&wed by age and extent of coronary artery disease. In an angiographic study of MIS patients followed up long-term after mywardial infarction, White et al. (6) showed that left ventricular volume was the
most
importam
prognostic
factor
and end-ryunlic
volume
additional prognostic information to the ejeclivn fraclion when the latkr was ~50%. Allhough left ventricular end-syrtohc volume may he mvre impvrlanl prognostically rhan lcrt ventricular enddiastolic volume (61. rhis study found thal prediction of left ventricular end-diastolic volume wa\ mvrc rehable than prediclion of end-systolic volume at year. This difference may have been due in pan to rhc grearer inaccuracy of measuring the smaller linear rys~olic dimension rhan the corresponding diastolic dimension. Echocardmgraphlc methods generally underesrimate left ventricular volume assessed with angiographic methods (17) and the measuremen1 error may be relatively greater wilh the echocsrdiographic systolic dimensions. Limitationsof thestudy. The mam limitation of fhis study relates to patient selection. A relatively small IIzmhcr of padents were included on the basis of rhc prwnc.: of moderate lefl ventricular dysfunction .i to IO days after myocardial infarclion. Patients with mild left vcmncular dysfuncrivn and ejection fraclion >45% were excluded. a, were patients wirh clinical heart failure requiring trcmment. Although study of a larger series vf patients with a broader spectrum of lefr ventricular dy’;funcGvn would ht desirable to confirm our findings. rhls wll he d~ficull rv achieve considering ihe many possible intcrvcntwnr aher myocardial inpwctivn that may modify left venwcular funcrivn. In this rcspec~ h is notable that none of our patients received thrombotytic therapy. which ha? been shown toreduce left ventricular volume (IX). and nvne wre taking medication affecting the prvgrepq oi left ventricular dilation. Even earlier prediction vf left ventricular d&nlun uvuld
provided
I
be preferable
to guide inlervenlion
immcdi~lcly
after the
reperfusion has nm hcen achieved. At present. further smdieb in prvgre I IX ml. with 140 ml
I SD ahox Ihc mean Vi). Wnh USE vi a univariare model from this study [LVEDV = 7.07 (4A-EDD) - 156.21, a terr ucntricular end-dmrolic volume uf I40 ml at I year would be related to an >mn~alfour chamber apical end-diastolic dimen>ion IQ-EDD) * f 47 mm. Thus. if B man asressed week ailer m)ocardlal infarction had a few chamber apical enddiasiulic dimenwn 37mn he would have a 95% chance of having left ventricular sod-diastvlic volume SD above normal 81 I year. If tuch a leti ventneular end-diasrolic
I
I
volume WB prechcled by applicauon of !his univariate modci or oh; three variable model. ~reaunenr :v prevent dilation
ml:ht be conaldered. Conclusions. This preliminary study ha5
ABERNETHY. SMITH.
MBCHB.
NORMAN
DMU. GREG GAMBLE.
SHARI%.
MD. FRACP.
FACC,
MS
nRer mycordial infarction would prwlict later loft ventricular dilation. Forty4ght patientswith unrompliratedtransmuralmywardis, infarctionhad echocardiography 5 II 10 daysnflrr m)axxardisl inFaWionand ~fyllment of clinics,variablesincludingpeak orestine kinase and sum of electrowdiagraphic ST segment elrvntion.L% ventriculardimension;were measuredirom the echocardiogram in theparaarnsl YEWandalsoin theapicalfour andtwochamberviewsat the kvctof the mitral lestlee. papillary mu~~lwand apex. A cardiacwslt notian scorewas abtsiwd by sqmentat anslysir aT the apical V,WS. Ech-rdigraphic IdR ventricularvolumewps measuredshrr the apical
L~PHSwith we al a Simapron’r rule method.Initial e,iniQ, a,,., whaeardiographie variat& werecorre,aledwith the Mt rentrieu,ar wtume a, I year. There HBS a &i&ant relation hetwen the initial four ood twu chamberend-diastolic dimemiansand the Id wntricular
apicaltewt ti.ur chamberR’l; 0.66. p = 0.&4Bt.tso chamber R’ = 0.61. p = O.Wtt,l. Other clinicalrariabb. pansternalletI ventriculardimendoasand cardiac~a,, motionMT~ were rot rigniticantl~relatedto ,eR ventricukwwbme. A pawerR!,three wiable mode,obtnillPdby multipleqresSw and includingthe inttiat tw chamberapicaldimension.cardiacsat, motionwore and bodysurfatpa~1 accounted lor 82% otthe variationin ,eR
I )ewfrom
After transmural myocardial infarction. early iofarcr e~~ansion and regional dilation may be followed by progresrive global ventricular dilation and dysfunrtn 1-S). Left yenwicular volume is the strongestpredictor of survival after myocardial infarclion. more powerful than the extent of coronary aneiy disease 16.71. Experimental animal and clinical studieshave show that ilnpiotenSin.cvnverIinaenzyme inhibition can modify ventricular dilation after myocardial infarction (8.9). Rarher than Irea all patients in thas fashion, it might he possible to wxat patent\ velecuvely if those most likely to develop lefr ven~ncular dilation after myocardial infarction could be identified. Left ventricular volume is not easily measured. requinng time-consuming laboratory techniques for accurate a~essment. The aim uf this study was to determine which practxal clinical or echocardiographic criteria would predict left ventricular dilation during the year oiler rransmur;ll myocardial mfarclion.
t
Methods Patient utwlmn. ConsiderLd for thi\ stud, were patients ;4mslcd IO the Auckland coronary care units with detinile tnmmuml myucardial infarction who had not received rhmmbolytic treatment. Patients who were clinically stable wthoul evidence al myocardial ircheniv or requirement for trcalment for arrhythrnna or heart failure undenvent echacardiognphy 5 to IO day\ after myocardial infarction. Those with adequate image quabty and cchocardiogmphic left ventricula ejection faction , >,
A more powerfoul lhrrc variable model predicting 82% of the wn.moo in left ventricular end-diastolic volume at (R’ = 0.82. p i 0.01) and in&ding the apical diastolic dimcnwn from the two chamber view (?A-EDD). the cardnc wall motion score (WMS) and body sulfate orea (BSAI ulil*:
I year
LYEDV
- 3 7 l?A-EDD,\,
,, ,J
8.8 Icardiac WMS,,,
,,J
4612 ms.4,,,,,J- Y&L l”, Baseline ventricolar volume was strongly predictive of volume, a, I vea, (RI = 0.85. p < 0.01,. A single variable model predict& 85% of the variation in end-diastolic vol. ume \,‘.I>
Discussion Echoeardiogrsphic prediction of ventricular volume 1 year after myorardiat infarction. This study has shown that simple linear echocardiographic measurements week after myocardial infarction correlate wth lefr venlricular enddiastolic volume at I year. The apical diastolic dimensions yield the \troqest correlalions of the single baseline variables with left ventricular end-diastolic volume. Furthermore. mulllple regression has prodw J a powerful three variable model predicling 82X of the variaion in left ventricular end-diastolic volomc at I year. This model used the two chamber apical diastolic dimension that, like Ihe other dimensions. can be dotined readily by m aimizing the endocardial echocardiogram and freezing the image in diaslole. Although the simple cardiac wall motion score obtained corrclatcd poorly by i&elf wilh lefl venlricular volume because of intercorrelation wilh the other two variables. it provided imponant additional information for the model. 11 is not unusual to encoonter a variahk that individually has poor correlation but has a synergistic effect with other variables because information from this variable may be unique and directly additive to the model. This ha5 been recognized by previous studies 11.13) that have shown that cardiac wall motion is an imponant predictor of left vc~~~r&dx volume alad prognosis after myocardial infarction. More sophisticated asseaament of wall motion might have yielded a better correlation with left ventricular volume. but our aim was to assess a simple method that coulo be easily applied. The contribution of body surface area in our model is unlikely 10 be a type I error because body surface area consistently appeared in mw of the multivariable models and was an importam indcpendeot variable. Although a so& estimated value for peak creatine kinase did not correlate with left ventricular volume. more
I
frequent crcatine kinase measurements and integration of the creatine kinale time curve as an estimate of infarct size might have correlated better. Similarly, multiple precordial ST segmem mapping (14) would have provided more exact ECC asseswwd of infarct size than was provided by a single I2 lead ECG. Pathagenosis of left ventricular dilation after myoeardtul infarction. Left ventricular dilation after myochrdial infarction signifies a poor prognosis. Early dilation within the 1st 2 to 3 days after myocardial infarction is attributed to infarct scgmem expansion 13) lhat begins within minutes of the onset of ischemia (4). This may be a consequence of reduced systolic ejection and increased left ventricular end-diastolic volume and pressure. causing increased wall stress (51. Increased wall stress causes myotibril stretching and thinning and compression of the inlercellular space resulting in infarct exoansion (15) and it is irreversible at 3 h (41. This early in& expansion may increase the length of the inimct ~eement bv as much as 65% (2). The result of earlv infarct expansion is an increased left v&tricolar volume that allows cardiac output to be maintained at a lower left ventricular tilling prcsswc (5). Patients who do not develop early infarct expansion are unlikely to develop left ventricular dilation subsequently and in some cases the infarct segment may shrink as .hcaling occon 13). Conversely, patients with early infarct segment expansion commonly develop later global venlricular dilation over subsequent months (2). Latr left ventricular dilation occurs in both the infarcted and noninfarcted segments 12). lo response to left ventricular dilation and incrcaed wall stress. compensatory hypertw phy may follow in the noninfarcted segment (5). Thus. ventricular dilation ailer myocardial infarction is due to early stretching of the infarct segment and later generalized ventricular enlargement. Although this adaptation allows initial maintenance of cardiac output, the increase in muscle mass and wall tension promores further hytxrtrophy and eventual myocardial failure 116). In this study much of the early infarct segment expansion md regional left ventricular dilation would have occurred by the time of the baseline echofardiogram. However. further significant left ventricular dilation continued over the followine. war. esoeciallv durina thr 1st 3 months (9). This study de&nsl&s that simple fncar crhocardiogmphic measure ment~ are sensitive enough to detect early changes in left veo!i.icular size that correlate with left ventricular volume at 1 year. Prediction of left ventricular volume at I year can be achieved by using a combination of simple measurements obtained early after myocardial infarction. Prognostic importance of lelt ventridar dllatlon. A study (7) of 733 patients after myocardial infarction showed that ejection fraction was the most important indicator of sorviva1 aftcr myocardial infarcrion. f&wed by age and extent of coronary artery disease. In an angiographic study of MIS patients followed up long-term after mywardial infarction, White et al. (6) showed that left ventricular volume was the
most
importam
prognostic
factor
and end-ryunlic
volume
additional prognostic information to the ejeclivn fraclion when the latkr was ~50%. Allhough left ventricular end-syrtohc volume may he mvre impvrlanl prognostically rhan lcrt ventricular enddiastolic volume (61. rhis study found thal prediction of left ventricular end-diastolic volume wa\ mvrc rehable than prediclion of end-systolic volume at year. This difference may have been due in pan to rhc grearer inaccuracy of measuring the smaller linear rys~olic dimension rhan the corresponding diastolic dimension. Echocardmgraphlc methods generally underesrimate left ventricular volume assessed with angiographic methods (17) and the measuremen1 error may be relatively greater wilh the echocsrdiographic systolic dimensions. Limitationsof thestudy. The mam limitation of fhis study relates to patient selection. A relatively small IIzmhcr of padents were included on the basis of rhc prwnc.: of moderate lefl ventricular dysfunction .i to IO days after myocardial infarclion. Patients with mild left vcmncular dysfuncrivn and ejection fraclion >45% were excluded. a, were patients wirh clinical heart failure requiring trcmment. Although study of a larger series vf patients with a broader spectrum of lefr ventricular dy’;funcGvn would ht desirable to confirm our findings. rhls wll he d~ficull rv achieve considering ihe many possible intcrvcntwnr aher myocardial inpwctivn that may modify left venwcular funcrivn. In this rcspec~ h is notable that none of our patients received thrombotytic therapy. which ha? been shown toreduce left ventricular volume (IX). and nvne wre taking medication affecting the prvgrepq oi left ventricular dilation. Even earlier prediction vf left ventricular d&nlun uvuld
provided
I
be preferable
to guide inlervenlion
immcdi~lcly
after the
reperfusion has nm hcen achieved. At present. further smdieb in prvgre I IX ml. with 140 ml
I SD ahox Ihc mean Vi). Wnh USE vi a univariare model from this study [LVEDV = 7.07 (4A-EDD) - 156.21, a terr ucntricular end-dmrolic volume uf I40 ml at I year would be related to an >mn~alfour chamber apical end-diastolic dimen>ion IQ-EDD) * f 47 mm. Thus. if B man asressed week ailer m)ocardlal infarction had a few chamber apical enddiasiulic dimenwn 37mn he would have a 95% chance of having left ventricular sod-diastvlic volume SD above normal 81 I year. If tuch a leti ventneular end-diasrolic
I
I
volume WB prechcled by applicauon of !his univariate modci or oh; three variable model. ~reaunenr :v prevent dilation
ml:ht be conaldered. Conclusions. This preliminary study ha5
