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Heart failure

Management of heart failure in people with diabetes


Page 5 of 8:
Summary
Diabetes and heart failure
Early signs of heart failure
How is heart failure detected?
Treatment options for heart failure
Which treatment options are suitable?
Tight glycaemic control and minimising risks
Treatment for diabetes with heart failure
References

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Pharmacological options
Non-pharmacological options

The main goal of therapy in heart failure is to treat the underlying cause of the left ventricular dysfunction and remove all the precipitating factors, thus improving the quality of life and length of survival. This means that therapy should be targeted towards relief of both pulmonary and systemic congestion in the short term, and slowing of the progression and potentially reversing the course of left ventricular dysfunction and prolonging survival in the long term. These can both be targeted with the use of either non-pharmacological or pharmacological approaches.

Initially, attention should be directed at reducing the standard coronary risk factors. This is particularly important in people with diabetes when aiming to prevent the development of heart disease as well as preventing the progression of heart disease to heart failure.

Steps to minimise the risks include:

• stopping smoking.
• losing weight (where necessary).
• limiting alcohol consumption.
• dietary changes.
• exercising.
• lowering cholesterol levels.
• lowering blood pressure.

Recommendations for cholesterol levels can be seen in the Viewpoint on Revascularisation procedures in coronary heart disease.

Pharmacological options

Even when patients successfully control their lifestyle risk factors for heart failure, most will still need medication and many receive two or more drugs. The pharmacological agents available for the treatment of heart failure are outlined below.

1. ACE inhibitors
ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II and are used in the treatment of hypertension, heart failure and diabetic nephropathy. The SOLVD, CONSENSUS, and VHEFT II trials all demonstrated improved survival in people with heart failure with the use of ACE inhibitors [Cohn et al, 1986; Cohn et al, 1991; Pfeffer et al, 1992; The CONSENSUS Trial Study Group, 1987; The SOLVD Investigators, 1992]. Both the HOPE and TRACE studies demonstrated the beneficial effects of ACE inhibitors and found that these were more profound in people with diabetes when compared with those without diabetes [Gustafsson et al, 1999; Heart Outcomes Prevention Evaluation Study Investigators, 2000; Yusuf et al, 2000]. These findings imply that ACE inhibitors have anti-ischemic and anti-remodelling effects that appear to be interrelated [Lavine and Gellman, 2002].

However, ACE inhibitors may not be effective in all patients. Initiation of ACE inhibitor treatment is contraindicated in bilateral renal artery stenosis and angioedema during previous ACE inhibitor therapy [Remme and Swedberg, 2001]. These agents are excreted by the kidneys and may accumulate in people with renal insufficiency. In addition to this, ACE inhibitors also inhibit bradykinin degradation, which may be responsible for the cough sometimes seen with their use [Lavine and Gellman, 2002].

ACE inhibitors are currently the only pharmacological agents that have been demonstrated to halt the transition from left ventricular dysfunction to heart failure. However, the dosages used are often too low and care should be taken to ensure the maximum effect is achieved [Lavine and Gellman, 2002].

2. Diuretics
Diuretics promote the excretion of urine. Loop diuretics are the main class of diuretics used in heart failure. By blocking ion transport in the loop of Henle, they help avoid volume overload. However, they can cause potassium depletion, prerenal azotemia and other electrolyte disorders, which can become more acute in the setting of renal insufficiency, as can be seen in some people with diabetes [Lavine and Gellman, 2002]. If hyperkalaemia persists, the patient may be switched to potassium-sparing diuretics [Remme and Swedberg, 2001].

Care should be taken to ensure diuretics are used appropriately as overuse may produce fatigue and electrolyte imbalance, and underuse can cause congestion [Lavine and Gellman, 2002].

3. Beta-blockers
Beta-blockers were initially contraindicated in people with heart failure but now have an important role in symptomatic relief and survival benefits. Beta-blockers have demonstrated improvements in ejection fraction, reductions in risk of heart transplant and mortality [Heidenreich et al, 1997; Lechat et al, 1998; Merit-HF Study Group, 1999; The International Steering Committee, 1997; Waagstein et al, 1993]. Results from the MOCHA trial suggested that higher doses are more advantageous [Cohn et al, 1997; Merit-HF Study Group, 1999; Zuanetti, 2000]. However, the general rule is to start at very low doses and uptitrate to the wanted effect. If the patient experiences side effects, efforts should be made not to discontinue beta-blocker therapy, as their proven efficacy is sizeable [Cohn et al, 1997]. It has also been suggested that the effects of this therapy may be even greater in people with diabetes [Lavine and Gellman, 2002].

4. Inotropic agents
Inotropic agents, including digoxin, increase the force of contraction of cardiac muscle. Although digoxin has been used for over 30 years, its efficacy has only recently been established. Digoxin exerts its effects on the force of contraction by increasing the availability of myocardial calcium, increasing ejection fraction, reducing symptoms, improving exercise capacity and decreasing the number of hospitalisations [Garg, 1996; Packer et al, 1993]. Its effect on mortality is neutral, but it does appear to work across the severity spectrum, including patients with diabetes [Garg, 1996].

5. Vasodilators
The use of vasodilators, such as nitrates, has now been superceded by the use of ACE inhibitors. However, the use of hydralazine has demonstrated efficacy in improving survival, increasing ejection fraction and reducing symptoms, even if its effects are not as salutary as ACE inhibitors [Cohn et al, 1986; Cohn et al, 1991]. For this reason, isosorbide dinitrate and hydralazine are often recommended for those patients who are unable to tolerate ACE inhibitors. It must also be remembered that the use of nitrates alone may assist with symptoms of pulmonary congestion and angina in patients with left ventricular dysfunction and coronary artery disease [Lavine and Gellman, 2002].

6. Angiotensin II receptor antagonists
Angiotensin II receptor antagonists have a similar effect to ACE inhibitors but do not have as many associated renal problems [Cody et al, 1988; Textor, 1997]. However, those patients who are intolerant to ACE inhibitors may also be intolerant of this therapy [Lavine and Gellman, 2002].

Recently, the angiotensin II inhibitor losartan has been shown to increase parasympathetic activity in the heart. This implies that angiotensin II inhibitors could slow the progression of autonomic dysfunction, which is associated with increased mortality [Maser and Lenhard, 2002]. However, more research is needed in this area.

7. Aldosterone antagonists
Aldosterone antagonists reduce mortality and hospitalisation when used in addition to maintenance therapy (digoxin, diuretic and ACE inhibitor) [Pitt et al, 1999].

8. Calcium channel antagonists
Calcium channel antagonists are rarely used as a main therapy for heart failure but some may be useful in the therapy of hypertension in people with heart failure [Lavine and Gellman, 2002].

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Non-pharmacological options

1. Sodium intake
Controlling sodium intake is more important in the management of advanced heart failure than in mild heart failure [Remme and Swedberg, 2001]. Sodium restriction assists with fluid volume control and minimizes the dosage of heart failure drugs used [McConaghy and Smith, 2002]. However, salt substitutes should be used with caution, as they may contain potassium. In large quantities, in combination with an ACE inhibitor, they may lead to hyperkalaemia [Good et al, 1995].

2. Exercise training
Patients with stable heart failure should be encouraged to carry out daily physical and leisure time activities that do not induce symptoms [McConaghy and Smith, 2002; Remme and Swedberg, 2001]. Moderate exercise can prevent muscle de-conditioning and improve quality of life [Tokmakova et al, 1999]. However, strenuous or isometric exercises should be discouraged and work tasks assessed for suitability [Remme and Swedberg, 2001].

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