Cardiovascular

The ageing cardiovascular system

Advanced age is the most potent risk factor for cardiovascular disease. This vulnerability stems from:

Cumulative exposure to risk factors (extrinsic ageing)

This was looked at in more detail in the WHO MONICA project (see ‘Further reading’, p.256), which looked at coronary risk factors in 38 populations across 21 countries for a decade
This showed that not all risk factors increased with age—male smoking decreased (although not female) and cholesterol showed a small downwards trend. Body mass index (BMI) increased for both sexes
Thus, it is not inevitable, and can be modified by behaviour, eg athletes who continue to exercise into older age may show fewer signs of cardiovascular ageing than an unfit younger person

Disease acquisition

Often occult
Affected by risk factor accumulation

Intrinsic ageing

The relative contributions of these factors to the clinical picture are unclear. Table 10.1 addresses the three important questions:

What are the common changes with age?
How does that impact on function?
What are the clinical implications?

Further reading

Evans A, Tolonen H, Hense HW, et al. (2001). Trends in coronary risk factors in the WHO MONICA Project. Int J Epidemiol 30: S35-S40.

Table 10.1 An overview of age-related changes and their effects

Age-related change	Impact on function	Clinical implications
Proximal arteries become thicker, dilated, elongated and less elastic	Systolic pressure peak increases, causing hypertension Increased peripheral vascular resistance (variable)	Intimal thickening probably predisposes to atheroma Systolic hypertension common in older patients CXR may show enlarged aortic knuckle ‘unfolding’ of the aorta
Fibrosis and fat infiltration of the sinoatrial (SA) node and conducting system	Slower conduction from SA node and through the conducting system	First degree heart block and bundle branch block common Left axis deviation more frequent More vulnerable to clinically significant bradyarrhythmias
Maximum heart rate falls by 10% at rest and 25% during stress	Decreases capacity for cardiac output—largely compensated for at rest, but limits response to stress	Less able to mount a tachycardia, so less reliable sign of acute illness
Left ventricular wall thickens as myocyte size increases	Increases cardiac filling pressures and allows compensation for drop in heart rate	A degree of cardiac enlargement seen on CXR is normal. Worse with hypertension, so always check BP and treat as needed
Left atrial size increases due to alterations in cardiac filling		Predisposes to AF
Myocardial contractility impaired at high demand	Contractility preserved at low stimulation, but with stress cannot increase meaning (along with heart rate factors) that cardiac output cannot be increased	Decreased cardiac reserve to stress—may become haemodynamically compromised in response to acute illness earlier than younger patients
Increased circulating catecholamines with down regulated receptors (especially B adrenergic)	Impairs ability to mount a stress response	As above, this table—decreased cardiac reserve to stress More prone to heart failure
Impaired oxygen consumption on exercise	Varies considerably between individual older patients—unchanged in those used to exercise, up to 60% reduction in unfit	Contributes to reduced cardiovascular reserve to stress

Chest pain

A common complaint in all settings. May be primary symptom (presenting to GPs and general medical take) or mentioned only in response to direct questioning. Also occurs during inpatient stays for other reasons.

There are very many causes, the majority of which become more common with age. Many are benign, but some are serious and even life threatening, so a thorough and sensible approach is needed.

Common conditions not to be missed include: cardiac pain; pleuritic pain due to pulmonary infarction or infection; peptic pain (including bleeding ulcers); pain from dissecting aortic aneurysm and pneumothorax (especially in COPD).

Other possibilities include: muscular pain (eg after unaccustomed exertion); costochondritis (local tenderness at sternal joint); pain from injury (eg after a fall); referred pain from the back and neck (eg osteoarthritis) and referred pain from the abdomen.

Differentiating these depends on accurate history taking and careful examination, both of which can be more of a challenge in older patients. Presentation may be atypical, and the patient may have many other problems so teasing out which are the important symptoms can be difficult (experience improves the ability to ‘feel’ your way around the history). ▶It may be the last symptom mentioned in a long list, however, mention of chest pain should always trigger a careful assessment.

History

Is this a new symptom? (may suffer from chronic angina)
If not, is it any different from the usual pain? (intensity, pattern)
What is the nature of the pain? (pleuritic, heavy, tight. This is often hard to do, and hand gestures can help—a clenched fist for a heavy pain, a stabbing action for a sharp pleuritic pain)
Where is it located? (including radiation)
How acute is the onset and what is the duration?
Are there any associated symptoms?

Patients with cognitive impairment can be particularly difficult to assess, but allowing free conversation may reveal symptoms, followed by closed questions that may prompt appropriate answers. Family members may have noted signs or symptoms and are an invaluable aid to assessment, eg clutching the chest after walking.

Remember that cardiac symptoms may differ for each patient and they will describe the pain in their own terms. Many older adults with ischaemia will deny ‘pain’ and instead describe ‘discomfort’. Some will just experience weakness, dyspnoea, or nausea.

Examination

How does the patient look? A sweaty, clammy patient needs urgent and exhaustive assessment, whereas a patient drinking tea and chatting is less likely to have a devastating condition
What are the basic observations?
Signs of shock alert to a serious condition—IHD, pulmonary infarction, dissection, sepsis, blood loss—but remember these may be late signs and are less useful in older patients. The patient may usually be hypertensive, so a BP of 120/80 may be very low for them; they may be on a β-blocker, so unable to mount a tachycardia, etc.
Temperature may be raised in sepsis
Low oxygen saturation always needs explaining (unless chronic) and may indicate an intrapulmonary problem
Is the jugular venous pressure (JVP) elevated? (heart failure)
Look at the chest wall for shingles, bruising and localized tenderness
Different blood pressures in the arms may indicate dissection (but may also occur with atheroma)
Listen to the heart—are there any new murmurs (dissection or infarction) or a rub (pericarditis)?
Listen to the lungs—is there consolidation (sepsis) or a rub (consolidation or infarction)?
Look at the legs—is there any clinical DVT?

Investigations

Some tests can be less useful in older patients, and should be individually tailored to the patient. Sending off every single test on all patients with chest pain will only lead to confusion.

ECG—should be done on the majority of patients with chest pain. Remember the baseline ECG may well be abnormal in an elderly person, and comparison with old traces is extremely useful. If your patient has a very abnormal ECG (eg left bundle branch block (LBBB)) it is useful to give them a copy to carry with them
CXR—looking for lung abnormalities and widening of the mediastinum. Remember that the aorta often ‘unfolds’, so a careful look at the contours of the aortic arch and/or comparison with old films is needed to assess possible dissection. Remember that a patient can look fairly well in the early stages of aortic dissection
Blood tests—basic haematology, biochemistry, and inflammatory markers are often useful. Remember that in acute blood loss, the haemoglobin may not drop immediately, and that an elderly septic patient may take a day or two to develop an elevated white cell count and CRP
Troponin—useful in a patient with suspected cardiac chest pain (for risk stratification). It is NOT a useful test if you do not think this is cardiac pain—there are many false positives that will only cause confusion
D-dimer—only useful if negative in cases of suspected thromboembolism. There are a huge number of causes of a positive d-dimer (including old age itself); a positive result does not imply the diagnosis of PE
Further tests (eg CT thorax for suspected dissection, exercise testing for angina, lung perfusion scans for thromboembolism, etc.) depend on clinical factors

▶Always attempt to explain a chest pain—both for the patient and future clinicians. A ‘diagnosis’ of non-cardiac chest pain is rarely helpful.

Stable angina

Coronary artery disease is clinically evident in 20% of those > 80 years. Management is often suboptimal. It is unacceptable to leave a patient with symptoms, however frail, until all available options have been looked at, and it has been proven (by trying it) that a certain treatment cannot be tolerated. A stepwise, slow introduction of tablets allows insight into adverse effects and may require multiple clinic visits. Symptom diaries can assist with this process.

Stable angina

Risk factor reduction

Cholesterol and BP less likely to be lowered in older patients, but the risk reduction is equal if not greater than for younger subjects
Diabetic control is less likely to be tight, in part due to justifiable concerns about the dangers of hypoglycaemia
Lifestyle advice (exercise, smoking and diet) should be given

Aggravating conditions

Such as heart failure, anaemia, thyroid disease, arrhythmias, valvular heart disease. More common in older people and should be corrected.

Medication

Under utilized, particularly aspirin (concerns about bleeding) and β-blockade but there is evidence that they are both equally useful in reducing risk
A trial and error approach to treatment is needed—add one or two treatments at a time to minimize the risk of side effects (most commonly orthostatic hypotension) and stop if there are problems, trying something else instead
Start on low doses, and titrate upwards (eg atenolol 25mg)
Long-acting agents (eg diltiazem MR) reduce compliance problems
Nicorandil (10-20 mg bd) is often better tolerated than other anti-anginals in this age group.
Choice of medication should be pragmatic—if a patient has a bradycardia for example, a negatively chronotropic drug is usually inappropriate (consider using amlodipine 5-10mg). If a patient has heart failure, a cardio selective β-blocker (eg carvedilol, metoprolol, bisoprolol) is a better choice than a fluid-retaining calcium channel blocker
GTN can cause considerable problems with hypotension, and instruction on correct use is essential. Tablets can be spat out once the pain starts to settle, so (in theory) the dose can be titrated to symptoms. In practice, the spray is often easier to use. It should be used sitting down if possible and prophylactically before significant exertion

Revascularization

Should be considered (ideally after risk stratification by stress testing), as for younger patients, if symptoms persist despite maximal medical therapy (see

‘Revascularization procedures’, p.264).

Palliation

Consider if diffuse disease, not amenable to revascularization with ongoing symptoms (eg home oxygen therapy, opiates to allow sleep).

HOW TO … Rationalize antianginals in older patients

When?

With advancing age and frailty, mobility may reduce and so angina symptoms may become less frequent, or even stop
It is not uncommon to find an octogenarian on four antianginals, who has not had angina for many years
Use a low pulse or BP reading as a trigger to review the medication
Do not hesitate to rationalize this—there are many pitfalls from polypharmacy, and requirements will change with time

How?

If cognitive impairment, confirm with carers that they are genuinely asymptomatic from angina
Review observations—if bradycardic, stop β-blockade first; if hypotensive, start with the symptomatic medications first (eg nitrates) before those with disease-modifying properties
Select one drug to modify, then reduce in a stepwise fashion (eg reducing dose and/or frequency)
Patients and family may be resistant to medication changes after years of healthcare professionals emphasizing the importance of their tablets. Some are frightened of a recurrence of disabling symptoms so explain to the patient, carers and GP what you are doing
Clarify contingency plan: ‘This is a trial, and if it does not suit you, you may get angina pains again. If that happens, please just start taking your old doses again’
Ensure there is back-up if there are concerns (eg telephone number)

Review

Set a date for review of impact
Assess whether there have been any symptoms, and reassess the pulse and BP
If all is well, continue with careful reduction in medication

Goal

Aim to use as few medications as possible, while maintaining control of symptoms
If the BP allows, continue those with disease-modifying properties (β-blockade, ACE inhibitors), but in frail older people it is more important to avoid orthostatic hypotension and falls
Once the medication has been titrated down to an optimum level (balancing pulse, BP, symptoms, and disease modification) communicate the final list to the GP

Acute coronary syndromes

CHD incidence rises with increasing age. An acute coronary syndrome describes a scenario in which the myocardial cells are not receiving enough blood and oxygen to meet their demands. There is a range of syndromes from unstable angina to non-ST elevation MI (NSTEMI) to ST elevation MI (STEMI). Management in general is as for younger patients, but there are some points relating to older patients in particular.

Atypical presentation

More likely to present with atypical or vague symptoms (eg intense dyspnoea, syncope, weakness, abdominal pain)
Symptoms may be obscured by comorbidity
ECG changes may not be present in up to a quarter of acute MI with the full diagnostic triad (chest pain, ECG changes, and biochemical changes) present in under a third of those > 85 years
ECG may be difficult to interpret because of pre-existing abnormalities (LBBB, pacing)
Vital signs or symptoms may be obscured by medication (β-blockade, pain medication)

Different pathology

More pre-existing coronary artery disease with more multivessel disease
NSTEMI more likely than an STEMI
More likely to develop heart failure, AV block, AF, and cardiogenic shock after a coronary event

Later presentation

Increased prevalence of angina so less alarmed by chest pains
May modify lifestyle to avoid symptoms (if climbing a hill gives them chest pain, they may just stop doing it)
Increased occurrence of ‘silent ischaemia’ (especially in people with diabetes)
Increased social/attitudinal factors (I didn’t want to bother the doctor’)
A third of patients > 65 with MI will present later than 6hr after symptom onset

Increased comorbidity

Making diagnosis difficult (eg a patient with COPD who has exertional breathlessness) and therapy less well tolerated (eg β-blockers with peripheral vascular disease)
Also as comorbidities add up, so frailty increases and medications are generally less well tolerated

Older patients with acute coronary syndromes have a higher inpatient mortality so should be prioritized for specialist monitoring where there are limited resources; however, it is known that they are:

Less likely to receive aggressive acute therapy (eg less thrombolysis, angiography and angioplasty, coronary artery bypass grafting (CABG), and maximal medical treatment)
Less likely to have full secondary prevention measures implemented

Management of the older cardiac patient is therefore more difficult and more likely to result in death than in younger patients. Sometimes there are good reasons for withholding therapy (eg patients presenting later are less often eligible for thrombolysis, side effects may restrict secondary prevention) but often the justification is less robust. Lack of evidence in older people does not mean that there is no benefit—rather that it has not been proven, as is the case with many commonly used therapies (eg loop diuretics in pulmonary oedema).

Common sense dictates when to use an aggressive approach, considering the patient as a whole including:

Patient preference where possible
Comorbidities (alter risk profile)
Current medication
Frailty and likely life expectancy
Apparent biological age rather than chronological age

There are many well-defined treatment algorithms, and older patients should be included at every step unless there are good reasons not to. If you plan to exclude a patient from treatment, you should clearly document your rationale.

Revascularization procedures

Includes percutaneous coronary angiography and intervention (PCI) and CABG.

When?

Used when stable symptoms persist despite maximal medical therapy, when unstable symptoms fail to settle, or for acute myocardial infarction (primary PCI)
Risk stratify with exercise testing and troponin measurements. Older patients may be unable to exercise, but consider bicycle exercise, stress echocardiography or an isotope myocardial perfusion scan to look for evidence of reversible ischaemia

What are the risks?

PCI—higher risk of death, renal failure and infarction in elderly. Age is an independent predictor of increased complication, but so too are diabetes, heart failure and chronic renal impairment, all of which are more common in older patients.
CABG—increased early mortality and stroke in older patients

What are the benefits?

PCI—may be only way to control intrusive symptoms in stable angina, and the only way to settle an acute coronary syndrome. Variable evidence from studies—all agree increased early complications, but longer-term benefits in older patients are reported as equivalent or even better
CABG—probably better with triple vessel disease, poor exercise tolerance, poor left ventricular function and diabetes. Generally well tolerated in elderly, with similar long-term improvements in symptoms and quality of life to younger patients. New minimally invasive techniques, that do not require bypass, are likely to reduce the early complications without impairing outcome

Overall recommendations

Consider all patients who fail medical treatment for revascularization procedures, regardless of age. The early complication rate is higher in older patients, but the eventual benefit is equal if not better than for younger patients.

Approach a cardiologist with a record of treating older patients. Crucial to include the patient in the decision, with a frank and individualised discussion about risks and benefits.

Myocardial infarction

This includes both NSTEMI and STEMI. Around two-thirds of all myocardial infarctions occur in patients > 65 and a third in patients > 75. Overall, the incidence of MI has decreased, but this is not the case for older patients. Despite this, evidence regarding optimal management is lacking, as older patients tend to be underrepresented in clinical trials. Table 10.2 summarizes what is known.

As a general rule, all appropriate therapies should be considered in all patients post-MI, regardless of age. While evidence is lacking in older patients, it is more reasonable to extrapolate from a younger population than to deny treatment. This approach must of course be tempered with common sense and individually tailored decision making.

Prior to discharge

Medication

May include aspirin ± clopidogrel, statin, β-blockade, ACE inhibitor, and GTN spray
Use medications unless they are contraindicated, or the risk > benefit
Be alert for common side effects (more likely with advancing age), eg orthostatic hypotension, gastrointestinal bleeding

Education

Diet, nutrition, cholesterol control
Smoking cessation
Activity restrictions and graded reintroduction
Recurrent symptoms and what to do
Routine follow up after stents

Cardiac rehabilitation

Used after acute coronary syndromes and multiple presentations of congestive heart failure
Involves structured exercise programme
Proven to improve exercise tolerance and decrease readmission
Under used for older cardiac patients—less referral, and sometimes there are upper age limits in place
Benefit seen in older patients is equivalent to that in younger patients, although they start from a less fit baseline
Older people adhere well to programmes and seem to suffer no complications
Some adaptations are needed (more time to warm up and cool down, longer breaks, avoidance of high impact activity, lower intensity for a longer time)
Benefits include improved fitness, increased bone mineral density, improved mood and fewer falls as well as improved cardiovascular fitness

Table 10.2 The current evidence base regarding various treatments for MI

Therapy	Evidence
Aspirin	Equivalent risk reduction in elderly population
Primary PCI	This is usually the strategy of choice where presentation is early. It reduces death and recurrent MI compared with a conservative strategy. Procedural risks are greater with frail patients and the role for PCI in those > 80 with multiple comorbidities has not been well studied. Resource limitations may impact
Thrombolysis	Not indicated for unstable angina or NSTEMI
	Has a role in STEMI regardless of age
	Must be administered <12hr after onset (ideally <3hr) and is used where PCI is not available or feasible
	Increased risk of complications, eg cerebral bleeding (but can predict those at higher risk if hypertensive, low body weight, previous stroke or on warfarin)
	Contradictory evidence regarding mortality—large RCTs suggest increased absolute risk reduction of mortality in elderly patients (eg ISIS-2) but these are selected, probably fitter patients, and do not include the very old. Observational trials of actual practice suggest equivalent benefit in older patients, or possibly even a survival disadvantage. Probable equivalent proportional mortality reduction, so absolute reduction greatest in elderly who have the highest mortality
	Overall, consensus is that thrombolysis can be used in older patients, with rare exceptions for the very frail or where individual risk seems to outweigh benefit
Low molecular weight heparin	Full dose is effective in NSTEMI, and possibly more effective in older patients
GP IIb/IIIa inhibitors	Trials using this therapy in unstable angina and NSTEMI show benefit that is equal in the older patients

Hypertension

Hypertension is an important risk factor for vascular disease. Historically underdiagnosed and undertreated, especially in older patients, although this is improving in the UK as GPs now have financial incentives to treat hypertension.

The incidence of hypertension overall rises with age, reaching a prevalence of 60-80% beyond 65. After this age, systolic BP (SBP) rises linearly while diastolic BP (DBP) falls, leading to widening of the pulse pressure and relative frequency of isolated systolic hypertension (Table 10.3). Isolated systolic hypertension reflects reduced arterial compliance which is disease related and not a part of ‘normal’ ageing per se.

Hypertension is an independent risk factor for stroke, IHD, peripheral vascular disease, congestive heart failure, renal failure, and dementia in all age groups, but in older patients it is SBP and widened pulse pressure that are the strongest predictors of adverse cardiovascular outcome.

Assessment

Ask about symptoms (including hypotensive), comorbidity, smoking
Measure with a well-maintained, calibrated device, with an appropriate sized cuff:
- Check supine and standing BP (orthostatic hypotension can cause symptoms when treatment initiated)
- Take at least two measurements in a single consultation
- Never initiate treatment based on a single reading
- Consider ambulatory measurements if drug resistance, variable BP, white coat hypertension, or postural symptoms
Examine for evidence of target organ damage (stroke, dementia, carotid bruits, cardiac enlargement, IHD, peripheral vascular disease, renal disease, retinal changes)
Consider secondary hypertension—Rare in older patients, but consider if drug resistant, severe hypertension or with suggestive examination or laboratory findings. Consider medications (NSAIDs, steroids, SSRIs), Cushing’s syndrome, sleep apnoea, primary aldosteronism, phaeochromocytoma, or renal artery stenosis
Investigations to look at target organs (urinalysis, blood urea, and electrolytes, ECG) and for risk factor analysis (glucose, lipids)

Treatment thresholds and goals

Depends on individual
In active elderly population with reasonable life expectancy treat as for younger patients—ie > 160/100mmHg
Use lower threshold (> 140mmHg) in high-risk patients (eg smokers, diabetics, evidence of target organ damage, high estimated 10-year risk)
No clear evidence for optimal target. Probably the lower the better as long as tolerated
The usual limit to treatment is symptomatic postural hypotension; consider using alternative agents which may cause less orthostatic drop (eg ARBs, calcium channel blockers)
Caution in isolated systolic hypertension—try not to lower DBP <65mmHg
There are even fewer data for very elderly (> 85) people and a pragmatic approach based on apparent biological age is appropriate

Table 10.3 British Hypertension Society definitions of high BP (2004)

	Grade	Systolic BP (mmHg)	Diastolic BP (mmHg)
Mild	1	140-159	90-99
Moderate	2	160-179	100-109
Severe	3	> 180	> 110
Isolated systolic hypertension	1	140-159	<90
Isolated systolic hypertension	2	> 160	<90

Hypertension: treatment

Similar approach to that used in younger patients, but it is important to bear the following in mind:

Side effects are more common and more debilitating in older patients (due to more sluggish baroreceptors and reduced cerebral autoregulation)
There is a greater risk of drug interactions as older patients are more often victims of polypharmacy
Comorbidity is common and should direct the choice of antihypertensive agents (see ‘HOW TO … Use antihypertensives in a patient with comorbid conditions’, p.271)
Hypertension should be seen as a risk factor and the decision to treat should be weighed along with other risk factors. In a very frail elderly person with a limited life expectancy, the side effects might far outweigh any future benefits from risk factor modification. This, however, should be an active decision reached if possible with the patient, and not a simple omission
Begin with lower doses and titrate up slowly (‘start low and go slow’) to minimize adverse reactions. It is better to be on something at a low dose than nothing at all

Non-pharmacological measures

Lifestyle modifications are as important and effective in reducing BP in older patients as in the young. Salt restriction, weight reduction, and regular exercise are particularly effective. Moderate or absent alcohol intake is advised. Smoking cessation and decreasing saturated fat intake helps with overall risk reduction.

Choice of medication

Many large trials have compared the different classes of antihypertensive but with little consistency in results. Overall, it seems that it is lowering the BP per se that is the important factor, and this benefit continues up until at least 84 years (possibly beyond—evidence pending). In older patients, with much comorbidity, there may be compelling reasons for using, or not using certain agents (see

‘HOW TO … Use antihypertensives in a patient with comorbid conditions’, p.271). Try to use a drug that will treat both BP and a coexisting disease to limit polypharmacy. If not, then the British Hypertension Society recommends using the A/CD approach: