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European Journal of Heart Failure 2000 2(2):133-136; doi:10.1016/S1388-9842(00)00068-4
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© 2000 European Society of Cardiology

Heart failure in the elderly: a diastolic problem?

Michael Lye* and Nicolas Wisniacki

Department of Geriatric Medicine, University of Liverpool Liverpool, UK

* Corresponding author. University Clinical Departments, The Duncan Building, Daulby Street, Liverpool L69 3GA, UK. Tel.: +44-151-706-4062; fax: +44-151-706-4064. E-mail address: m.lye{at}liv.ac.uk (M. Lye).

Key Words: Ageing • Diastolic function • Heart failure • Mechanisms

Received December 14, 1999; Revised February 7, 2000; Accepted February 29, 2000


   1. Introduction
Top
 1. Introduction
2. Age changes in...
 3. Age changes in...
 4. Heart failure in...
 References
 
It is difficult to differentiate the normal ageing process from age-related pathology especially in relation to effects on the cardiovascular system of humans. The difference between the two processes is not entirely semantic — normal cardiovascular ageing is inevitable whereas most pathologies are potentially, at least, preventable or subject to a variable degree of amelioration [1]. With increased understanding many processes previously thought to be ageing are seen to be age-related pathology. Thus, atherosclerosis, because of its almost ubiquitous occurrence in older subjects, was thought previously to be an ageing phenomenon but now we can show it obviously fails four out of the five ageing criteria (Table 1) and therefore it is an example of an age-related pathology. Many studies of ageing in humans have been focused upon individuals over 60 years of age but not much older. Age changes are more likely to be manifest in much older individuals, those so-called selective survivors — the ‘old-old’ — who have escaped cardiovascular pathology earlier in life. These are the people — the ‘old-old’ — who demonstrate the dual processes, often interacting, of ageing and age-related pathology. The consequence of this combination is to modify the pathophysiology of disease such that knowledge of that condition derived from studies in ‘young-old’ (60–75 years) are not readily applicable to the ‘old-old’ patient. Similarly with disease management. With a rapidly increasing older population no longer can ‘old-old’ subjects and patients be excluded from major cardiovascular studies of diseases and their treatment.


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  		Table 1 Criteria used to define an ‘ageing process’a

 

   2. Age changes in cardiac structure
Top
 1. Introduction
 2. Age changes in...
3. Age changes in...
 4. Heart failure in...
 References
 
Increased stiffness of peripheral and central arteries with increasing age is due to proliferation of collagen cross-links, increased thickness of smooth muscle (hypertrophy) and loss of elastic fibres [2]. Age-related structural changes within the right ventricle are of little concern. Within the higher pressure left ventricle there is a progressive increase in wall thickness with increasing age [3,4]. This process is independent of any age-related pathological increase in systolic and/or diastolic blood pressure. The main element is myocyte hypertrophy with a small degree of myocytic hyperplasia. There is accumulation of interstitial connective tissue, and in the ‘old-old’, an accumulation of amyloid deposits.


   3. Age changes in cardiac function
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 1. Introduction
 2. Age changes in...
 3. Age changes in...
4. Heart failure in...
 References
 
3.1. Systolic function
At rest, in subjects carefully screened to exclude coronary artery disease and hypertension, haemodynamics show little change by increasing age [5]. In response to increased demands, usually exercise but also any form of pathological stress due to illness, increasing age in otherwise healthy subjects changes systolic responses (Table 2). Exercise increases in the ejection fraction and the heart rate is attenuated and thus, stroke volume only increase can by ‘moving up’ the Frank–Starling curve [6,7]. These age changes in cardiac responses to exercise are mimicked by β-adrenergic blockade [8] but the use of β-adrenergic agonists does not reverse this ‘ageing process’ [9]. Peripheral factors, blood flow and muscle mass changes with increasing age rather than cardiac systolic changes explain a significant proportion of the decline in exercise tolerance with age.


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  		Table 2 Changes in exercise haemodynamic variables between 20 and 80 years of agea

 
3.2. Diastolic function
Ageing in healthy adults is associated with decreases in the rate and volume of early diastolic left ventricular filling [3,10]. Initially it was thought that the structural changes described above entirely accounted for the decline in diastolic function [4], but recent findings of partial reversibility brought about by the use of calcium channel antagonists [11] and exogenous angiotensin II [12] emphasis the dynamic and therefore potentially reversible nature of the process. This reduction in left ventricular compliance makes a significant direct contribution to the attenuated cardiac responses to exercise in older adults [13]. The aged heart requires atrial contraction to maintain adequate diastolic filling so it is unfortunate that atrial fibrillation is so common in otherwise healthy elderly subjects and, particularly, in elderly patients with heart failure [14].


   4. Heart failure in the ‘old-old’ patient
Top
 1. Introduction
 2. Age changes in...
 3. Age changes in...
 4. Heart failure in...
References
 
Chronic heart failure is a disease of ‘old-old’ people. Only 17% of people with heart failure are below 65 years of age [15] yet most of the interventional studies of the treatment of chronic heart failure have focused on this minority group [16] and have extrapolated the results to the older majority [16]. The interaction of cardiovascular ageing and age-related cardiovascular pathology alters the pathophysiology of heart failure in the older patient as well as giving rise to the increased prevalence and incidence of heart failure in the elderly. Improved survival following myocardial infarction, cardiac surgery and improved treatment of heart failure itself will continue to add more patients to the epidemic of heart failure [17].

As medical undergraduates most older clinicians were taught that heart failure without, and often with, valve defects was mainly a problem of impaired ventricular systolic contractility secondary to coronary artery disease and/or hypertension. The only exceptions to this general rule were the rare specific cardiomyopathies. Clinical features alone cannot reliably assess systolic or diastolic haemodynamics [18,19]. The emergence of haemodynamic assessment tools from the laboratory and into the clinical arena played a major part in what can only be termed a revolution in our understanding of the pathophysiology of heart failure. Subsequently this new knowledge underwrote therapeutic innovations.

Unfortunately older patients missed out on many of these advances and it was only the ready availability of echocardiography that exposed older patients to haemodynamic investigations. The almost routine use of echocardiography in older chronic heart failure patients has revealed many patients to have good cardiac contractility [20]. Normal or preserved systolic function in heart failure has been assumed to imply diastolic dysfunction (‘diastolic heart failure’) but it is necessary to measure directly or indirectly diastolic function in order to confirm the haemodynamic diagnosis [5]. The guidelines for the diagnosis of diastolic heart failure have been published by the European Society of Cardiology but unfortunately fail to focus on elderly patients [21]. To label all above the age of 50 years as a group is to fail to recognize the heterogeneity of a population living for a further 40 years! The correlation of Doppler indices with increasing age impairs the sensitivity and specificity for detecting abnormalities of diastolic function in the ‘old-old’ if the results are extrapolated from data acquired in ‘young-old’ individuals [22].

Heart failure with preserved systolic function (diastolic heart failure) rises in incidence with age (Table 3). Probably less than 10% of heart failure patients below the age of 60 years have preserved systolic function [14] whereas up to 70% of patients over the age of 80 years have preserved systolic function [23]. Not all workers believe that there is a specific entity of normal systolic function heart failure [24,25]. It is, however, difficult to dismiss the accumulating data on the incidence and prevalence of normal systolic function heart failure in older patients if sufficient ‘old-old’ patients are included in the studies [5]. Survival for patients with diastolic heart failure is better than for those with systolic heart failure [26] with the latter dying of sudden death and the former to disease progression [27]. Other workers, however, report the prognoses as being similar [28]. Surprisingly both types of heart failure patients are as likely to be readmitted to hospital; systolic dysfunction patients with heart failure and diastolic heart failure patients with other co-morbidities [29].


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  		Table 3 Age and prevalence (%) in heart failure patients of normal systolic functiona

 
What is the basis for the development of normal systolic function heart failure in the elderly? The age changes described above must be relevant. Atrial fibrillation, whether associated with coronary artery disease or not, is a significant factor [14]. Additionally, conditions associated with left ventricular hypertrophy and/or metabolic disruption of energy dependent relaxation are particularly common in the ‘old-old’ patient. These include hypertension [8], atrial fibrillation [14], diabetes mellitus (IDDM and NIDDM) [30], amyloidosis [31] and coronary artery disease itself [21]. Some workers have suggested that there is a high incidence of specific non-ischaemic cardiomyopathies in older patients [32,33]. The roles of micronutrient deficiency and oxidizing free radicals on cardiac morphometry and the aetiology of heart failure in the experimental situation [34–36] open exciting possibilities. Both these factors have been implicated as major players in the biology of normal mammalian ageing [37,38].


   References
Top
 1. Introduction
 2. Age changes in...
 3. Age changes in...
 4. Heart failure in...
 References
 

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