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European Heart Journal - Cardiovascular Imaging Advance Access published November 7, 2014 EDITORIAL European Heart Journal – Cardiovascular Imaging doi:10.1093/ehjci/jeu221 The association of left ventricular mass with coronary atherosclerosis and myocardial ischemia: cause and effect or simple association? Leonardo Roever1,2*, Ibraim M. Pinto 3, and Antonio Carlos Palandri Chagas 1,4 1 Heart Institute (InCor), HCFMUSP-University of Sa˜o Paulo Medical School, Av. Dr. Ene´as de Carvalho Aguiar
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  EDITORIAL Theassociationofleftventricularmasswithcoronaryatherosclerosisandmyocardialischemia:causeandeffectorsimpleassociation? Leonardo Roever  1,2 * , Ibraim M. Pinto 3 , and Antonio Carlos Palandri Chagas 1,4 1 Heart Institute (InCor), HCFMUSP-University of Sa˜o Paulo Medical School, Av. Dr. Ene´as de Carvalho Aguiar, 44 05403-900 Sa˜o Paulo, Brazil;  2 Federal University of Uberlaˆndia,Uberlaˆndia, Brazil;  3 Institute Dante Pazzanese of Cardiology, Sa˜o Paulo, Brazil; and  4 Faculty of Medicine ABC, ABC Foundation, Santo Andre´, Brazil Lima and colleagues 1 describe a parallel independent associationof the presence of coronary artery atherosclerosis, myocardialinfarction, and left ventricular mass (LVM). Previous publicationsreporter  2 – 5 similarfindingsinsomewhatdifferentsubsetsofpatientsandtheysupportthepotentialroleofhigherLVMasanindependentpredictor of adverse events in addition to coronary atherosclerosisand myocardial ischaemia.The current paper contributes to an expanding body of evidence that emphasizes the independent risk associated with the presenceofhigherLVMandintriguinglyshowsastrongrelationshipinpatientswith previous myocardial infarction. They also found that LVM andconcentric remodelling are associated with a greater degree of cor-onaryatheromaburdeneveninpatientswithoutLVhypertrophythatis also consistent with previously published data. 6,7 LVM may also be the consequence of a number of several con-founding risk factors such as hypertension, dyslipidaemia, obesity,smoking status, gender, aging, as well as the presence of previousmyocardial infarction. 2,3,8 In this CORE320 substudy, the LVM index (LVMi) was associatedwith rest perfusion defects and the total ischaemic score (summedstress score  ≥ 1) regardless of cardiovascular risk factors and ob-structive coronary artery disease (CAD), but not with the extentof reversible perfusion defects (summed difference score  ≥ 1).Therefore, LVMi was only associated with the overall perfusiondefects (summed stress score  ≥ 1) when patients had previousinfarcts. The authors theorize that this would be a consequence of  thereplacementofmyocyteaftercelldamageornecrosisbyfibrosis.Theyeitherponderthatinterstitialfibrosisfromchronicexposuretocardiovascular risk such as metabolic syndrome, obesity, hyperten-sion, and diabetes ultimately lead to replacement fibrosis in thelater stages of disease, an consideration also made by previousauthors. 7 – 12 LV hypertrophy might be expected to be found in patients withprevious myocardial infarction for it is an adaptive response duringpost-infarction remodelling and attenuates progressive dilatation,and stabilized contractile function. 8 Salcedo  et al. 13 demonstrated thatCADandLVMiareindependentpredictorsofmyocardialischae-mia inpatients withoutmyocardial infarction. Otherstudiesdemon-strated that LV hypertrophy increases the incidence of perfusiondefectsinhypertensivepatientswithoutCAD,andthatLVremodel-lingisanindependentpredictorofabnormalcoronaryflowreserveinhypertensive patients. 13 – 15 ItispossiblethatmyocardialischaemiawouldbefoundinpatientswithLVhypertrophyevenintheabsenceofsignificantobstructionin the coronary arteries, for patients presenting this condition haveincreased myocardial oxygen demand, increased coronary vascular and minimal vascular resistance along with decreased myocardialoxygen supply dependent on coronary blood flow, and decreasedrelative myocardial blood flow and coronary flow. 16 Interestingly, however, Lima and colleagues confirmed the find-ings of previous authors that the correlation between CAD sever-ity,perfusiondefects,andLVMmaybefoundevenintheabsenceof myocardial hypertrophy, thus suggesting that this parameter mightbe included in the risk stratification of patients with known sus-pected CAD. 1,4,7 This information might, in turn, have an impacton patient management for both the LVM and the concentric re-modelling may respond well to proper treatment. 7 Therefore, even though the proper link between CAD severity, perfusion defects,and LVM was not fully clarified, the authors provide clinically signifi-cant information.The study by Kishi  et al. 1 benefits from having used multislicecomputed tomography as a tool to assess LVM and CAD, for this techniquepresentshighreproducibility,andallowsforthequantifica- tion of lesion severity and myocardial mass. These characteristicsmake the contribution of their findings even stronger and, for the time being, allow us to consider that the authors add another piece to the growing puzzle of the impact of LVM tissue on coronaryatherosclerosis and myocardial infarction. The multiple featuresof this disease state continue to fascinate us while a completeunderstanding of its pathogenesis still continues to elude us. Conflict of interest:  none declared. The opinions expressed in this article are not necessarily those of the Editors of   EHJCI , the European Heart Rhythm Association or the European Society of Cardiology. * Corresponding author. Tel: + 55 11 30695259; Fax: + 55 11 30695261, Email: leonardroever@hotmail.comPublished on behalf of the European Society of Cardiology. All rights reserved. & The Author 2014. For permissions please email: journals.permissions@oup.com. European Heart Journal – Cardiovascular Imagingdoi:10.1093/ehjci/jeu221   European Heart Journal - Cardiovascular Imaging Advance Access published November 7, 2014  b  y  g u e s  t   onN  ov  em b  er 7  ,2  0 1 4 D  ownl   o a d  e d f  r  om   References 1. KishiS,MagalhaesTA,GeorgeRT,DeweyM,LahamRJ,NiinumaH etal. Relationshipof left ventricular mass to coronary atherosclerosis and myocardial ischemia: TheCORE320 Multicenter Study.  Eur Heart J Cardiovasc Imaging   2014.2. LangRM,BierigM,DevereuxRB,FlachskampfFA,FosterE,PellikkaPA etal. Recom-mendations for chamber quantification: a report from the American Society of Echocardiography’sGuidelines andStandards Committee andthe Chamber Quan- tification Writing Group, developed in conjunction with the European AssociationofEchocardiography,abranchoftheEuropeanSocietyofCardiology.  JAmSocEcho-cardiogr   2005; 18 :1440–63.3. LevyD,GarrisonRJ,SavageDD,KannelWB,CastelliWP.Leftventricularmassandincidence of coronary heart disease in an elderly cohort. The Framingham HeartStudy.  Ann Intern Med   1989; 110 :101–7.4. BluemkeDA,KronmalRA,LimaJAC,LiuK,OlsonJ,BurkeGL et al. Therelationshipof left ventricular mass and geometry to incident cardiovascular events: the MESAStudy.  J Am Coll Cardiol  2008; 52 :2148–55.5. Ghali JK, Liao YL, Cooper RS. Influence of left ventricular geometric patterns onprognosis in patients with or without coronary artery disease.  J Am Coll Cardiol 1998; 31 :1635–40.6. Cooper RS, Simmons BE, Castaner A, Santhanam V, Ghali J, Mar M. Left ventricular hypertrophy is associated with worse survival independent of ventricular functionand number of coronary arteries severely narrowed.  Am J Cardiol  1990; 65 :441–5.7. TruongQA, ToepkerM, Mahabadi AA,Bamberg F,RogersIS,BlanksteinR  et al. Re-lation of left ventricular mass and concentric remodeling to extent of coronaryartery disease by computed tomography in patients without left ventricular hyper- trophy: ROMICAT study.  J Hypertens  2009; 27 :2472–82.8. Lin FY, Nicolo D, Devereux RB, Labounty TM, Dunning A, Gomez M  et al.  Nonob-structivecoronaryarterydiseaseasdetectedby64-detectorrowcardiaccomputed tomographic angiography is associated with increased left ventricular mass.  J Cardi-ovasc Comput Tomogr   2011; 5 :158–64.9. LiebW,XanthakisV,SullivanLM,AragamJ,PencinaMJ,LarsonMG etal. Longitudinal trackingofleftventricularmassovertheadultlifecourse:clinicalcorrelatesofshort-and longterm change in the Framingham offspring study.  Circulation  2009; 119 :3085–92.10. Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction:pathophysiology and therapy.  Circulation  2000; 101 :2981–8.11. Mewton N, Liu CY, Croisille P, Bluemke D, Lima JA. Assessment of myocar-dial fibrosis with cardiovascular magnetic resonance.  J Am Coll Cardiol  2011; 57 :891–903.12. WeberKT,BrillaCG.Pathologicalhypertrophyandcardiacinterstitium:fibrosisandrenin-angiotensin-aldosterone system.  Circulation  1991; 83 :1849–65.13. SalcedoEE,MarwickTH,KorzickDH,GoormasticM,GoRT.Leftventricularhyper- trophysensitizesthemyocardiumtothedevelopmentofischaemia. EurHeartJ 1990; 11 (Suppl G):72–8.14. Houghton JL, Frank MJ, Carr AA, von Dohlen TW, Prisant LM. Relation amongimpairedcoronaryflowreserve,leftventricularhypertrophyandthalliumperfusiondefects in hypertensive patients without obstructive coronary artery disease.  J AmColl Cardiol  1990; 15 :43–51.15. Pringle SD, Dunn FG, Tweddel AC, Martin W, Macfarlane PW, McKillop JW  et al. Symptomaticandsilentmyocardialischaemiainhypertensivepatientswithleftven- tricular hypertrophy.  Br Heart J  1992; 67 :377–82.16. Scha¨fer S, Kelm M, Mingers S, Strauer BE. Left ventricular remodelingimpairs coronary flow reserve in hypertensive patients.  J Hypertens  2002; 20 :1431–7.17. Camici PG, Olivotto I, Rimoldi OE. The coronary circulation and blood flow in leftventricular hypertrophy.  J Mol Cell Cardiol  2012; 52 :857–64. Editorial Page 2 of 2  b  y  g u e s  t   onN  ov  em b  er 7  ,2  0 1 4 D  ownl   o a d  e d f  r  om 

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