Heart Failure (Heart Failure audit)

Whether due to problems arising from coronary artery or valve disease, inherited heart muscle abnormalities (‘cardiomyopathies’), inflammation of the heart (‘myocarditis’) or other causes, the chambers of the heart may increase in size and contractile function of the left and right ventricles may reduce. (When that reduction in function is of the left ventricle, this is referred to as “heart failure with reduced ejection fraction” or HFrEF). This may be associated with fatigue and breathlessness, though occasionally it is relatively asymptomatic, and may be associated with dangerous heart rhythm abnormalities and a reduced survival rate. The left ventricular ejection fraction is a measure of the pumping capability of the heart, usually assessed with an echocardiography scan. This ejection fraction is used to distinguish different types of cardiac dysfunction and identify treatments which may be beneficial in some, but not all, patients.

Symptoms may similarly occur in people who develop thickened heart muscle, again from a variety of causes. The cardiac muscle, which is often described as being stiff retains the ability to contract or pump but does not relax normally. The cavity of the main heart chamber can reduce in size, and this leads to back pressure on the blood vessels in the lungs. The ensuing syndrome of heart failure can be exactly the same, but this combination is referred to as ‘heart failure with preserved ejection fraction’ or HFpEF, with its own treatment options.

Historically, symptoms of heart failure could only be improved by the use of diuretics (‘water tablets’) and in some people by the use of digoxin, but over the last twenty five years, or so, new treatments have had a substantial impact on reducing the rate of deterioration of heart muscle problems, making the patients less prone to dangerous heart rhythm abnormalities and have helped improve symptoms, quality of life, and life expectancy. These ‘disease-modifying treatments’ for people with HFrEF include beta blockers, mineralocorticoid receptor antagonists (MRAs) and ACE-inhibitors (ACEis) or angiotensin receptor blockers (ARBs). More recently, the Angiotensin-Neprilysin Inhibitor (ARNI) sacubitril valsartan has emerged as a replacement for ACEi or ARBs in certain patients with chronic heart failure. And most recently a new class of drugs, the SGLT2 inhibitors, including dapagliflozin and empagliflozin have also been shown to confer benefit for patients with HFrEF.

Certain patients who remain symptomatic on optimal therapy, can be identified from characteristics seen on their electrocardiograms (ECGs), alongside repeat echocardiography, as people who are likely to benefit from a particular form of pacemaker known as cardiac resynchronisation therapy, or CRT. Patient well-being and outcomes can be transformed with this treatment. These devices may also be able to monitor the patient’s heart rhythm and provide special pacing techniques or shock treatment should any life-threatening rhythms occur. Other devices provide these functions but without the resynchronisation function – so called implantable cardioverter defibrillators (ICDs).

To date most of the emerging research studies shown to deliver improved outcomes have been in patients with HFrEF, but there are still important treatments available for those with HFpEF. Ongoing research continues to try and identify drugs that will improve outcomes for people with HFpEF, in the way it has for those with HFrEF.

Heart Failure Summary Report 2023

National Heart Failure Audit 2023 Summary Report  (updated October 2023)

Key messages document and Line of Sight table