Dr Nigel Rowell discusses the assessment and management of this elderly patient, providing details of the lifestyle and pharmacological review that should be undertaken
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Your patient is a 70-year old male with a history of hypertension and myocardial infarction (5 years previously), who has heart failure (with left ventricular dysfunction). He is on an optimal dose of both an angiotensin-converting enzyme inhibitor and a beta blocker. His heart failure has been fairly stable for the last few months but he is still moderately symptomatic (New York Heart Association classification III).
It would be easy at first glance to say that nothing more could be done for this man, and, indeed, cardiac patients so often tolerate their symptoms with the same outlook. They say, ‘it’s what I expect—I have a bad heart’. Fortunately, evidence and an understanding of the pathophysiology of heart failure offer him more.
Improved life expectancy and quality of life
Since the mid-1980s, a number of landmark, successful drug trials have brought an increase in life expectancy and, perhaps more importantly, quality of life for patients with heart failure. From the frusemide-only days of that era we can now add to our arsenal angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta blockers, spironolactone, and biventricular pacing; all with the gold standard quality mark of well conducted trials. Revascularisation is also more widely available to heart failure patients who have concomitant angina or in whom some evidence of reversible ischaemia is found.
The landmark studies are the famous acronyms that specialist registrars in cardiology incant—Studies Of Left Ventricular Dysfunction (SOLVD);1 Candesartan cilexetil in Heart failure Assessment of Reduction Mortality and morbidity (CHARM);2 Cardiac Insufficiency BISoprolol study (CIBIS);3 and Carvedilol Prospective Randomized Cumulative Survival study (COPERNICUS),4 to name just a few.
It is important not to underestimate how much difference these therapies make in the more severe grades of heart failure—New York Heart Association (NYHA) grades III and IV (see Box 1). Angiotensin-converting enzyme inhibitors are the single most valuable tool as they show a 23% relative risk reduction in mortality across all classes of heart failure.5
Box 1: Classification of NYHA
The physiology of heart failure
In order to understand the treatment of heart failure, it helps to review the physiology. The kidney ‘gets it wrong’ when it finds itself underperfused by a failing heart and perceives this to be the result of a lack of fluid. It therefore sends hormonal signals, via the renin–angiotensin system, in the form of increased aldosterone to hang on to fluid, and powerful vasopressor agents (the angiotensins) to increase blood pressure. The heart is then faced with an increased fluid load and vascular resistance—the very things it could do without.
This is the basis for diuretic, ACE inhibitor (or ARB), and beta blocker therapy in heart failure. In a patient with heart failure, I would recommend the therapy steps:
- ‘start low and go slow’ is a useful rule in all heart failure therapies
- when starting an ACE inhibitor, a low dose, such as 1.25 mg/day of ramipril (once daily), or 2.5 mg of lisinopril (once daily), should be used—blood pressure and urea/electrolytes should be checked at the initiation of therapy and after 1 week
- a small rise in serum creatinine is nearly always seen; however, ACE inhibitor therapy should be stopped if serum creatinine is greater than 50% above the baseline reading or greater than 220 µmol/l6
- in patients who are intolerant of ACE inhibitors, the use of an ARB should be considered. Candesartan would be the ARB drug of choice as it has a large evidence base in patients with more severe heart failure (NYHA grades III and IV) who are intolerant of ACE inhibitors. Candesartan is licensed for this indication—a suitable starting dose would be 4 mg, increased no more frequently than every fortnight to a maximum of 32 mg.
Beta blockers may produce benefit in heart failure by blocking sympathetic activity. They probably have more than one mechanism but think of them as ‘chilling’ the heart out and enabling it to go about its daily work without the added pressure from adrenaline, and with more time to perfuse itself between beats. The antiarrhythmic effects of carvedilol probably explain the early benefit on mortality in LVSD as observed in the CAPRICORN study.7 Beta blockers also alter myocardial metabolism favourably.8
It is not just pharmacotherapy that can make a difference. Dyssynchronous hearts—where two walls of the left ventricle beat at different times—can be corrected by insertion of a pacemaker with leads on either side of the ventricle to resynchronise its actions. This brings profound benefits to the right patients.
Already we can see that it is worth taking a closer look at our 70-year-old patient. He is on an optimum dose of an ACE inhibitor, which is good. The quality and outcomes framework (QOF) in England and Wales demonstrates use of ACE inhibitors or ARBs at 40–80% in heart failure for patients who can tolerate the therapy and for whom there is no contraindication. All beta blockers are not the same in heart failure; only bisoprolol, carvedilol, and nebivolol have an evidence base.9 Atenolol is not a drug of choice in this grade of heart failure.
Before planning additional therapy, it will be worthwhile reassessing the patient clinically. Several questions should be asked, which are:
- is he suffering concomitant angina?—if so, referral for angiography with a view to revascularisation would be a good idea10,11
- is he suffering from fluid overload?—the jugular venous pressure is difficult to see, but it is a more useful measure than ‘creps in the chest’.10 Adjustment of his diuretic requirement can be started. It should be noted that ankle oedema in men is probably more helpful than in women, in whom it is often misleading; for example, a local audit found 179 presentations for ankle oedema over 3 years of whom only 13 patients had heart failure
- what does his ECG look like?—broad complexes of left bundle branch block and a QRS width of >120 ms should prompt consideration of referral for biventricular pacemaker assessment.
Other pathology commensurate with the patient’s age group should not be forgotten. Are his symptoms worsening because of anaemia or lung pathology? According to the guideline from the Scottish Intercollegiate Guidelines Network (SIGN on the management of chronic heart failure), the GP’s investigations should include:10
- chest X-ray—to exclude the lurking lung primary in this age group as the patient may have been a smoker
- full blood count—colon cancer again becomes common at this age, and anaemia may be the reason his heart failure (or angina) has worsened
- thyroid function test
- urea and electrolytes—essential as both a baseline and for monitoring diuretic and ACE inhibitor therapy
- B-type natriuretic peptide—a marked rise would be an indication to perform an up-to-date echocardiogram
- fasting blood glucose.
A review of all the patient’s medication should be carried out. Computerised systems facilitate this, but beware the patient who ‘hoards’ old prescriptions. Take note of prescription of the following drugs:
- calcium channel blockers—these would be contraindicated in this grade of heart failure because they are negatively inotropic and offer the heart no protection against the ravages of the neuroendocrine system described above, and there is no evidence to support their use here
- aspirin use remains controversial, so a pragmatic approach should be adopted—if he is on aspirin for ischaemic heart disease it should not be stopped,10 but neither should it be started unless he experienced an upturn in angina (in which case he would be referred on anyway)
- statins—the patient may be taking these already, but, if not, one should not necessarily be started at this stage in his cardiovascular career. Results from the controlled rosuvastatin multinational trial in heart failure (CORONA)12 study on statins in heart failure are expected in 2008, which should help to clarify their use
- medication prescribed for co-morbidities should also be reviewed. The main culprits here would be anti-inflammatories—their use can be a big disadvantage as they negate the effects of heart failure therapy by causing fluid retention and further renal impairment, and every effort should be made to take patients with heart failure off these drugs
- check on what over-the-counter medication or herbal remedies the patient may be taking.13
Other pharmacological treatment that you may consider for this patient includes candesartan.10 The ‘CHARM-Added’ arm of the CHARM trial demonstrated benefits on mortality and chronic heart failure hospitalisations when candesartan was added to an optimal dose of an ACE inhibitor’.14
Spironolactone may also be beneficial in patients with moderate to severe heart failure due to LVSD,10 but is to be avoided in the presence of renal impairment or high potassium content as it can disrupt the patient’s renal function and potassium levels.15
Digoxin is worth considering for patients with heart failure who are in sinus rhythm if they are still symptomatic after optimum therapy.10
At this point, referral would probably be a sensible option, to fine tune the neurohormonal blockade outlined above, and to consider further investigation of coronary anatomy, valves, and any dyssynchrony.
What of the patient’s lifestyle? This man may be frightened, even depressed, and worried about taking any exercise for fear of making himself worse. The impact on his family and carers will be considerable. His social background is where GPs have the knowledge to help. Exercise actually improves well being and reduces hospital admissions, and a graded exercise plan should be adopted. The heart failure specialist nurse can help with this, as well as with education, and should be involved at this grade of heart failure.
Alcohol and fluid excess are no friends to a failing heart and should be addressed—even just one less pint down at the pub can help!
Depression is also common in heart failure, with prevalence rates around 50%.16 It is, however, surprisingly difficult to treat. Very few trials support antidepressant use in combination with commonly used medications. However, regular reviews by a health professional do seem to improve psychological health.
To summarise treatment of the patient in this case, I would:
- carry out baseline investigations as above
- consider using the ARB candesartan in addition to an ACE inhibitor to improve cardiovascular mortality and morbidity
- refer the patient for consideration of spironolactone in line with the guidance10
- refer the patient for consideration of resynchronisation or revascularisation therapy10
- increase community support with the heart failure specialist nurse.
Dr Nigel Rowell has received honoraria for educational activities from a number of pharmaceutical companies including Takeda UK Ltd. He is also an adviser to A. Menarini Pharmaceuticals UK Ltd.
- Studies of left ventricular dysfunction (SOLVD)—rationale, design and methods: two trials that evaluate the effect of enalapril in patients with reduced ejection fraction. Am J Cardiol 1990; 66 (3): 315–322.
- McMurray J, Ostergren J, Pfeffer M et al; CHARM committees and investigators. Clinical features and contemporary management of patients with low and preserved ejection fraction heart failure: baseline characteristics of patients in the Candesartan in Heart failure-Assessment of Reduction in Mortality and morbidity (CHARM) programme. Eur J Heart Fail 2003; 5 (3): 261–270.
- Lechat P. Beta-blockade treatment in heart failure: the cardiac insufficiency bisoprolol study (CIBIS) project. CIBIS Committees and Investigators. Cardiac Insufficiency Bisoprolol Study. J Cardiovasc Pharmacol 1990; 16 (5): S158–S163.
- Louis A, Cleland J, Crabbe S et al. Clinical Trials Update: CAPRICORN, COPERNICUS, MIRACLE, STAF, RITZ-2, RECOVER and RENAISSANCE and cachexia and cholesterol in heart failure. Highlights of the Scientific Sessions of the American College of Cardiology, 2001. Eur J Heart Fail 2001; 3 (3): 381–387.
- Garg R, Yusuf S. Overview of randomized trials of angiotensin-converting enzyme inhibitors on mortality and morbidity in patients with heart failure. Collaborative Group on ACE Inhibitor Trials. JAMA 1995; 273 (18): 1450–1456.
- McMurray J, Cohen-Solal A, Dietz R et al. Practical recommendations for the use of ACE inhibitors, beta-blockers, aldosterone antagonists and angiotensin receptor blockers in heart failure: putting guidelines into practice. Eur J Heart Fail 2005; 7 (5): 710–721.
- Dargie H. Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial. Lancet 2001; 357 (9266): 1385–1390.
- Andersson B, Lomsky M, Waagstein F. The link between acute haemodynamic adrenergic beta-blockade and long-term effects in patients with heart failure. A study on diastolic function, heart rate and myocardial metabolism following intravenous metoprolol. Eur Heart J 1993; 14 (10): 1375–1385.
- Cleland J, Loh H, Windram J. Are there clinically important differences between beta-blockers in heart failure? Heart Fail Clin 2005; 1 (1): 57–66.
- Scottish Intercollegiate Guidelines Network (SIGN 95). Management of chronic heart failure. A national clinical guideline. Edinburgh: SIGN, 2007.
- Scottish Intercollegiate Guidelines Network (SIGN 96). Management of stable angina. A national clinical guideline. Edinburgh: SIGN, 2007.
- National Institute for Clinical Excellence. Management of chronic heart failure in adults in primary and secondary care. Clinical guideline 5. London, NICE, 2003.
- Pfeffer M, Swedberg K, Granger C et al; CHARM Investigators and Committees. Effects of candesartan on mortality and morbidity in patients with chronic heart failure: the CHARM-Overall programme. Lancet 2003; 362 (9386): 759–766.
- Effectiveness of spironolactone added to an angiotensin-converting enzyme inhibitor and a loop diuretic for severe chronic congestive heart failure (the Randomized Aldactone Evaluation Study [RALES]). Am J Cardiol 1996; 78 (8): 902–907.
- Gottlieb S, Khatta M, Friedmann E et al. The influence of age, gender, and race on the prevalence of depression in heart failure patients. J Am Coll Cardiol 2004; 43 (9): 1542–1549.G