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 Sao Paulo Medical School, Av. Dr. Eneas de Carvalho Aguiar, 44 05403-900 Sao Paulo, Brazil; 2Federal University of Uberlandia,
Uberlandia, Brazil; 3Institute Dante Pazzanese of Cardiology, Sao Paulo, Brazil; and 4Faculty of Medicine ABC, ABC Foundation, Santo Andre, Brazil

that CAD and LVMi are independent predictors of myocardial ischaemia in patients without myocardial infarction. Other studies demonstrated that LV hypertrophy increases the incidence of perfusion
defects in hypertensive patients without CAD, and that LV remodelling is an independent predictor of abnormal coronary flow reserve in
hypertensive patients.13 15
It is possible that myocardial ischaemia would be found in patients
with LV hypertrophy even in the absence of significant obstruction in
the coronary arteries, for patients presenting this condition have
increased myocardial oxygen demand, increased coronary vascular
and minimal vascular resistance along with decreased myocardial
oxygen supply dependent on coronary blood flow, and decreased
relative myocardial blood flow and coronary flow.16
Interestingly, however, Lima and colleagues confirmed the findings of previous authors that the correlation between CAD severity, perfusion defects, and LVM may be found even in the absence of
myocardial hypertrophy, thus suggesting that this parameter might
be included in the risk stratification of patients with known suspected CAD.1,4,7 This information might, in turn, have an impact
on patient management for both the LVM and the concentric remodelling 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 significant information.
The study by Kishi et al. 1 benefits from having used multislice
computed tomography as a tool to assess LVM and CAD, for this
technique presents high reproducibility, and allows for the quantification of lesion severity and myocardial mass. These characteristics
make 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 coronary
atherosclerosis and myocardial infarction. The multiple features
of this disease state continue to fascinate us while a complete
understanding 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.com
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2014. For permissions please email: journals.permissions@oup.com.

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Lima and colleagues1 describe a parallel independent association

of the presence of coronary artery atherosclerosis, myocardial
infarction, and left ventricular mass (LVM). Previous publications
reporter2 5 similar findings in somewhat different subsets of patients
and they support the potential role of higher LVM as an independent
predictor of adverse events in addition to coronary atherosclerosis
and myocardial ischaemia.
The current paper contributes to an expanding body of evidence
that emphasizes the independent risk associated with the presence
of higher LVM and intriguingly shows a strong relationship in patients
with previous myocardial infarction. They also found that LVM and
concentric remodelling are associated with a greater degree of coronary atheroma burden even in patients without LV hypertrophy that
is also consistent with previously published data.6,7
LVM may also be the consequence of a number of several confounding risk factors such as hypertension, dyslipidaemia, obesity,
smoking status, gender, aging, as well as the presence of previous
myocardial infarction.2,3,8
In this CORE320 substudy, the LVM index (LVMi) was associated
with rest perfusion defects and the total ischaemic score (summed
stress score 1) regardless of cardiovascular risk factors and obstructive coronary artery disease (CAD), but not with the extent
of reversible perfusion defects (summed difference score 1).
Therefore, LVMi was only associated with the overall perfusion
defects (summed stress score 1) when patients had previous
infarcts. The authors theorize that this would be a consequence of
the replacement of myocyte after cell damage or necrosis by fibrosis.
They either ponder that interstitial fibrosis from chronic exposure to
cardiovascular risk such as metabolic syndrome, obesity, hypertension, and diabetes ultimately lead to replacement fibrosis in the
later stages of disease, an consideration also made by previous
authors.7 12
LV hypertrophy might be expected to be found in patients with
previous myocardial infarction for it is an adaptive response during
post-infarction remodelling and attenuates progressive dilatation,
and stabilized contractile function.8 Salcedo et al. 13 demonstrated

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Editorial

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