Heart failure: what it is and how it is treated

What is heart failure?

Heart failure (HF) is not a single diagnosis but a complex clinical syndrome. According to the official guidelines of the European Society of Cardiology (ESC), it is defined as a condition in which there is a structural or functional abnormality of the heart, leading to raised pressures within the cardiac chambers and/or an inability of the heart to deliver a cardiac output sufficient for the metabolic needs of the organs and tissues.

Explained in plain terms:

Think of the heart as the central pump of a house, constantly moving water through the pipes. When that pump weakens, or becomes too stiff to fill properly, it stops pushing enough blood out to the body.

When the heart begins to pump less blood, the body tries to redirect its resources to the most vital organs, such as the brain. As a result, less blood passes through the kidneys per unit of time. Because the kidneys are filtering less blood, they “assume” the body is short of fluid and begin to retain water and salt. This retained excess fluid returns to the circulation and starts to leak into the tissues and the lungs.

Causes

Heart failure is always the consequence of another underlying disease that gradually damages the heart muscle:

• Coronary artery disease and previous myocardial infarction: The most common cause. A previous heart attack causes part of the heart muscle to die and be replaced by scar tissue, which cannot contract. The remaining healthy muscle has to work twice as hard to compensate, and over time it becomes exhausted.
• Valvular disease: Stenosis or regurgitation of the aortic, mitral or tricuspid valve. These force the heart to work against persistently high pressure, or to pump the same volume of blood several times over.
• Obesity and metabolic disorders: Excess body weight dramatically increases the volume of blood the heart must pump, while also driving chronic inflammation and fatty infiltration of the myocardium.
• Endocrine disease: Diabetes directly damages myocardial cells (diabetic cardiomyopathy), while thyroid disease — whether overactive or underactive — disturbs the normal metabolism and rhythm of the heart.
• Other causes:
• Cardiomyopathies — primary diseases of the heart muscle.
• Myocarditis — inflammation of the heart muscle.
• Toxic damage (chronic alcohol use, chemotherapy).
• Uncontrolled rhythm disturbances, for example atrial fibrillation with a rapid ventricular rate.

Symptoms and clinical picture

Fluid retention and reduced blood flow account for the main features of the condition:

• Fatigue and reduced exercise tolerance: The brain and muscles do not receive enough oxygen and nutrients. Patients tire during ordinary exertion — climbing a few steps or taking a short walk — that they previously managed without difficulty.
• Breathlessness: Excess fluid collects in the lungs. This forms a physical barrier to the free passage of oxygen from the air into the blood across the alveolar membrane.
• Breathlessness and cough when lying flat (orthopnoea): In advanced stages, when the patient lies down, fluid from the lower limbs redistributes back towards the chest. This raises the pressure in the lungs and provokes coughing — often at night — and breathlessness, forcing patients to sleep propped up on several pillows or even sitting.
• Passing urine at night (nocturia): During the day, while standing, the kidneys work with difficulty because of gravity and the reduced pumping capacity of the heart. At night, lying down, blood flow to the kidneys temporarily improves, which increases urine production and causes frequent waking.
• Swelling of the legs (peripheral oedema): This appears around the ankles and lower legs, because fluid pools in the lowest parts of the body during the day.
• Swelling that eases by morning: Because the body lies flat overnight, fluid redistributes evenly and the kidneys filter more effectively. For most patients the swelling in the legs is therefore markedly reduced, or temporarily gone, in the morning.

The link with high blood pressure, and why treatment matters

Arterial hypertension (high blood pressure) is the most common condition accompanying heart failure. The relationship runs both ways:

• High pressure forces the heart to pump against great resistance, which leads first to thickening of the muscle, then to dilatation and exhaustion.
• Once heart failure is established, inadequate control of blood pressure further worsens the pumping function.

Without correct and timely treatment, the two conditions enter a vicious circle. They cannot be controlled in isolation and quickly lead to vascular complications — myocardial infarction, stroke, progressive kidney failure and severe pulmonary crises.

How is the diagnosis made?

A diagnosis of heart failure is made only by a doctor specialising in cardiology, on the basis of a combined assessment:

• Clinical examination: Assessment of symptoms, listening to the heart and lungs, checking for oedema and measuring blood pressure.
• Electrocardiogram (ECG): Helps detect signs of a previous heart attack, rhythm disturbances or thickening of the heart muscle.
• Echocardiography (ultrasound of the heart): The single most important imaging method. It allows direct visualisation of the structure of the heart, the thickness of the walls and the function of the valves, and measurement of the ejection fraction.
• Laboratory tests and natriuretic peptides (BNP / NT-proBNP): Natriuretic peptides are specific protein markers released into the blood by the heart when it is subjected to stretch — that is, overloaded with volume or pressure. Normal levels almost always, though not invariably, rule out heart failure, while high levels confirm the diagnosis and indicate its severity.

Treatment according to the European Society of Cardiology (ESC): the “four pillars”

Modern drug treatment of heart failure with reduced ejection fraction rests on foundational therapy known as the four pillars. These medicines should be started as early as possible, as they are proven to save lives and reduce hospital admissions:

• RAAS / ARNI inhibitors:
• ACE inhibitors (ACEi) or angiotensin receptor blockers (ARBs).
• Where possible, an ARNI (sacubitril/valsartan) is preferred — a newer medicine that replaces the ACE inhibitor or ARB and blocks two damaging pathways at once.
• Beta blockers: They prevent the harmful effect of stress hormones (adrenaline and noradrenaline) on the heart, slow the pulse and allow the heart to rest and fill more effectively.
• Mineralocorticoid receptor antagonists (MRAs): For example spironolactone or eplerenone — they block the hormone aldosterone, reduce salt and fluid retention and prevent fibrosis, the replacement of healthy muscle by scar tissue.
• SGLT2 inhibitors: For example dapagliflozin or empagliflozin. Originally developed to treat diabetes, these medicines have transformed cardiac protection. They help the kidneys excrete excess sugar and sodium and improve the energy metabolism of the heart muscle. Patients are often puzzled to be prescribed a “diabetes drug” by their cardiologist when they do not have diabetes.

Additional medicines, depending on the clinical picture:

• Diuretics (loop diuretics): Very important for rapid relief of breathlessness and swelling, by increasing the excretion of excess fluid.
• Ivabradine: For patients with a high heart rate who are already on the maximum dose of a beta blocker.
• Vericiguat, digoxin, iron preparations (where iron is deficient) and other specific treatments according to the individual patient.

Future articles will look in more detail at each component of the assessment and treatment of heart failure.