In this population‐based sample of older adults, diastolic dysfunction was common and increased in frequency with age. In contrast to the female preponderance documented in studies of heart failure with normal EF,7
we found that diastolic dysfunction was equally common in men and women. Co‐morbid cardiovascular conditions such as hypertension, ischaemic heart disease, diabetes, obesity and systolic dysfunction were predictors of diastolic dysfunction, independent of age and sex. Advanced (moderate or severe) diastolic dysfunction rarely equated to “diastolic” heart failure. Indeed, 76% of patients with advanced diastolic dysfunction did not have overt symptoms or a history of CHF. We observed that advanced DD‐NEF was as common as systolic dysfunction (EF
50%) and more likely to be present in the preclinical phase of disease. Despite the frequent absence of symptoms, subjects with advanced DD‐NEF had evidence of structural remodelling, including increased left atrial size and LV mass, and raised N‐BNP concentrations compared with subjects with normal or mildly impaired diastolic function. Furthermore, DD‐NEF was independently associated with a reduction in general health status.
Several factors enhance the validity of results from this study compared with previously published surveys. Our estimates of systolic and diastolic dysfunction are less likely to be affected by selection bias arising from a low participation rate5
or misclassification error resulting from the failure to use comprehensive Doppler methods to distinguish subjects with normal diastolic function from those with moderate diastolic dysfunction.6
Nonetheless, the consistency in prevalence and clinical predictors of diastolic dysfunction between our study and the only other study that employed detailed Doppler methods of estimating LV filling pressure5
provides reassurance as to the generalisability of our findings.
This study extends previously published observations on the relationship between DD‐NEF and CHF status.5
In addition to surveillance of medical records, the incorporation of a clinical examination to detect symptoms and signs of CHF has provided a more robust classification of clinical status of subjects with DD‐NEF. By using an array of clinical scores that offer varying degrees of sensitivity and specificity, we have confirmed the existence of a preclinical phase of advanced diastolic dysfunction that is detectable by comprehensive Doppler echocardiography. Indeed, the prevalence of preclinical advanced DD‐NEF is 10‐fold greater than that of advanced systolic dysfunction. There is scant evidence regarding the prognostic significance of preclinical diastolic dysfunction. Despite their lack of symptoms, subjects with preclinical advanced DD‐NEF have biochemical and morphological evidence supporting the presence of current and chronic rise of LV filling pressures as assessed by N‐BNP concentration and left atrial size, respectively. Further, as left atrial size has been shown to be an independent risk marker for the development of atrial fibrillation,19,20
and cardiovascular death,23
preclinical DD‐NEF is likely to be a condition that portends a poor cardiovascular prognosis. Our conclusion is supported by longitudinal data from a study of Olmsted County residents, which has shown that people with advanced diastolic dysfunction, most of whom were in a preclinical stage of disease, had a 10‐fold higher risk of all cause death than subjects with normal diastolic function after adjustment for age, sex and EF.5
Despite evidence from convenience samples that patients with heart failure24,25,26
or DD‐NEF have a subtle decrease in LV long‐axis systolic dysfunction,26,27
subjects with diastolic dysfunction with an EF > 50% have recently been classified as having isolated diastolic dysfunction.5
Our results suggest that this term may be an oversimplification. We have observed that, in subjects with an EF > 50% and no regional wall motion abnormalities, advancing diastolic dysfunction was associated with a decrease in long‐axis systolic function and CHF status was related to a reduction in radial systolic function, although EF remained within “normal” limits. Furthermore, there was a trend towards an increase in LV end diastolic size with advancing diastolic dysfunction and in subjects with symptomatic DD‐NEF. Thus, at least some subjects with advanced DD‐NEF may have cardiac remodelling as a pathophysiological response to co‐morbid cardiovascular conditions (hypertension, ischaemic heart disease or obesity), with increased LV filling pressure related to an increased ventricular capacitance rather than a shift in the end diastolic pressure–volume relationship caused by a pure decrease in LV compliance. Although recent studies have provided an insight into the mechanisms underlying such a response by showing that patients with advanced DD‐NEF have load‐dependent alterations in diastolic function caused by increased LV systolic and arterial stiffness,28
more work is required to confirm these findings.
A low participation rate from women aged > 80 may have resulted in an underestimation of the true prevalence of LV dysfunction in the source population. Although echocardiography is widely accepted as a safe and convenient method for the diagnosis and follow up of patients with diastolic dysfunction,12
it is recognised that Doppler echocardiographic methods reflect integrative properties of diastolic function that lack specificity.29
In this study of survey participants, we could not justify the use of invasive methods for the assessment of active and passive diastolic LV properties. Most (97.6%) of our sample was white and our results may not be applicable to non‐white populations. As our data are cross sectional, we were unable to determine temporal relationships (and thus causal relationships) between clinical parameters, cardiac remodelling and diastolic function.
The burden of DD‐NEF in the community will probably increase with the ageing population and escalating rates of obesity and diabetes in the community. Whether this burden can be reduced by screening efforts remains to be determined. Our observations suggest that, as preclinical advanced DD‐NEF is relatively common and associated with cardiac markers that portend a poor cardiovascular prognosis, screening efforts may be warranted. Before community‐based screening programmes for LV (systolic and diastolic) dysfunction are adopted, however, more data are required detailing the natural history of the disease, the efficacy of treatment for preclinical LV dysfunction, the screening performance of biomarkers and ultimately the cost effectiveness of screening strategies. As DD‐NEF is rare in subjects without co‐morbid cardiovascular conditions, the efficiency of screening programmes could be optimised by targeting high‐risk groups, defined according to age (> 70 years) or risk factor status (hypertension, ischaemic heart disease, diabetes or obesity).
Diastolic dysfunction is common in the community and is often unaccompanied by overt symptoms and signs of CHF. Despite the absence of symptoms, subjects with advanced DD‐NEF have accompanying structural abnormalities that reflect an increased risk for adverse cardiovascular outcomes and have a reduced quality of life.