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(Circulation. 1997;96:3294-3299.)
© 1997 American Heart Association, Inc.
Articles |
Cardiovascular Death and Left Ventricular Remodeling Two Years After Myocardial Infarction
Baseline Predictors and Impact of Long-term Use of Captopril: Information From the Survival and Ventricular Enlargement (SAVE) Trial
From the Brigham and Women's Hospital, Harvard Medical School, Boston, Mass, and University of Pennsylvania Medical Center (Philadelphia).
Correspondence to M. St. John Sutton, FRCP, Division of Cardiology, Hospital of the University of Pennsylvania, 3400 Spruce St, Philadelphia, PA 19104.
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Abstract |
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Background We quantified cardiovascular death and/or left ventricular (LV) dilatation in patients from the SAVE trial to determine whether dilatation continued beyond 1 year, whether ACE inhibitor therapy attenuated late LV dilatation, and whether any baseline descriptors predicted late dilatation.
Methods and Results Two-dimensional echocardiograms were obtained in 512 patients at 11±3 days and 1 and 2 years postinfarction to assess LV size, percentage of the LV that was akinetic/dyskinetic (%AD), and LV shape index. LV function was assessed by radionuclide ejection fraction. Two hundred sixty-three patients (51.4%) sustained cardiovascular death and/or LV diastolic dilatation; 279 (54.5%) had cardiovascular death and/or systolic dilatation. In 373 patients with serial echocardiograms, LV end-diastolic and end-systolic sizes increased progressively from baseline to 2 years (both P<.01). More patients with LV dilatation had a decrease in ejection fraction: 24.8% versus 6.8% (P<.001) (diastole) and 25.7% versus 5.3% (P<.001) (systole). Captopril attenuated diastolic LV dilatation at 2 years (P=.048), but this effect was carried over from the first year of therapy because changes in LV size with captopril beyond 1 year were similar to those with placebo. Predictors of cardiovascular death and/or dilatation were age (P=.023), prior infarction (P<.001), lower ejection fraction (P<.001), angina (P=.007), heart failure (P=.002), LV size (P<.001), and infarct size (%AD) (P<.001).
Conclusions Cardiovascular death and/or LV dilatation occurred in >50% of patients by 2 years. LV dilatation is progressive, associated with chamber distortion and deteriorating function that is unaffected by captopril beyond 1 year.
Key Words: remodeling • myocardial infarction • trials
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Introduction |
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Left ventricular remodeling after MI can be an insidious process resulting in progressive changes in LV chamber size, shape, muscle mass, and function.1-6 The rise in systolic and diastolic wall stress that accompanies LV dilatation, as well as activation of both circulating neurohormones and local autocrine tropic factors, is believed to be important in sustaining this response.7,8 Progressive LV dilatation post-MI is associated with adverse cardiovascular events9-12 and in particular plays an important role in the development of congestive heart failure.6 Post-MI LV remodeling can be partly attenuated by the early administration of ACE inhibitor therapy,13-20 which is associated with improved survival.18,21-28 However, despite the prognostic importance of LV dilatation after MI, little is known regarding its incidence, for how long after MI this dynamic process continues, or whether long-term use of ACE inhibitor therapy beyond 1 year remains efficacious.
The aims of this study were to quantify the incidence of cardiovascular death and/or LV dilatation in a large population of survivors of acute MI from SAVE18 and to determine the impact of LV dilatation on LV chamber shape and function over a minimum of 2-year follow-up. We assessed whether LV dilatation continued beyond 1 year after MI and, if so, whether this late LV dilatation was attenuated by the continued administration of ACE inhibitor therapy. In addition, we wanted to determine whether any patient demographics or echocardiographic descriptors at baseline predicted increased risk for cardiovascular death and/or progressive LV dilatation.
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Methods |
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The SAVE Trial echocardiographic substudy consisted of 512 patients who sustained an acute MI (301 had Q-wave MI) with residual LV dysfunction (LV ejection fraction <40%) and were randomized to treatment with captopril or placebo for a minimum duration of 2 years and a mean of 3.5 years.18 Of these 512 patients, 103 died during follow-up; 89 were cardiovascular deaths. An additional 62 either missed, refused, or had repeat echocardiograms of insufficient technical quality to permit quantitative analysis. Three hundred seventy-three patients had serial high-quality two-dimensional echocardiograms at baseline (mean, 11±3 days) and 1 year and 2 years after MI.
Transthoracic two-dimensional echocardiograms of the short axis of the LV were recorded from the left parasternal region at three levels: the mitral valve and the high and mid papillary muscle levels. The long axis of the LV was imaged from the apex in the four-chamber view and in either the apical long axis or apical two-chamber views.
All two-dimensional echocardiograms were submitted to the core laboratory at the Brigham and Women's Hospital for assessment of technical quality and suitability for quantitative analysis. The definition of a technically acceptable two-dimensional echocardiogram was one that included images of both the long and short axes of the LV in a minimum of three of the five views. Two-dimensional echocardiographic images were transferred to the hard disk of a Freeland Medical off-line computer analysis system and digitized to obtain LV cavity areas at end diastole and end systole. LV short-axis cavity areas were summed, and the average short-axis areas at end diastole and end systole were calculated. Similarly, LV long-axis cavity areas were summed, and average long-axis areas were calculated at end diastole and at end systole. Thus, LV size was quantified from multiple orthogonal echocardiographic views and defined as the sum of the average short-axis and average long-axis cavity areas at end diastole and end systole as described previously19 at baseline (mean, 11 days after MI) and 1 and 2 years after MI.
MI size was estimated by two-dimensional echocardiography as the percentage of the total LV cavity perimeter that was either akinetic or dyskinetic in each of the multiple echocardiographic images, and the average value for all images (%AD) was calculated, similar to that described angiographically.29
LV shape index, calculated as the ratio of the average LV short-axis cavity area to average long-axis cavity area at end diastole and end systole, was used as a measure of LV distortion (a ratio of unity would represent a sphere).
LV myocardial areas at end diastole and end systole were calculated from the three parasternal LV short-axis echocardiographic images by subtracting the cavity area from the total epicardial area. The ratio of myocardial to cavity area was used as a surrogate for the ratio of LV mass to volume and is an indirect indicator of wall tension.
LV dilatation was defined using the previously reported two-dimensional echocardiographic reproducibility analysis19 as an increase in LV end-diastolic or end-systolic area above baseline values of >1.96 times the SDs of the difference between the three independent assessments of LV size.19 The overall incidence of post-MI LV dilatation and/or death was an objective ascertainment independent of treatment assignment.
The incidences of LV dilatation in patients randomized to treatment with placebo or captopril were compared at 1 and 2 years after MI, and the interval change from 1 to 2 years was calculated in the two-treatment groups to determine whether LV dilatation occurring beyond 1 year was attenuated by the continued long-term therapy with the ACE inhibitor captopril.
In surviving patients, the effect of LV dilatation on LV function was evaluated with radionuclide angiography. Decreased LV function was defined as a reduction in ejection fraction of >9 units from baseline to the repeat study at the end of the trial. The 9-unit decrease in LV ejection fraction was prespecified18 as an important change in radionuclide ejection fraction that was unlikely to be produced by a technical difference but rather result from a biological change.18
To identify potential predictors of death and/or progressive LV dilatation, we assessed the relationships among the clinical demographics, echocardiographic measurements at baseline, and progressive LV dilatation. The clinical demographics examined included age; sex; heart rate; blood pressure; history of hypertension, diabetes, or prior MI; radionuclide ejection fraction; use of thrombolytic agents, aspirin, diuretics, or ß-adrenergic receptor blockers; percutaneous angioplasty, coronary artery bypass graft surgery, heart failure, and angina. Baseline echocardiographic measurements were entered into this analysis individually. These measurements included LV cavity areas at end diastole and end systole, an estimate of %AD, LV cavity shape, and the ratio of LV short-axis myocardial-to-cavity areas.
Statistical Analysis
Changes in echocardiographic measurements
over time were assessed using two-way repeated measures ANOVA, with
time being the "within-subjects" variable. Assessment of the
effect of therapy over time was made by evaluating the interaction term
in the model. Patients were considered to have developed LV dilatation
if they met the criteria previously reported in the SAVE
echocardiographic substudy, which was based on the
reproducibility analysis.19
Cardiovascular cause of death was established in every
case by the mortality committee as described in the parent
trial.18 The analyses for predictors of
dilatation required the creation of a "time to first dilatation"
variable. The event of dilatation and the time of dilatation were
noted for each patient in the cohort. If patients did not develop LV
dilatation, they were censored (ie, removed from the analysis
as a nonevent) at the time of their 2-year echocardiogram. This allowed
a Cox proportional hazard analysis, in which we examined the
relationships with the occurrence of dilatation, with the time of
occurrence being the dependent variable. We were able to examine
the relationship between independent variables and the time to
first dilatation. The P value, relative risk, and confidence
intervals provided for changes in the independent variables are
based on the Cox analysis.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The cumulative incidence of adverse cardiovascular events in this echocardiographic SAVE substudy was similar to that occurring in the parent SAVE trial18: 85 patients had a revascularization procedure after randomization, and 74 patients sustained recurrent MI (48 in the first year, 14 in the second year, and 12 thereafter). Of the 512 patients in the echocardiographic cohort, 103 died, 89 of these patients sustained a cardiovascular death, 182 (35.5%) met the criterion for LV dilatation in diastole, and 204 (39.8%) met the criterion for systolic dilatation at 2 years. The combined end point of cardiovascular death and/or diastolic dilatation was reached in 263 patients (51.4%), whereas 279 patients (54.5%) sustained a cardiovascular death and/or had systolic dilatation.
Of the 373 survivors who had serial echocardiograms at baseline and 1
and 2 years; LV end-diastolic cavity area increased
progressively from a mean value of 69.6±11.7 cm2
at baseline to 72.1±13.3 cm2 at 1 year
(P<.01), and 73.0±14.8 cm2
(P=.02) at 2 years (Fig 1
). LV
end-systolic cavity area increased progressively from a mean of
49.7±11.1 cm2 at baseline to 52.3±14.0
cm2 at 1 year (P<.01) and 53.7±16.2
cm2 (P<.001) at 2 years (Fig 1). The
number of 2-year survivors who developed LV dilatation, defined by the
strict criteria based on the reproducibility analysis, was 113
of 373 (30.3%) at end diastole (P<.01) and 125
of 373 (33.5%) at end systole (P<.01) at 1 year; this
increased further to 132 of 373 (35.4%) at end diastole
(P<.01) and 144 of 373 (38.6%) at end systole
(P<.01) at 2 years, regardless of treatment assignment (Fig 2). The effect of captopril on LV
enlargement in patients at 1 year has been demonstrated in SAVE
patients.19 In this study, we evaluated the
treatment effect of captopril on the number of patients who developed
LV dilatation and on LV dilatation per se beyond 1 year compared with
placebo (Fig 3). At 2 years, captopril
was still efficacious in attenuating LV dilatation in
diastole (P=.048) (Fig 4); however, the attenuation of LV
dilatation beyond 1 year was a "carried over" effect from the first
year of therapy, after which LV sizes at end diastole and
end systole in the captopril increased in parallel with the placebo
treatment group (Fig 4). This was best demonstrated by comparing the
interval changes in LV size at end diastole and at end
systole between 1 and 2 years, which were similar in the captopril
versus the placebo treatment arms in the 373 patients who survived and
had serial echocardiograms (Table 1).
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LV dilatation from baseline through 2-year follow-up was
associated with progressive LV distortion with increase in the LV shape
index toward a more spherical configuration (Table 2, Fig 5).
In patients who met the criteria for LV dilatation, the degree of
distortion to a more spherical ventricle was even greater (Table 2, Fig 5).
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Progressive LV dilatation was also accompanied by deterioration in LV
performance, shown by the greater number of patients who
experienced a 9-unit fall in radionuclide ejection fraction from
baseline to the end of study. Of the 373 2-year survivors, 362 (97%)
had both initial and end-of-study radionuclide ejection fractions
determined, whereas 11 had no end-of-study ejection fraction
determination. Forty-seven of the 362 patients (13%) had a fall in
ejection fraction of >9 units. A significantly greater proportion of
patients who met the criteria for LV dilatation had a 9-unit fall in
ejection fraction: 24.8% with diastolic dilatation versus
6.8% without dilatation (P<.001) and 25.7% with
systolic LV dilatation versus 5.3% without dilatation
(P<.001) by 2 years after MI (Table 3).
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Of the multiple baseline clinical and echocardiographic
demographics assessed in a Cox proportional hazard model, patient age
(P=.023), a history of prior MI (P<.001), lower
radionuclide LV ejection fraction (P<.001), development of
angina (P=.007), baseline heart failure (P=.002),
use of diuretics (P=.018), presence of an S3 gallop
(P=.03), increased heart rate (P=.009), baseline
echocardiographic measures of LV areas at end
diastole (P<.001) and at end systole
(P<.001), and MI size (%AD) (P<.001) all
predicted cardiovascular death and/or LV dilatation
(Table 4). In addition, two-dimensional
echocardiographic estimates of cavity shape index and
muscle-to-cavity area ratio were strongly predictive of
cardiovascular death (P=.003;
P<.001) and development of severe heart failure
(P=.006; P=.002) but did not predict repeat MI
(Table 5).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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LV remodeling after acute MI is stimulated by the interaction of a number of factors such as the magnitude of the loss of contractile elements, the abrupt alteration in systolic and diastolic loading conditions, activation of circulating neurohormones and local autocrine tropic factors, and patency of the infarct-related coronary artery.1-8,11,30-32 In experimental animal models of MI and in increasing numbers of studies of acute MI in humans, LV dilatation has been shown to commence within the first hours of coronary artery occlusion.4-6,13,17,18 LV size early after MI has emerged as a powerful predictor of long-term survival,9,10,19 and the progressive dilatation that continues after the infarct zone has healed histologically is associated with the development of progressive LV dysfunction and congestive heart failure.6 Furthermore, the extent of the increase in LV size after MI relates to mortality and the risk of experiencing a major cardiovascular adverse event.19 This late phase of LV dilatation involves the entire ventricle, has a more protracted time course, and has only been documented in small groups of selected patients followed up for variable lengths of time after MI.6,29
This prospective study of a large cohort of after MI patients with
impaired LV function (ejection fractions <40%) demonstrates that
>50% sustain cardiovascular death and/or develop LV
dilatation during the initial 3.5-year follow-up period. Of the
survivors of acute MI who had serial echocardiograms at baseline and 1
and 2 years; more than one third had developed LV dilatation by 2
years. This latter figure underestimates the true incidence of LV
dilatation after MI because this subanalysis required that all
patients survive 2 years and censored the highest-risk group of
patients who died from a cardiovascular cause within
the 2 years of follow-up (89 patients). Importantly, there was
progressive LV dilatation beyond 1 year with significant increases in
the mean values for diastolic and systolic cavity
areas from baseline to 1 year and from 1 to 2 years, indicating that in
a proportion of patients, LV remodeling continues insidiously. In this
SAVE echocardiographic study population, LV dilatation
after MI correlated with the echocardiographic estimate
of MI size at baseline (%AD) (Table 4
). In addition, increasing LV
size at end diastole and end systole was associated with
increasing distortion of cavity shape and progressive deterioration in
LV performance compared with those who did not develop
ventricular dilatation35 (Tables 2 and 3; Fig 5).
Deterioration in LV function with progressive LV dilatation was
demonstrated by the significantly larger number of patients who
experienced a 9-unit reduction in radionuclide ejection fraction (from
baseline to the end of study), in whom there was a threefold to
fourfold increased risk of death compared with patients who did not
develop LV dilatation. In a previous study, we demonstrated that LV
dilatation is strongly associated with adverse
cardiovascular events at long-term
follow-up.19 Echocardiographic
estimates of baseline LV ratio of short-axis muscle to cavity area and
of shape index used in this study also emerged as powerful predictors
of survival and adverse cardiovascular events (Tables 4 and 5).
Progressive LV dilatation is not a universal finding after MI even in SAVE patients with LV dysfunction and ejection fractions of <40%. Although the precise mechanisms by which LV dilatation is obviated after MI have not been elucidated, it may relate to the combination of a number of factors, including patency of the infarct-related coronary artery,30,31 recovery of stunning, blunting of neurohormonal activation,8 interaction between neurohormones and the fibrinolytic system, initial MI size,4 and adequate LV hypertrophy to normalize wall stress, reduce wall tension, and minimize LV dilatation and distortion.
Post-MI LV remodeling has generally been regarded as a process that is completed over a period of months, as the myocardium remote from the infarct zone dilates and hypertrophies to offset the change in loading conditions induced by the early loss of contractile elements when the repair of the infarct zone is completed histologically. Our study indicates that LV dilatation can continue beyond 1 year, long after the infarct repair is completed; with further increases in end-diastolic and end-systolic chamber sizes occurring in more than one third of survivors by 2 years.
Early LV dilatation after MI can be attenuated by the administration of ACE inhibitors,13-20 and the linkage between attenuation of LV dilatation and reduction in adverse cardiovascular events has been demonstrated.19 Although the effect of ACE inhibitor therapy on attenuating LV dilatation was still present at 2 years compared with placebo; this effect was a "carry over" from the initial year of therapy. Evidence for this was that there were parallel increases in LV end-diastolic and end-systolic sizes beyond 1 year in the captopril and placebo treatment groups such that the interval changes between 1 and 2 years were similar in the two groups. This novel observation suggests that patients appeared to "escape" from ACE inhibitor therapy beyond 1 year in terms of its impact on attenuation of LV dilatation.
Early identification of patients prone to
cardiovascular death and LV dilatation is of paramount
importance to stratify those at high risk in whom prolonged treatment
(up to 1 year) might reduce the likelihood of severe adverse
cardiovascular events. LV end-systolic size and
ejection fraction have been previously shown to be powerful predictors
of survival9,10,19; in the present study, we
demonstrated that echocardiographic estimates of
infarct size, myocardial-to-cavity area ratio, and cavity distortion
(shape index) also correlated strongly with
cardiovascular death and severe congestive heart
failure, although not with repeat MI (Tables 2, 4, and 5). Because
little information is available regarding baseline demographics that
predict cardiovascular death and/or progressive LV
dilatation, we examined a large number of baseline clinical
demographics, LV geometry by transthoracic
echocardiography, and therapeutic interventions
that are all well known to have a direct impact on survival. The
baseline descriptors that predicted cardiovascular
death and/or progressive LV dilatation were patient age, resting
radionuclide ejection fraction, history of prior MI, development of
angina, baseline heart failure (increased resting heart rate, an S3
gallop, use of diuretics), and
echocardiographic measurements of LV cavity areas and
%AD (Table 4).
We conclude from this large cohort of SAVE patients that cardiovascular death and/or LV dilatation occurs in >50% of survivors of acute MI with LV dysfunction in the initial 3.5 years of follow-up. Progressive LV dilatation is associated with distortion of ventricular shape, deterioration in systolic function, and increased risk of adverse cardiovascular events. Late LV dilatation beyond 1 year appears to be refractory to continued treatment with captopril in this study, indicating that patients may escape from the attenuating effect of ACE inhibitor therapy on LV dilatation. Patients with a history of prior MI, low ejection fraction, early heart failure, or older age and those demonstrating continued changes in echocardiographic indices of LV geometry and function identify a particularly high-risk group for progressive dilatation and adverse cardiovascular events.
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Selected Abbreviations and Acronyms |
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Received June 19, 1997; accepted August 2, 1997.
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