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Heart failure treatment strategies in primary care

In the second article of a two-part feature on heart failure, Professor Bun Tan answers GP Dr Stefan Cembrowicz's essential questions on treatment

In the second article of a two-part feature on heart failure, Professor Bun Tan answers GP Dr Stefan Cembrowicz's essential questions on treatment

1. Our PCT introduced a heart failure algorithm, but it didn't mention the use of digoxin. The last heart failure patient I saw was in fast atrial fibrillation (pulse 130 beats per minute) and might not have survived the wait for an ECHO as mandated. When and how should digoxin be used nowadays?

There are two properties of digoxin which are useful therapeutically:

• slowing the AV node conduction: for example for rate control of fast atrial fibrillation

• positive inotropic effects to improve myocardial contractility.

You are quite right in using it to treat fast atrial fibrillation in the heart failure patient you mentioned without waiting for the echocardiographic results. Two points are relevant here. Atrial fibrillation can be diagnosed clinically (irregularly irregular pulse, apico-radial deficits, absence of 'a' wave in the jugular venous pulsation). An ECG would confirm it. The presence of heart failure symptoms and signs can often be established clinically without recourse to echocardiography.While the use of digoxin to control ventricular rates in fast atrial fibrillation is widely accepted, that for its positive inotropism has attracted much more controversy. One reason is that the positive inotropic effect of digoxin is difficult to detect in a patient at rest (hence the scientific confusion), but becomes manifest during exercise. Because of this unusual property, digoxin approaches the property of an ideal inotrope – it is not desirable to flog the failing heart unnecessarily at rest, but it kicks in during exercise when the chronic heart failure patient really needs the extra inotropic support to ameliorate exercise intolerance. In a large-scale randomised placebo-controlled trial, it reduced hospitalisation rates of heart failure patients and did not show any increase in mortality. Digoxin is still the only orally active agent licensed for use as a positive inotropic agent to treat heart failure. There are now two main types of treatment for heart failure:

• for prophylactic purposes to improve prognosis (prolong life and reducing frequency of hospital readmissions)

• for functional reasons to improve quality of life, such as symptomatic relief and improving exercise tolerance.

The drugs that are mainly prescribed for prognostic improvement are certain ß-blockers (see below), ACE inhibitors, angiotensin receptor blockers (ARBs) and aldosterone antagonists; drugs which are useful to improve symptoms and exercise ability include diuretics and digoxin.With the latter, the prescriber can start, stop and adjust the dose according to responses and the patient can tell us whether s/he has improved or not, remembering that it has a rather narrow therapeutic window. However, with the former, no one can tell whether the patient has derived any benefit prognostically, except by making the assumption that s/he will behave the same way as the average participants in the large-scale trials that provided the evidence for efficacy.

2. What is the place for ß-blockers in the management of heart failure?

In 1996 a paper in the NEJM showed heart failure patients treated with ß-blockers had reduced mortality, and this has been confirmed by other subsequent trials. ß-blockers are now specifically indicated to treat heart failure patients.

ß-blockers are powerful negative chronotropic and inotropic agents and, in sufficiently high doses, can depress the myocardial contractile force of failing hearts enough to cause shock or death. The negative chronotropic effect is easily detected by the slowing of the heart rate. In general, it is best to avoid bradycardia of below 50 beats per minute at rest. In chronic heart failure, the sympathetic system is activated and the catecholamines released are cumulatively toxic to the cardiac myocytes. This leads to further losses of contractile elements in the failing heart resulting in progressively hastened deterioration of cardiac dysfunction. ß-blockers are the most effective means to reduce these catecholamine-induced harmful effects.This is probably the most important factor explaining the beneficial effects of ß-blockers in trials of chronic heart failure patients in the past decade. To gain this beneficial effect of ß-blockade therapy, clinicians need to avoid the acute cardiodepressant effects and introduce ß-blockade with very low doses, and titrate the dosage upwards cautiously and slowly over weeks and months (for example carvedilol 3.125mg bd increasing to 25mg bd, or bisoprolol 1.25mg bd increasing to 10mg od). ß-blockers are still contraindicated in acute heart failure and severe decompensated heart failure. During exacerbation of chronic heart failure, the ß-blockade dosage may also need to be temporarily reduced or stopped, and reintroduced later if tolerated. Patients with other contraindications to ß-blockers, such as confirmed asthma or peripheral vascular disease, would not be able to benefit from ß-blockade therapy for heart failure.

3. What non-drug measures are important in the treatment of heart failure, for example, salt and fluid restriction? How much fluid per day and how much alcohol can patients drink? What about regular weighing and flu vaccines? What is the risk from NSAIDs?

These non-drug treatments are as important as and complementary to pharmacological therapy of heart failure.

• Strict fluid balance is essential. Ask patients to chart daily weights (using an accurate and reliable scale), limit fluid and salt intake (daily fluid not to exceed 1.5 l/day, no added salt, avoid salty food or drugs containing much sodium), and advise patients to adjust their diuretics dosage up and down to maintain a constant ideal body weight. Be careful to prevent the situation when the patient has to drink enough to catch up with over-diuresis having been over treated with diuretics.

• Related to the above point are education and monitoring by clinicians, including reviewing patients' weight charts, their electrolyte balance and renal function.

• Alcohol produces four undesirable effects in heart failure patients: – extra fluid volume loading in the case of beer and lager– propensity to precipitate atrial fibrillation which can worsen heart failure symptoms markedly– cardiotoxicity of ethanol is well-known, and in patients who already have reduced number of cardiomyocytes, this will hasten their cardiac demise– ethanol is also a known cardiodepressant; advise abstinence or only in limited quantities.– All attempts to avoid exacerbation of heart failure should be implemented, and these include flu vaccination, asking patients to avoid (if possible) close contacts with persons suffering from upper respiratory tract infection. Early signs of any form of infection (tooth abscess, urinary tract infection, cholecystitis) should trigger aggressive treatment.– Weight reduction for overweight or obese heart failure patients.– Avoid NSAIDs and other agents likely to impair renal function (ACE inhibitors and ARBs in patients with renal artery stenosis), and agents likely to retain fluid (steroid, some calcium antagonists, glitazones, liquorice, ginseng), or use with caution and under close supervision and monitoring.

4. Is exercise therapy valuable?

The heart is a muscular organ, and functions best by being conditioned with regular exercise. Trials show that exercise training of heart failure patients confer significant benefits. Both aerobic and strength training are beneficial.

Advise patients to exercise within their physical limits (about 70-85 per cent of their peak exercise heart rate), ideally at least 30 minutes a day and three or more times a week. Patients should avoid exercises when they are infected (such as coryza, flu). Exercise therapy is contraindicated in patients suffering from heart failure during active viral myocarditis or endocarditis.

5. What is the place for biventricular pacing?

In heart failure patients with ventricular contractile dyssynchrony (for example LBBB with QRS duration >120ms, or echocardiographic evidence of dyssynchronous contraction), cardiac resynchronisation therapy (CRT) via atrio-biventricular pacing is the only treatment in recent randomised controlled trials to produce the four main desirable outcomes of heart failure therapy – improving:

• symptoms • exercise capacity • rates of hospitalisation • longevity.

None of the pharmacological agents (ß-blockers, ACE inhibitors, ARBs, aldosterone receptor blockers) could produce such a 'royal flush' of desirable outcomes. So far the indication for CRT is limited to heart failure patients in the New York Heart association (NYHA) class III or worse.

6. For patients terminally ill at home, when should home oxygen be started? What other measures may be helpful at this stage?

The first point to make here is that labelling any heart failure patient as terminal or end-stage should not be undertaken lightly. Ideally very ill heart failure patients should be checked by a specialist cardiologist. Once this diagnosis has been correctly made, it is necessary to consider withdrawing therapies aimed at prolonging life (for example implanted ICD, ß-blockers, ACE inhibitors, ARBs) provided the withdrawal is not accompanied by any symptomatic or functional deterioration.

Therapies aimed at relieving any distressing symptoms, including domiciliary oxygen, analgesics and sedatives, may need to be introduced whenever appropriate. Cardiac drugs which aim to improve or control symptoms and function, such as diuretics, digoxin and nitrates, should not be discontinued, and the dose adjusted as necessary (for example, reduce/stop diuretics if the patient has inadequate fluid intake).

Bun Tan is a consultant cardiologist at Leeds General Infirmary

Competing interests None declared

Take-home points

• The positive inotropic effect of digoxin is difficult to detect in a patient at rest, but is seen during exercise so it approaches the property of an ideal inotrope: it improves quality of life by symptomatic relief and also exercise tolerance.

• To gain the beneficial effect of ß-blockade, avoid the acute cardiodepressant effects and introduce ß-blockade with low doses, and titrate upwards cautiously and slowly over weeks and months.

• ß-blockers are still contraindicated in acute heart failure and severe decompensated heart failure: during exacerbation of chronic heart failure the ß-blockade dosage may need to be temporarily reduced or stopped, and reintroduced later if tolerated.

• Daily fluid should not exceed 1.5 l/day, and patients should adjust their diuretics dosage up and down to maintain a constant ideal body weight.

• Trials show exercise training confers significant benefit; both aerobic and strength training are beneficial.

What I will do now

Dr Cembrowicz responds to the answers to his questions

• Be pleased that I put my patient on digoxin; happily they survived and were then able to go on the ECHO waiting list.

• Remind the PCT about the omission of digoxin in their 'guidelines'!

• Reflect that the old drugs reduce symptoms, the new drugs improve prognosis. The old ways are sometimes the best.

• Be aware that cautious titrated introduction of cardioselective ß-blockers is an important part of heart failure management.

• Observe that the toxic effect of catecholamines is intuitively apparent in many patients – now we know why stress is so bad for you.

• Regularly weigh heart failure patients; easy to do and can help manage heart failure.

• Advise that fluid restriction is important – although many patients believe the opposite.

• Tactfully nudge my obese, beer-drinking patients towards lower volume drinks or even abstinence.

• Watch out for sepsis as a cause of deteriorating heart failure.

• Think of patients with end-stage heart failure as comprising an important aspect of terminal care. Withdrawal of (newer) life-prolonging therapies in favour of (older) symptom-reducing ones is quite a major concept.

Stefan Cembrowicz is a GP in Bristol

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