Effect of Revascularization on Left
Ventricular Remodeling in Patients With
Heart Failure from Severe Chronic
Ischemic Left Ventricular Dysfunction
Roxy Senior, MD, Avijit Lahiri, MB, MRCP, and Sanjiv Kaul, MD
Few data exist regarding the effect of revascularization
on left ventricular (LV) geometry in patients with severe
LV systolic dysfunction and viable myocardium. We hy-
pothesized that patients with chronic ischemic LV dys-
function but viable myocardium will have improved LV
geometry after revascularization, which in turn will im-
prove long-term outcome. Accordingly, 70 patients with
severe ischemic LV dysfunction (LV ejection fraction
<0.35) were studied at rest. They then either underwent
revascularization (n 36) or were treated medically
(n 34). Fifty-four patients had viable myocardium,
and 16 did not. They were evaluated for change in LV
function and geometry (size and shape) a mean of 21
months later. Further follow-up was performed for a
mean of 3.5 years to determine outcome. Patients with
viable myocardium had improvement not only in re-
gional and global function, but also in LV geometry
(shape and size), which was independent of and in-
cremental to the improvement in function. On long-
term follow-up, change in LV end-systolic volume was
the only multivariate discriminator between 15 pa-
tients who died and 55 who did not, irrespective of
whether they had undergone revascularization. Thus,
measurement of the effect of revascularization of vi-
able myocardium in chronic ischemic heart disease
should not only include improvement in resting re-
gional and global LV function, but also LV geometry.
Improvement in LV geometry contributes to better LV
systolic function, which in turn is the best predictor of
survival after revascularization. 2001 by Excerpta
Medica, Inc.
(Am J Cardiol 2001;88:624 – 629)
T
he beneficial effect of revascularization of dys-
functional myocardium in chronic ischemic heart
disease has traditionally been measured by its effect
on improvement of resting regional and global left
ventricular (LV) function.
1–4
It has been argued, how-
ever, that because the endocardium is responsible for
most of the wall thickening seen at rest, regional
functional recovery may not occur after revasculariza-
tion, even when most of the myocardium excluding
the endocardium is viable.
5
In this situation, benefit
from revascularization may be achieved by restoration
of adequate flow to viable mid- and epimyocardium,
which in turn will prevent infarct expansion and LV
remodeling, and thus prevent heart failure and death.
We recently reported the effect of revascularization
of viable myocardium in a series of prospectively
recruited patients with chronic ischemic heart disease
whose main symptom was congestive heart failure.
6
We recorded a second echocardiogram in these pa-
tients after revascularization to test the hypothesis that
patients with viable myocardium will benefit from
revascularization by favorably altering LV geometry
as well as resting LV function. We further postulated
that patients with improved LV function and geometry
will have a better outcome than those whose LV
function and geometry were unchanged or became
worse. Although several studies have described the
prognostic value of preoperative echocardiography for
predicting survival after revascularization,
6–9
this is
the first attempt to examine the value of both the pre-
and postrevascularization echocardiogram for predict-
ing long-term outcome.
METHODS
Study design: All patients underwent a baseline
clinical assessment, rest echocardiography, low-dose
dobutamine echocardiography, and coronary angiog-
raphy. After these tests, the patients underwent either
revascularization or were treated medically based on
the physician’s preference. The results of the echocar-
diogram were not divulged to the patient’s physician.
At 21 8 months after the initial echocardiogram, a
second echocardiogram was recorded to measure
changes in the left ventricle caused by revasculariza-
tion or the lack thereof. Patients were then followed
for a mean of 3.5 1.8 years to determine outcome.
Patient selection: This is a report of 70 patients from
an original cohort of 87 consecutive patients who have
been previously described.
6
These patients were se-
From the Department of Cardiovascular Medicine, Northwick Park
and St. Mark’s Hospitals and Institute of Medical Research, Harrow,
United Kingdom; and the Cardiovascular Division, University of Vir-
ginia, Charlottesville, Virginia. This study was supported in part by
grants from Northwick Park Hospital Cardiac Research Fund, Harrow,
United Kingdom; Dupont Pharmaceuticals, Wilmington, Delaware;
and the Michael Tabor Grant, Harrow, United Kingdom. Dr. Kaul was
supported by Grant HL-48890 from the National Institutes of Health,
Bethesda, Maryland; an Established Investigator Award from the
American Heart Association, Dallas, Texas; and a travel grant from
Dupont Pharmaceuticals, Wilmington, Delaware. Manuscript received
March 6, 2001; revised manuscript received and accepted May 4,
2001.
Address for reprints: Roxy Senior, MD, Department of Cardiology,
Northwick Park Hospital, Watford Road, Harrow, Middlesex HA1
3UJ, United Kingdom. E-mail: nphcardiology@netscapeonline.co.uk.
624 ©2001 by Excerpta Medica, Inc. All rights reserved. 0002-9149/01/$–see front matter
The American Journal of Cardiology Vol. 88 September 15, 2001 PII S0002-9149(01)01803-3