This study provides estimates of the prevalence of LV dysfunction in a large community sample of very old British people, its relationship with limiting dyspnoea and the extent to which its presence is recognised in the UK National Health Service. We found that around half of 87–89 year olds had LV systolic dysfunction or isolated moderate/severe diastolic dysfunction. Nearly two-thirds of these people had limiting dyspnoea. Over 80% of those with symptomatic significant LV dysfunction remained undiagnosed. A pre-existing diagnosis of HF was present in 10% of participants, and in just over a third of these no echocardiographic evidence of significant systolic or diastolic LV dysfunction or severe valve disease was found.
LV systolic dysfunction underlies the majority of HF (termed HF-REF) at younger ages, however the importance of HF with a preserved LVEF (HF-PEF) is increasingly recognised in older age groups. Numerous studies have shown that the proportion of HF patients who have a normal or near normal EF increases with age and HF-PEF is responsible for approximately 50% of HF cases over the age of 70 years.14
In comparison with HF-REF patients, those with HF-PEF are more likely to be female, more likely to have multiple comorbid conditions, particularly hypertension and diabetes, and less likely to have coronary artery disease.14
The underlying pathophysiology of HF-PEF is much debated and involves complex mechanical and metabolic abnormalities of ventricular function.17
While not the only contributory cause of HF-PEF, LV diastolic dysfunction is an important component.15
Our study is among the first to incorporate detailed measurement of both systolic and diastolic function in the home setting in a cohort of the very old.
Almost all previous population based studies of LV dysfunction have recruited small numbers aged over 85 years. Our data indicate a substantially higher prevalence of LV dysfunction than previous studies involving ‘younger old’ people and most of the few studies including the very old. We attribute this to our inclusive recruitment strategy, the domiciliary approach and the advanced age of our sample. The prevalence of LV systolic dysfunction in our population (32% with LVEF 50% or less, 9% with LVEF 40% or less) was more than twice that of most previous studies (see supplementary table S2 in the online appendix). For example, the Olmsted County study10
(n=298, aged 75+ years) found that 13% had an EF of 50% or less and 4% of 40% or less; the Belfrail Study20
(n=556, aged 80+ years) found 6% with an EF of 50% or less and 2% with an EF of 40% or less; the UK ECHOES study21
(n=66, aged 85+ years) found 17% with an EF of 50% or less and 3% with an EF less than 40%; and the Leiden 85-Plus Study (n=81, aged 90 years) found 9% with an EF of <50%.22
The Leiden study highlights the selection bias introduced by hospital based assessment in the very old; only 30% of those eligible were able to attend hospital for echocardiographic assessment and those who attended were significantly healthier than those who could not.22
Our findings are comparable to the recently reported Jerusalem study (n=450, aged 85 years) which reported 44% with EF less than 55% and 14% with EF less than 45%.23
The prevalence of severe systolic dysfunction in our study is also broadly comparable with previous studies by Raymond et al24
and the Rotterdam study group,25
both of which focused on more severe systolic dysfunction.
It is likely that coronary artery disease is a major contributor to the high prevalence of LV systolic dysfunction that we observed. MI (defined by a pre-existing diagnosis in the GP records or Minnesota coded ECG) was significantly commoner in those with LV systolic dysfunction than in those without (30.3% vs 14.8%; p<0.001). Moreover, 32% of MI cases were identified on the ECG alone (ie, did not have a pre-existing GP diagnosis). Previous data from the Rotterdam study supports the notion that unrecognised MI is an important long term risk for the development of HF in older people.26
As we did not specifically explore regional wall motion abnormalities among those with preserved LVEF, it is possible that we may have somewhat underestimated the prevalence of mild abnormalities of LV systolic function. Nevertheless, our observation that among those with both biplane and semiquantitative measured LVEF >50%, only two people had a Wall Motion Score Index >1.25 (equivalent to two akinetic segments of the 16 segment Wall Motion Score Index), suggests that any such underestimate is slight. Differences in blood pressure even within the ‘normal range’ are associated with incident HF.27
Perhaps surprisingly, we did not observe an association between a previous GP diagnosis of hypertension and LV systolic dysfunction (p=0.713); our previous observation that hypertension is substantially underdiagnosed in our cohort may account for this finding.7
Comparison of the prevalence of LV diastolic dysfunction between our study and previous investigations is complicated by differences in the grading schemes used. While the general approach is similar across studies, specific criteria and cut-off points vary widely.10
To address this issue we also analysed our diastolic function data using the scheme implemented by Bursi et al
in the Olmsted County study.15
Although a smaller number of participants could be classified using the approach of Bursi et al
, the proportion of classifiable participants with moderate or severe diastolic dysfunction was very similar to that yielded by our approach (30.9% vs 31.0%). Notwithstanding the difficulties inherent in between study comparisons, we found a prevalence of LV diastolic dysfunction (31% for moderate/severe dysfunction and 20% for isolated moderate/severe dysfunction) that was substantially higher than most previous studies (see supplementary table S2 in the online appendix). For example, among those aged 75 years and above in the Olmsted County study,10
moderate or severe LV diastolic dysfunction was about half as common as in our sample. Only the Canberra Heart Study28
(n=118 aged 80–86 years) and the Belfrail Study20
(n=458, aged 80+ years) have reported the prevalence of isolated LV diastolic dysfunction in the very old; the Canberra study found 11% with isolated moderate/severe dysfunction and the Belfrail Study found 3% with isolated severe dysfunction. Our cross sectional results, in a large sample of the very old, support the data from prospective studies in younger cohorts13
indicating that progressive deterioration in diastolic function is part of biological ageing and is likely to contribute significantly to the substrate for the development of HF with preserved ejection fraction (HF-PEF). The biological processes underlying these observations require further study.
We found a high prevalence of significant LV dysfunction accompanied by limiting dyspnoea in the very old, the majority of which was undiagnosed. These findings were robust to adjustment for significant intrinsic lung disease defined by spirometric criteria. We did not adjust for other potential causes of dyspnoea (eg, severe anaemia or renal impairment) as such conditions were rare among our participants. While some prevalence studies have defined HF as LV dysfunction plus dyspnoea,21
we are conscious that we did not apply Framingham or similar criteria for the diagnosis of HF. Our category of symptomatic LV dysfunction should therefore not be considered as equivalent to HF. Nevertheless, approximately 25% of our participants had undiagnosed LV systolic dysfunction potentially amenable to therapies known to prolong survival and enhance quality of life.31–33
The importance of preventing the progression of asymptomatic LV systolic dysfunction to HF is well recognised.2
However, no therapy has been proven to be effective in preventing the progression of preclinical diastolic dysfunction to HF-PEF, or indeed in improving outcomes in established HF-PEF.35
The strengths of this study include its population based sample, which included both the institutionalised and cognitively impaired—excluded from many previous studies in this age group21
—and its domiciliary echocardiographic approach. We have previously shown that up to 50% of very old people would be unwilling to participate in a study requiring hospital attendance,6
and hospital based echocardiography assessment is known to introduce selection bias in this age group.22
The Newcastle 85+ Study cohort was sociodemographically representative of the local population, and of England and Wales, including the proportion in care homes.7
Rather than rely on self-reported diagnoses, which are known to be unreliable at this age,39
we ascertained disease diagnoses from GP records.
Some limitations merit comment. We did not assign or validate HF diagnoses using Framingham or other criteria. Isovolumic relaxation time, used in our classification of diastolic function in atrial fibrillation, is known to be difficult to measure precisely. Of note, it was used to assign only 22 participants and the principal conclusions of the study remain unchanged if those participants are removed. The methodological challenges of accurate measurement of left atrial volume, Valsalva manoeuvres and pulmonary venous flow (variably incorporated into the diastolic function classification schemes in previous studies) precluded their use in this domiciliary study of very old people. Participants in this study cannot be considered a random sample of the very old population; they had elected to participate in the Newcastle 85+ Study and made a subsequent additional commitment to undergo cardiac assessment. It is therefore possible that study participants were in somewhat better health than the general population of the very old; we may therefore underestimate the true prevalence of LV dysfunction. Our population was of overwhelmingly white ethnicity and British origin, and although representative of the very old in the UK,38
may not be typical of people of this age in other parts of the world.