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Cardiac Condition
Heart Failure
When the heart cannot pump efficiently enough to meet the body's demands. Modern treatment — including carefully titrated medication — can transform quality of life and significantly improve long-term outcomes.
Overview
What Is Heart Failure?
Heart failure is a clinical syndrome in which the heart is unable to pump sufficient blood to meet the body's demands — or can only do so at the cost of abnormally elevated filling pressures within the heart.
The term "heart failure" does not mean the heart has stopped. It means the heart's pumping capacity has been compromised — by damage to the heart muscle, stiffening of its walls, or a structural problem — to the point where it can no longer meet the body's normal requirements without difficulty. Most patients live active lives with the condition, provided it is diagnosed and treated appropriately.
Cardiologists classify heart failure by measuring the ejection fraction — the proportion of blood the left ventricle pumps out with each heartbeat. A normal ejection fraction is 55% or above. This single measurement has profound implications for which treatments are effective.
HFrEF
Reduced Ejection Fraction
Ejection fraction below 40%. The heart muscle is weakened and pumps less blood than normal. This is the form with the most established evidence base for drug therapy.
HFmrEF
Mildly Reduced Ejection Fraction
Ejection fraction of 40–49%. A transitional category — may represent a recovering or deteriorating heart. Treatment follows similar principles to HFrEF.
HFpEF
Preserved Ejection Fraction
Ejection fraction 50% or above, but the heart muscle is stiff and does not relax properly. Common in older patients and those with hypertension or diabetes. Increasingly treatable with modern agents.
Heart failure affects over one million people in the UK. Despite significant advances in treatment over the past decade, it remains a serious condition that requires expert monitoring and active management. With the correct treatment, many patients see meaningful improvements in their symptoms, exercise capacity, and life expectancy.
Aetiology
What Causes Heart Failure?
Heart failure arises from any condition that damages, weakens, or overburdens the heart muscle over time. Identifying the underlying cause is essential — the right treatment depends on it.
- Coronary artery disease The most common cause. One or more heart attacks damage portions of the heart muscle permanently, reducing overall pump function. Even without a recognised heart attack, chronic reduced blood supply can gradually weaken the muscle.
- High blood pressure Sustained hypertension forces the heart to pump against abnormally high resistance, causing the muscular walls to thicken and eventually stiffen. This is the principal driver of HFpEF.
- Dilated cardiomyopathy The heart muscle weakens and the chambers enlarge without a clear obstructive cause. May be genetic, viral (post-myocarditis), or idiopathic. The most common presentation of HFrEF in younger patients.
- Valve disease Severe aortic stenosis or mitral regurgitation imposes chronic pressure or volume overload on the heart muscle. Heart failure secondary to valve disease is often reversible once the valve is repaired or replaced.
- Atrial fibrillation Persistent AF with an uncontrolled rapid ventricular rate can cause tachycardia-mediated cardiomyopathy — a reversible form of heart failure that recovers when the rate is controlled or rhythm restored.
- Alcohol & toxins Heavy alcohol use causes a direct toxic cardiomyopathy. Certain chemotherapy agents — notably anthracyclines and some targeted therapies — carry a risk of cardiac toxicity requiring monitoring.
- Inherited conditions Hypertrophic cardiomyopathy, familial dilated cardiomyopathy, and storage disorders (such as cardiac amyloidosis) are increasingly recognised causes, particularly in patients presenting at a younger age.
In some patients, more than one cause coexists. A thorough investigation — including cardiac imaging and sometimes genetic testing — is required to identify the primary driver and guide treatment correctly.
Identifying the underlying cause is the cornerstone of effective heart failure management
Coronary Expertise Dr Nijjer has dedicated his career to understanding coronary blood flow. Where heart failure is driven by coronary artery disease, his expertise in coronary physiology and intervention places him uniquely to address the underlying cause — not only the consequences.
How It Presents
Symptoms of Heart Failure
Heart failure symptoms arise because the failing heart cannot maintain adequate forward circulation — leading to fluid accumulation in the lungs and body, and reduced delivery of oxygen to the tissues.
Breathlessness Ankle swelling Fatigue Orthopnoea Paroxysmal nocturnal dyspnoea Reduced exercise tolerance Palpitations
Breathlessness on exertion is the most common presenting symptom. Patients notice they cannot walk as far or climb stairs as easily as before. As the condition progresses, breathlessness may occur with minimal activity or even at rest.
I have to sleep propped up on three pillows — if I lie flat I can't breathe
I wake in the night gasping — I have to sit at the edge of the bed for half an hour
My ankles are puffy by the evening and my shoes feel tight by mid-afternoon
Orthopnoea — breathlessness on lying flat — occurs because fluid redistributes from the legs to the lungs when supine. Patients describe needing increasing numbers of pillows to sleep. Paroxysmal nocturnal dyspnoea is the sudden awakening from sleep, often hours after falling asleep, with severe breathlessness and a need to sit upright or open a window.
Peripheral oedema — ankle and leg swelling — reflects fluid accumulating in the tissues as venous pressure rises. In severe cases, this can extend above the ankles to the calves and even the abdomen (ascites).
Heart failure symptoms may develop gradually over months. Many patients initially attribute breathlessness to ageing or deconditioning and delay seeking help. Early diagnosis allows treatment to begin before the heart deteriorates further.
Acute Heart Failure — EmergencySudden, severe breathlessness at rest — especially if accompanied by frothy or pink-tinged sputum, profound sweating, or collapse — represents acute pulmonary oedema. Call 999 immediately.
Investigation
Diagnosing Heart Failure
The diagnosis of heart failure is confirmed by a combination of symptoms, clinical examination, blood tests, and cardiac imaging. Dr Nijjer will build a precise picture of the type, severity, and underlying cause before formulating a treatment plan.
Investigations are selected according to clinical context — some patients are referred following an acute hospitalisation; others present to the cardiology outpatient clinic with gradually worsening breathlessness. In both cases, the aim is the same: to characterise the heart's function completely and identify any reversible cause.
- BNP / NT-proBNP Brain natriuretic peptide — a blood marker released by the heart under stress. An elevated level strongly supports the diagnosis of heart failure and correlates with severity. Serial measurements also track treatment response.
- ECG May reveal left ventricular hypertrophy, evidence of prior heart attack, bundle branch block (important for device therapy decisions), or atrial fibrillation as a contributing cause.
- Chest X-ray Demonstrates cardiac enlargement, pulmonary congestion (fluid in the lung fields), or pleural effusions — all characteristic of decompensated heart failure.
- Echocardiogram The cornerstone investigation. Measures ejection fraction, assesses left ventricular wall motion, identifies valve disease, and estimates filling pressures. Guides the choice of drug therapy and device eligibility.
- Cardiac MRI The gold standard for measuring ejection fraction precisely and characterising the heart muscle in detail. Can identify scarring (late gadolinium enhancement), myocarditis, infiltrative disease (amyloid, sarcoid), and iron overload — all of which alter treatment.
- Coronary angiography Indicated in most patients with newly diagnosed heart failure to determine whether coronary artery disease is the underlying cause — and whether it is amenable to angioplasty or bypass surgery. Dr Nijjer performs simultaneous pressure-wire assessment to identify which narrowings are truly compromising blood flow.
- Blood tests Full blood count, renal function, electrolytes, liver function, thyroid function, iron studies, and HbA1c — all interact with heart failure management and guide medication choices and dosing.
- Genetic testing Recommended in patients with a family history of heart failure, cardiomyopathy, or sudden cardiac death, and in younger patients without an obvious cause. Identifies inherited conditions and allows family members to be screened.
Echocardiography and cardiac MRI establish the type of heart failure and guide every treatment decision that follows
The New York Heart Association (NYHA) functional class is used to grade symptom severity on a scale of I–IV and is used alongside imaging to monitor progress over time and guide treatment escalation.
Expert Coronary Assessment Where heart failure may be ischaemic in origin, Dr Nijjer's specialist expertise in coronary physiology and intracoronary imaging allows him to determine precisely whether revascularisation — angioplasty or bypass — is likely to improve cardiac function.
Guideline-Directed Medical Therapy
Treating Heart Failure — The Four Pillars
For patients with heart failure with reduced ejection fraction (HFrEF), international guidelines now support four classes of drug — the four pillars of GDMT — each proven in large clinical trials to reduce mortality and hospitalisation. All four should be initiated and titrated to target dose in every eligible patient.
1
ACE Inhibitor or ARNI
Ramipril / Sacubitril-Valsartan
Blocks the renin-angiotensin-aldosterone system, reducing the hormonal drive that causes the heart to overwork. Sacubitril-valsartan (Entresto) offers additional benefit over ACE inhibitors and is now the preferred agent for most patients.
2
Beta-Blocker
Bisoprolol / Carvedilol / Nebivolol
Reduces the excessive sympathetic nervous system activation that drives heart failure progression. Slows the heart rate, reduces wall stress, and — over time — can improve ejection fraction. Must be started when the patient is stable, not during acute decompensation.
3
Mineralocorticoid Receptor Antagonist
Spironolactone / Eplerenone
Blocks the effects of aldosterone, reducing fluid retention, cardiac fibrosis, and adverse cardiac remodelling. Requires regular monitoring of potassium and renal function, particularly in older patients or those on ACE inhibitors.
4
SGLT2 Inhibitor
Dapagliflozin / Empagliflozin
Originally developed for diabetes, SGLT2 inhibitors reduce heart failure hospitalisations and cardiovascular death in HFrEF regardless of diabetes status. They also benefit patients with HFpEF — the first drug class proven to do so. Well tolerated with minimal monitoring requirements.
Medication Titration
Reaching Target Dose
Each of the four pillar drugs must be started low and titrated up at regular intervals — typically every two to four weeks — aiming for the target dose used in the clinical trials. The mortality benefit is substantially greater at target dose than at a low maintenance dose. Titration is guided by blood pressure, heart rate, renal function, and potassium at each review.
Dr Nijjer supervises this titration process systematically, reviewing patients at regular intervals until target or maximum-tolerated doses are achieved. The table below shows standard starting and target doses for the principal agents.
| Drug | Starting Dose | Target Dose | Key Monitoring |
|---|---|---|---|
| Sacubitril-Valsartan (preferred ARNI) | 24/26 mg twice daily | 97/103 mg twice daily | BP, renal function, potassium |
| Ramipril (ACE inhibitor) | 1.25–2.5 mg twice daily | 5 mg twice daily | BP, renal function, potassium |
| Bisoprolol (beta-blocker) | 1.25 mg once daily | 10 mg once daily | Heart rate, BP, symptoms |
| Carvedilol (beta-blocker) | 3.125 mg twice daily | 25–50 mg twice daily | Heart rate, BP, symptoms |
| Spironolactone (MRA) | 25 mg once daily | 50 mg once daily | Potassium, renal function |
| Eplerenone (MRA) | 25 mg once daily | 50 mg once daily | Potassium, renal function |
| Dapagliflozin (SGLT2 inhibitor) | 10 mg once daily | 10 mg once daily | eGFR (contraindicated <25) |
| Empagliflozin (SGLT2 inhibitor) | 10 mg once daily | 10 mg once daily | eGFR (contraindicated <20) |
In patients who cannot tolerate ACE inhibitors or ARNIs (most commonly due to cough), a combination of hydralazine and isosorbide dinitrate provides an alternative with proven mortality benefit, particularly in patients of African-Caribbean background.
Symptom Relief
Diuretics & Additional Therapies
- Loop Diuretics Furosemide and bumetanide are the primary agents for symptom relief — they rapidly remove excess fluid retained in the lungs and peripheries. The dose is adjusted according to daily weight, breathlessness, and renal function. These drugs relieve symptoms but do not alter the underlying disease course or reduce mortality.
- Ivabradine For patients who remain in sinus rhythm with a resting heart rate above 70 bpm despite optimal beta-blocker therapy, ivabradine selectively reduces heart rate without affecting blood pressure or contractility. It reduces hospitalisation for worsening heart failure and is indicated in ejection fraction ≤35%.
- Digoxin An older agent, now used selectively in patients with persisting symptoms despite the four pillars, particularly those with concurrent atrial fibrillation. Reduces hospitalisation rates but has no mortality benefit. Narrow therapeutic window requiring careful monitoring of levels, renal function, and potassium.
- Vericiguat A newer soluble guanylate cyclase stimulator licensed for patients who have recently deteriorated despite optimal medical therapy. Reduces the risk of further hospitalisation in this high-risk group.
- Iron Replacement Iron deficiency — found in over 40% of heart failure patients even without anaemia — worsens symptoms and functional capacity. Intravenous iron infusion (ferric carboxymaltose) significantly reduces breathlessness and improves quality of life and exercise tolerance.
Device Therapy
Devices & Advanced Treatment
For patients who remain symptomatic despite optimal medical therapy, or who carry a high risk of sudden cardiac death, device therapy offers powerful additional benefit.
- ICD — Implantable Cardioverter-Defibrillator Recommended for patients with an ejection fraction of 35% or below who remain at risk of sudden cardiac death despite at least three months of optimal medical therapy. The ICD monitors the heart rhythm continuously and delivers a life-saving shock if a dangerous arrhythmia is detected. In patients without an indication for pacing, a subcutaneous ICD (S-ICD) avoids the need for leads inside the heart.
- CRT — Cardiac Resynchronisation Therapy When heart failure is accompanied by a broad left bundle branch block on the ECG, the two sides of the heart beat out of synchrony. CRT uses a specialised biventricular pacemaker to resynchronise contraction, improving pump efficiency. Around 70% of eligible patients experience significant symptomatic improvement — some see the ejection fraction recover to near-normal levels. Most patients receive a combined CRT-D device, providing both resynchronisation and defibrillator protection.
- Conduction System Pacing An emerging technique in which the lead is placed within the heart's natural conduction system — either directly in the His bundle or the left bundle branch — to deliver more physiological pacing. Increasingly used where traditional CRT has failed or is not feasible.
Device eligibility is reassessed after every three months of optimal medical therapy. Ejection fraction can improve significantly with medication — a patient who initially appeared to need a device may no longer meet the criteria after treatment has taken effect.
For a small number of patients with end-stage heart failure refractory to all medical and device therapies, advanced options including left ventricular assist devices (LVAD) and cardiac transplantation are discussed in collaboration with a specialist heart failure centre. Dr Nijjer facilitates referrals to the appropriate tertiary centre and remains involved in the patient's care throughout.
Further Information
Additional Resources
The British Heart Foundation and the Heart Failure Matters patient platform both provide comprehensive information on living with heart failure, understanding medications, monitoring symptoms at home, and what to expect at a cardiology review appointment.
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Concerned About Heart Failure?
Whether you have a new diagnosis, are not responding to current treatment, or wish to have your medication reviewed by a specialist, Dr Nijjer offers prompt appointments at Harley Street and across London.