Detection and Management of Heart Failure

Heart failure detection and management rests on three moves that any physician can make: confirm the diagnosis early with a natriuretic peptide test, an ECG and an echocardiogram; start all four classes of guideline-directed drugs together rather than one at a time; and refer promptly when a patient stays symptomatic, so that devices, assist pumps or transplant can be considered before it is too late.

That was the framework Dr. Rajpal Singh R L, Director Cardiology, Fortis Hospitals, Bannerghatta Road, Bangalore, India, set out for physicians across Africa. He trained and worked in the UK for 17 years, including as a consultant, before returning to India 15 years before the session, and his practice follows the European Society of Cardiology (ESC) 2021 heart failure guidelines and their 2023 focused update. His organising question was a practical one: what should a general physician do for a heart failure patient at their own end, and when should that patient be referred?

This guide covers why heart failure has become so common, the mechanism every drug class targets, how treatment has evolved, the overall pathway, acute congestion and the heart failure clinic model. Three companion articles go deeper on diagnosing heart failure with natriuretic peptides, ECG and echo, on the four pillars of heart failure drug therapy and the drugs to avoid, and on when to refer for ICD, CRT, LVAD or transplant.

How heart failure guidelines grade their recommendations

ESC guidelines grade every recommendation by class (how strongly it is recommended) and by level of evidence (how good the data are). Dr. Singh anchored every recommendation in this system, and it is worth knowing before reading any heart failure guideline.

• Class I: the evidence shows the treatment is beneficial, useful and effective. It should be given.
• Class III: the treatment is not useful and may be harmful. It should not be given.
• Level of evidence A: data from multiple randomised controlled trials or meta-analyses.
• Level B: a single randomised trial or large non-randomised studies.
• Level C: consensus of expert opinion or small studies.

A "class 1A" recommendation, which appears repeatedly in heart failure care, therefore combines the strongest recommendation with the strongest evidence. Much of modern heart failure treatment sits in that category, which is why Dr. Singh described it as one of the most thoroughly researched fields in cardiology: almost every drug in routine use has a proven mortality or morbidity benefit, and the evidence is equally clear about which drugs cause harm.

Why heart failure is increasing

Heart failure is increasing partly because more people survive heart attacks with damaged heart muscle and live longer with it. It is common everywhere and its prevalence rises steeply with age: low single digits in younger adults, climbing into double figures in the elderly. It is more frequent in men, reflecting a heavier load of cardiovascular risk factors. Dr. Singh noted that about 30% of patients who come to an emergency department short of breath have heart failure of some kind, either a new acute episode or a worsening of established chronic disease.

The prognosis of untreated heart failure is poor. One-year mortality is high in men and women alike, in European and American data, and five-year mortality was substantial even with the treatment available when those figures were collected. Dr. Singh put it bluntly: undiagnosed heart failure carries mortality rates comparable with the most common cancers.

This is a paradox of progress. Treatment of heart attacks has improved, even if door-to-balloon and needle-to-thrombolysis times are still too long in many places. More patients survive the acute event with part of their heart muscle salvaged, live longer, and present years later with a damaged, degenerating myocardium. Fewer deaths from myocardial infarction on one side of the ledger translate into more heart failure on the other. Dr. Singh described the result as a real pandemic.

Despite this, heart failure remains underdiagnosed and undertreated. He described patients treated by senior doctors with low doses of a loop diuretic alone, with digoxin alone, or with cod liver oil capsules, when far better treatment exists.

The vicious cycle that every drug interrupts

The biology explains why modern treatment works. Once the heart muscle is injured, pump function falls. The body reads the lower output, through the carotid baroreceptors and through reduced blood flow to the kidneys, as a threat and activates two compensatory systems:

1. The sympathetic nervous system, which raises the heart rate. Over time the sustained adrenergic drive is toxic to the myocardium and worsens left ventricular dysfunction.
2. The renin-angiotensin-aldosterone system, which constricts blood vessels (raising afterload) and retains salt and water (raising preload).

Both limbs feed back into further heart failure, and the cycle continues unless it is treated. The value of this model is practical: each limb can be blocked by a different class of drug. Beta blockers target the sympathetic limb; angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers and angiotensin receptor-neprilysin inhibitors (ARNIs) target the renin-angiotensin limb; mineralocorticoid receptor antagonists block aldosterone. That is the logic of combining classes rather than choosing between them.

How heart failure treatment has evolved: from "diuretics, digoxin and death" to four pillars

Heart failure treatment has moved from diuretics and digoxin alone in the 1980s to combination drug therapy, devices and transplant today. Dr. Singh traced the change through four decades:

The shift on beta blockers was the most striking. When he started training in cardiology, giving a beta blocker to a heart failure patient was considered a crime; by the end of his training it was considered criminal not to. Trials such as CIBIS-II and CAPRICORN established beta blockers alongside ACE inhibitors. The RALES trial then rescued spironolactone, a drug that had been left on the shelf, by showing that it reduced hospitalisation and sudden cardiac death and improved quality of life. Device trials, including COMPANION and CARE-HF, then established cardiac resynchronisation therapy.

Today the treatments that improve both morbidity and mortality are sacubitril/valsartan (or an ACE inhibitor or angiotensin receptor blocker), beta blockers, mineralocorticoid receptor antagonists such as spironolactone or eplerenone, SGLT2 inhibitors, implantable defibrillators, resynchronisation devices and heart transplantation. Digoxin, the hydralazine and isosorbide dinitrate combination, and ivabradine are add-ons that improve symptoms and quality of life.

The heart failure management pathway at a glance

Heart failure management follows six steps: diagnose, classify, decongest, start all four drug pillars, follow up and refer. Dr. Singh's sequence for the general physician:

1. Establish the diagnosis. History, symptoms and risk profile, supported by an ECG, a natriuretic peptide level (BNP or NT-proBNP), an echocardiogram, a chest X-ray and routine blood tests.
2. Classify the heart failure by ejection fraction: reduced (HFrEF), mildly reduced (HFmrEF) or preserved (HFpEF).
3. Relieve congestion with diuretics.
4. Start guideline-directed medical therapy: all four pillars together, titrated as far as tolerated, ideally before discharge.
5. Follow up with an ECG and a natriuretic peptide level every six to twelve months in stable patients.
6. Refer patients who remain symptomatic on optimal therapy, or whose ECG and ejection fraction meet device criteria.

He framed heart failure in stages, from A (at risk, no symptoms or structural disease) through B (structural heart disease without symptoms) and C (symptomatic) to D (advanced, refractory disease with orthopnoea, paroxysmal nocturnal dyspnoea and repeated admissions). His message to primary care was to catch patients at stage A and stop them progressing. The detail of the diagnostic algorithm, the staging and the baseline investigations is in the companion article on diagnosis.

On drug therapy, his single most important instruction was to start all four pillars at once. "Which one do we start first?" is a question he is always asked, and his answer is all four, because they act on different mechanisms. The guidelines state that the four classes can be started simultaneously, without a specific sequence, and should not be delayed. Patients whose drugs are titrated aggressively before discharge do better than those whose treatment is started late. Doses, side effects and the drugs that must be stopped are covered in the four pillars article.

Managing acute congestion in heart failure

Acute congestion is treated first with appropriately dosed diuretics, with adjuncts chosen according to renal function and blood pressure. Several of the questions doctors raised during the session concerned acutely congested patients, and Dr. Singh's answers fill out the acute end of the pathway.

Congestive cardiac failure with ascites. A patient with severe ascites and peripheral oedema has congestive cardiac failure, a combination of right and left heart failure, and should usually be hospitalised. Where that is not possible, the priority is decongestion with appropriately dosed diuretics, with regular monitoring of creatinine and liver function tests. If renal function is preserved and there is no hepatorenal syndrome, the conventional heart failure drugs can be used; in a patient with liver cirrhosis he would consider a higher dose of spironolactone.

Acetazolamide as an adjunct. For patients in NYHA (New York Heart Association) class III or IV who need hospitalisation, Dr. Singh's unit now adds acetazolamide, orally or intravenously, to loop diuretics. In his experience it improves diuresis and speeds the resolution of congestion, provided renal function is not too poor. The ADVOR trial (2022) supports this: adding intravenous acetazolamide to loop diuretics in acute decompensated heart failure produced more successful decongestion.

Low blood pressure. If the blood pressure is low, Dr. Singh uses low-dose ("renal-dose") dopamine alongside diuretics, particularly in right heart failure with valve dysfunction, while acknowledging that no large long-term randomised trial supports it. In the ROSE-AHF trial, low-dose dopamine added to diuretics in acute heart failure did not improve decongestion or renal function. He no longer uses dobutamine routinely: it can tide a profoundly hypotensive patient over an acute phase, but used for longer it gives only a transient increase in output with no lasting benefit. More cardiologists, he noted, now prefer noradrenaline in that situation.

What a heart failure clinic does

A heart failure clinic standardises care: one team diagnoses, titrates drugs, monitors and decides on referral. It was Dr. Singh's strongest organisational recommendation, and his own clinic at Fortis runs on seven steps:

1. Referral and assessment by him or a colleague with an interest in heart failure; one cardiologist cannot run a clinic alone.
2. A heart failure investigation package: natriuretic peptides, full blood count, renal and liver function, ECG and chest X-ray, to identify the cause.
3. Treatment start and nurse-led titration. A heart failure nurse follows patients closely under clear instructions on when to check renal function and when to bring the patient back. At each visit the clinic checks NT-proBNP, creatinine and haemoglobin.
4. Risk assessment for sudden cardiac death once the patient is stable.
5. Disposition. Patients whose heart function has improved are seen once a year and discharged back to their general physician. Patients who remain symptomatic are assessed for resynchronisation therapy or a defibrillator.
6. Ongoing follow-up. A patient seen every six months will also have had a couple of telephone conversations with the heart failure nurse in between.
7. Advanced work-up for refractory disease: cardiac MRI, biopsy, and assessment for a left ventricular assist device (LVAD) or transplant.

The nurse also manages the problems that make patients abandon treatment. Beta blockers, for example, make many patients feel worse for the first one to two weeks before they improve, and a nurse who counsels patients about that dip keeps them on a drug that will ultimately save their lives. For any physician with an interest in heart failure, Dr. Singh's view was that a clinic is worth the investment because it brings the whole range of investigation and management together.

Advanced heart failure: devices, LVAD, transplant and palliative care

For patients who remain symptomatic despite optimal drugs, the next steps are devices and, in selected patients, mechanical support or transplant. Dr. Singh described himself as an avid user of cardiac resynchronisation therapy: as a consultant at the Wolverhampton Heart and Lung Centre he built up the CRT service, work recognised with a Clinical Excellence Award. In his summary, implantable defibrillators and resynchronisation devices make the difference to longevity, while for patients who are not suitable for those devices, LVADs and heart transplantation have excellent outcomes in selected patients. The criteria, procedures and practicalities are in the referral article.

He was equally clear about the other end of the spectrum. When a patient has reached the end of the road, whether because of the disease or because of finances, it is not wrong to discuss palliative care and to plan a comfortable life rather than more medication or more hospital admissions.

Key messages

Dr. Singh closed with the principles that should guide practice:

• Early recognition and diagnosis of heart failure is the key step.
• Systematic evaluation of risk factors, including family history, is mandatory: a family member with heart failure in their fifties is a reason to screen and watch relatives.
• Guideline-directed therapy for HFrEF now means four medications: a beta blocker, an ARNI (or ACE inhibitor or angiotensin receptor blocker), a mineralocorticoid receptor antagonist and an SGLT2 inhibitor. They should be continued, not started and stopped.
• Routine non-invasive assessment with natriuretic peptides, ECG and echocardiography makes a measurable difference.
• Defibrillators and resynchronisation devices have a clear role in symptomatic and advanced heart failure.
• In selected patients, LVADs and heart transplantation have excellent outcomes.

Physicians who want to compare approaches can read Dr. Biswarup Purkayastha's separate guide to heart failure and coronary artery disease in African patients. The questions doctors put to Dr. Singh during the session, on beta blocker tolerance, BNP, ascites, SGLT2 inhibitor infections and dobutamine, are covered in full in the Live Discussion. More on heart failure and related conditions is collected in the cardiology specialty hub.