The current study used the MESA cohort, composed of adults free of clinical cardiovascular disease (including myocardial infarction), to show that ALVSD is uncommon (prevalence of 1.7%) but nonetheless associated with significant morbidity (CHF and cardiovascular events) and mortality. LVMI improved the accuracy of LVEF for identifying individuals at risk for future incident CHF in the whole cohort and also had a good discrimination among individuals with ALVSD for incident CHF during the follow-up period.
The prevalence of ALVSD has been estimated to occur in 0.9 – 12.9% of the population14
. The wide range is due to differences in study design, setting, characteristics of the study sample, and LVEF threshold used to define ALVSD. The LVEF threshold used in previous studies ranged from 30-54 %14
. McDonagh et al defined ALVSD as LVEF < 30% in a cross-sectional survey of a selected urban cohort; in that study, the prevalence of ALVSD was 1.5% 13
. Older males were more likely to have ALVSD, and 83% had evidence of ischemic heart disease as the underlying etiology. In another large practice-based multi-ethnic cohort, using an LVEF threshold of 40%, prevalence of ALVSD was 0.89%12
. In a subset of the Strong Heart Study (some of whom had prevalent CHD and clinical CHF), Devereux et al reported that the prevalence of left ventricular dysfunction in Indian Americans, defined as LVEF <54%, was 14% (10). Gottdiener et al, in an elderly cohort (mostly Caucasian) reported a prevalence of ALVSD of about 0.8%22
. In the Framingham Heart Study, Wang et al showed that the prevalence of ALVSD (defined as LVEF <50%) in participants with and without prior MI was 3%14
. These studies are limited by differences in the LVEF threshold, small sample sizes, lack of racial diversity, and the use of echocardiography in estimating LVEF. In addition, almost all included participants with and without prior MI. The present study used a large multi-ethnic cohort and a more accurate measure of LVEF, cardiac MRI. We found that within population based adults free of clinical cardiovascular disease, the prevalence of ALVSD is 1.7% and is mostly in men and African Americans.
There is no consensus on how to best identify individuals with ALVSD in the community, and the best most cost-effective way to do so14
. The use of natruiretic peptides to screen for ALVSD in communities has yielded mixed results23-25
. Despite the relatively rare prevalence of ALVSD, its presence identified a group of participants at high risk for incident CHF, CVD, and all-cause mortality. Our data also suggest that individuals with ALVSD may not be more likely to have incident myocardial infarction, compared to those without ALVSD. Thus, these individuals may evade detection until late in their disease course, increasing the cost of therapy and worsening their prognosis.
African Americans with left ventricular dysfunction appear to be at higher risk for progression of heart failure and death from any cause than similarly treated whites26
. In the present cohort, African American males had the highest mean blood pressure and LVMI, and were more likely to have ALVSD and develop clinical CHF compared with other MESA participants. This suggests that community-wide screening for ALVSD and preemptive interventions in hypertensive African American men could be explored as an appropriate and cost-effective public health strategy to reduce heart failure burden in our communities. Current debate should focus on how best to screen for ALVSD in individuals without clinical CVD, since our data suggest these individuals are at higher risk for CHF, CVD, and all-cause mortality. More research is needed to determine if preemptive interventions might reduce the risk for CHF, CVD, and death in this high risk subgroup.
Unlike echocardiography, cardiac MRI more accurately measures left ventricular volumes, from which LVEF is derived16
. In addition, other variables, such as LVMI, can be measured during the cardiac MRI scan. The present study shows that adding LVMI as part of a cardiac risk assessment would significantly improve the prognostic accuracy of LVEF in predicting incident CHF. Furthermore, in individuals with ALVSD, LVMI would discriminate accurately among those most likely to progress to clinical CHF. Studies in other cohorts are needed to replicate and extend our findings.
The strengths of this study include the large sample size, long duration of follow-up, adjudicated outcomes, use of cardiac MRI, the multi-ethnic nature of the cohort and the fact that unlike other studies, all participants were free of clinical cardiovascular disease at baseline. However, given the relatively small prevalence of ALVSD, we did not explore stratified analysis due to limited statistical power. In addition, MESA is an observational study; although we adjusted for most covariates in our adjusted models, our results may still have been influenced by residual confounding. The cardiac MRI results including left ventricular ejection fraction was made available to participants and their clinicians (if participants consented). MESA does not include other ethnic groups such as American Indians and other Asian groups except Chinese. In addition the proportion of each ethnic group in MESA does not accurately reflect that of the US population. This limits the generalizability of our findings. Presently other cardiac MRI data including left atrial size and structure etc, likely to influence the development of congestive heart failure, cardiovascular events and mortality are not available in MESA. Inclusion of such data and a more comprehensive analysis of the MESA cardiac MRI data may further inform risk prediction of these outcomes in this population. Lastly, because the present study involved individuals without clinical cardiovascular disease at baseline, our results may not be applicable to other populations.