Heart failure has many causes, and several can coexist in the same person. Coronary artery disease is one of the most important causes because reduced blood flow to the heart muscle can produce myocardial infarction, permanent scar tissue and impaired ventricular contraction. Repeated or extensive myocardial injury can reduce the amount of functioning muscle available to pump blood.
Longstanding high blood pressure is another major cause because the left ventricle must generate higher pressure to eject blood into the systemic circulation. Over time, this pressure overload can cause ventricular hypertrophy, impaired relaxation and eventually structural and functional deterioration. Valve diseases can also cause heart failure by producing chronic pressure or volume overload. A narrowed valve increases the pressure required to move blood through it, while a leaking valve allows blood to flow backwards and forces the heart to handle an abnormal volume.
Cardiomyopathies are another important group of causes. Dilated cardiomyopathy involves ventricular enlargement and impaired systolic contraction and can have genetic, infectious, toxic, inflammatory or metabolic causes. Hypertrophic cardiomyopathy is characterised by abnormal myocardial hypertrophy and can impair ventricular filling; some forms are inherited through variants affecting sarcomeric proteins. Restrictive cardiomyopathies produce impaired ventricular filling because the myocardium becomes abnormally stiff. Arrhythmogenic cardiomyopathies can involve structural and electrical abnormalities that increase the risk of ventricular arrhythmias and cardiac dysfunction. Some cardiomyopathies are idiopathic, meaning no cause is identified despite investigation. Others are secondary to alcohol, certain medications or toxins, endocrine disorders, nutritional deficiencies, inflammatory conditions or genetic disease. Identifying the cause is important because treatment can differ substantially depending on the underlying mechanism.
Myocardial inflammation can cause heart failure. Myocarditis is inflammation of the heart muscle and can follow viral infection or result from other infectious, autoimmune or inflammatory processes. Severe myocarditis can impair contraction, provoke arrhythmias or cause cardiogenic shock. Certain systemic inflammatory disorders can also affect the myocardium or cardiac vessels. Infections can damage the heart through direct tissue injury, immune-mediated mechanisms or chronic structural effects.
Some parasitic infections are important causes of cardiomyopathy in particular geographic regions, while rheumatic fever can produce chronic rheumatic valve disease. These causes are less common in some high-income countries than coronary disease and hypertension but remain clinically relevant, particularly when a patient's age, travel history, exposures or systemic symptoms suggest an alternative mechanism.
Abnormal heart rhythms can contribute to heart failure when they substantially impair cardiac performance or persist for long periods. Persistent tachycardia can reduce ventricular filling time and increase myocardial oxygen demand, while very slow heart rates can reduce cardiac output. Atrial fibrillation can worsen ventricular filling because the atria no longer contract in a coordinated way, and rapid ventricular rates can place additional strain on the ventricles.
Certain sustained ventricular arrhythmias can directly impair cardiac output and cause severe haemodynamic instability. Conversely, heart failure can itself promote arrhythmias through chamber enlargement, fibrosis, neurohormonal activation and electrical remodelling. This creates a bidirectional relationship in which arrhythmia and structural heart disease can reinforce one another.
Congenital heart disease can cause heart failure when structural abnormalities produce abnormal blood flow or excessive workload on the heart. Large left-to-right shunts can increase pulmonary blood flow and volume load, while obstructive lesions can create pressure overload. Some congenital abnormalities are repaired early and may not cause heart failure for many years, whereas others can produce chronic physiological consequences despite correction. Pregnancy can also precipitate or reveal heart failure in susceptible individuals.
Peripartum cardiomyopathy is a form of dilated cardiomyopathy that develops toward the end of pregnancy or in the months following delivery. Its causes are incompletely understood and involve complex genetic, hormonal, vascular and inflammatory mechanisms. It is distinct from ordinary fluid retention or breathlessness of pregnancy and requires medical assessment when significant cardiac symptoms occur.
Systemic diseases and metabolic disorders can damage cardiac function or increase its workload. Severe anaemia reduces the blood's oxygen-carrying capacity, potentially increasing cardiac output demands. Thyroid disease can affect heart rate, contractility and vascular resistance; hyperthyroidism can promote tachyarrhythmias, while hypothyroidism can contribute to altered cardiovascular function. Kidney disease can promote hypertension, fluid retention and metabolic disturbances that strain the cardiovascular system. Diabetes contributes to coronary artery disease and can also be associated with diabetic cardiomyopathy. Sleep-disordered breathing, obesity and other metabolic conditions can increase cardiovascular workload and are associated with heart-failure risk. Some chemotherapy agents and other drugs can have direct cardiotoxic effects, making treatment history important when investigating unexplained ventricular dysfunction.
Environmental and behavioural factors influence the probability of several underlying diseases rather than acting as a single universal cause. Smoking increases cardiovascular risk, poor dietary patterns can contribute to hypertension and metabolic disease, excessive alcohol exposure can cause or worsen cardiomyopathy, and physical inactivity is associated with several cardiovascular risk factors. Genetic predisposition can influence coronary disease, cardiomyopathies, arrhythmias and other conditions.
Age increases the prevalence of heart failure because cumulative exposure to hypertension, coronary disease, valve disease and other cardiac insults increases over time, although heart failure is not an inevitable consequence of ageing. In many patients, the final syndrome reflects multiple interacting causes, such as hypertension and coronary artery disease together, rather than one isolated abnormality.
The cause of heart failure matters because treatment is partly directed at the underlying disease. Coronary disease may require revascularisation or intensive secondary prevention, valve disease may require intervention, tachyarrhythmias may require rate or rhythm management, and specific cardiomyopathies may require genetic assessment, disease-specific therapy or device treatment. Some causes are reversible or partially reversible when identified early, while others produce permanent structural damage.
Clinical evaluation therefore considers the patient's history, cardiovascular risk factors, medication and toxin exposure, family history, electrocardiogram, echocardiogram, laboratory tests and sometimes coronary imaging or cardiac magnetic resonance. Heart failure should not be regarded as a single condition with one cause; it is the endpoint of numerous processes that impair cardiac contraction, relaxation, filling or pressure handling.
