Chronic and congestive cardiac failure — aetiology, clinical features and management, including in an 85-year-old lady

Definition and classification. Heart failure is a clinical syndrome in which the heart is unable to deliver an output adequate for the metabolic needs of the tissues, or can do so only at raised filling pressures. Classify by ejection fraction — HFrEF (LVEF ≤ 40%), HFmrEF (41–49%) and HFpEF (≥ 50%); and by NYHA class I–IV. In older patients, diastolic dysfunction rather than systolic dysfunction is the primary cause of heart failure, and it carries a marked increase in all-cause mortality.

Aetiology. More than 75% of overt heart failure in older patients is associated with hypertension or coronary heart disease. Other causes: degenerative calcific aortic stenosis and mitral annular calcification, atrial fibrillation, cardiomyopathy (including wild-type transthyretin amyloidosis), thyroid disease, anaemia, chronic kidney disease and cor pulmonale. In India also consider rheumatic valve disease. Common precipitants of decompensation: infection, arrhythmia (especially new AF), myocardial ischaemia, non-adherence, high salt or fluid intake, anaemia, thyroid dysfunction, and drugs — NSAIDs, corticosteroids, thiazolidinediones, non-dihydropyridine calcium channel blockers and negatively inotropic agents.

Why ageing predisposes. Ageing produces reduced β-adrenergic responsiveness with a blunted heart rate response, arterial stiffening with increased afterload, and cardiac hypertrophy. There is retarded left ventricular filling and a higher left ventricular diastolic pressure both at rest and on exercise. Crucially, older people depend more on atrial contraction than on ventricular relaxation for left ventricular filling, and are therefore more likely to develop heart failure when atrial fibrillation supervenes. Because myocardial reserve is already used up to maintain normal resting function, older people decompensate readily when disease is superimposed.

Clinical features. Exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue and reduced exercise tolerance; signs of congestion — raised JVP, basal crackles, third heart sound, cardiac enlargement, hepatomegaly and peripheral oedema. In older patients the presentation is frequently atypical — confusion or delirium, falls, anorexia, weight loss, nocturia, functional decline or simply "off legs". Heart failure is often OVER-diagnosed in older adults: pedal and pretibial oedema alone is NOT sufficient for the diagnosis, since venous stasis produces an identical picture. Look for the other objective signs before accepting the diagnosis.

Investigations. Echocardiography determines the ejection fraction and is the key test — NICE recommends echocardiography as the initial test in those with a previous myocardial infarction, and natriuretic peptide (BNP or NT-proBNP) measurement in those without. Note that natriuretic peptides rise with age, renal impairment and atrial fibrillation, and are lowered by obesity, so interpret with care. Add ECG (a completely normal ECG makes heart failure unlikely), chest radiograph, full blood count, urea and electrolytes, creatinine, liver and thyroid function, glucose, HbA1c, iron studies and ferritin. Consider cardiac MRI or bone scintigraphy if amyloidosis is suspected. Specialist assessment should be considered in all.

Non-pharmacological management. Patient and carer education, daily weight monitoring with an action plan, salt and fluid moderation, smoking cessation and alcohol limitation. Supervised exercise training and cardiac rehabilitation improve symptoms and quality of life at any age. Give influenza, pneumococcal and COVID-19 vaccination. Treat the comorbidities that drive decompensation — hypertension, coronary artery disease, atrial fibrillation, diabetes, anaemia and iron deficiency, sleep apnoea, thyroid disease and depression. Multidisciplinary heart failure nurse-led follow-up reduces readmission.

Disease-modifying drugs for HFrEF. The mainstays for systolic dysfunction in older as in younger patients are diuretics for fluid overload, ACE inhibitors or ARBs, beta-blockers and aldosterone blockers. All patients with chronic symptomatic heart failure with reduced ejection fraction or left ventricular remodelling should receive an ACE inhibitor to improve function and survival; beta-blockers improve symptoms and survival. Low-dose spironolactone 12.5–50 mg reduced morbidity and mortality by 30% in NYHA class III–IV (RALES), with gynaecomastia as a notable adverse effect; eplerenone reduced mortality and hospitalisation in patients with mild symptoms (EMPHASIS-HF), with fewer side effects. Subgroup analyses of both MRA trials showed equal benefit in younger and older patients. Monitor electrolytes closely at initiation and periodically thereafter. Sacubitril–valsartan (ARNI) was superior to enalapril in PARADIGM-HF.

Diuretics, digoxin and other agents. Loop diuretics (furosemide, bumetanide) are the mainstay of symptomatic treatment of fluid retention and show some mortality benefit versus placebo; in resistant cases give them intravenously or combine with a thiazide (sequential nephron blockade). In older people monitor renal function, electrolytes and fluid status closely to avoid hypovolaemia, hypotension and falls. Digoxin reduces hospitalisation and improves symptoms in HFrEF in sinus rhythm but does not improve mortality (DIG trial); benefit was seen at all ages, with side effects comparable to placebo in older patients. In those over 70, start and maintain at 0.125 mg daily to achieve a level of 0.5–0.9 ng/mL, monitoring potassium and renal function; watch for gastrointestinal upset, heart block, arrhythmia and confusion, and consider discontinuation once the indication has passed. Hydralazine plus isosorbide dinitrate is recommended in self-declared Black patients and as an alternative when ACE inhibitors and ARBs cannot be used. Ivabradine (SHIFT) may be added for a persisting sinus rate ≥ 70/min.

Device and advanced therapy. If symptoms persist despite optimal medical therapy, refer to a specialist and consider cardiac resynchronisation therapy with or without a defibrillator in those with a wide QRS and reduced ejection fraction; pooled trial data show a survival benefit from primary-prevention ICDs that persists in older patients, and CRT benefits older adults. Ventricular assist devices have been used in selected older patients. Every device decision in the very old must weigh life expectancy, frailty, cognition and the patient's own goals — and deactivation of ICD shocks must be discussed as part of end-of-life planning.

Management of the 85-year-old lady — the geriatric answer. (i) Confirm the diagnosis objectively — do not rely on ankle oedema; obtain an echocardiogram, and expect HFpEF from hypertension, atrial fibrillation or aortic stenosis to be the likeliest substrate. (ii) Assess frailty, cognition, function, nutrition, continence, falls risk and social support by comprehensive geriatric assessment. (iii) Start low and go slow, introducing one drug at a time with careful uptitration and close monitoring of blood pressure, renal function and electrolytes. (iv) Review the whole drug chart — stop NSAIDs, minimise anticholinergic and sedative burden, and address polypharmacy. (v) Anticipate diuretic-related harm — postural hypotension, falls, incontinence precipitating immobility, acute kidney injury and hyponatraemia; time diuretics to protect sleep and toileting. (vi) Prioritise symptom relief, independence and quality of life over prognostic benefit where life expectancy is short; use the time-to-benefit principle before adding prognostic drugs. (vii) Recognise the family burden — heart failure imposes a significant burden on families, requires multifaceted care, and caregiver physical and emotional health should itself be an outcome that is assessed. (viii) Undertake advance care planning early, and involve palliative care for refractory breathlessness.

Four-pillar therapy and rapid sequencing. The 2022 AHA/ACC/HFSA guideline and the 2023 ESC focused update establish four foundational drug classes for HFrEF — ARNI (or ACE inhibitor/ARB), beta-blocker, mineralocorticoid receptor antagonist and SGLT2 inhibitor — to be started together at low dose and uptitrated within 4–6 weeks (the STRONG-HF strategy) rather than sequentially over months. SGLT2 inhibitors (dapagliflozin, empagliflozin) are now recommended across the whole ejection fraction spectrum, including HFpEF (EMPEROR-Preserved, DELIVER), and are notably well tolerated in older adults with no need for dose titration.

New options for HFpEF and HFmrEF, which is the dominant phenotype in the very old. FINEARTS-HF (NEJM 2024) showed that finerenone, a non-steroidal MRA, reduced worsening heart failure events and cardiovascular death in HFmrEF and HFpEF, with less hyperkalaemia than spironolactone. STEP-HFpEF (NEJM 2023) showed that semaglutide markedly improved symptoms, physical limitation and exercise function in obesity-related HFpEF. Together these give the first genuinely disease-modifying options for a phenotype the textbook describes as having no proven drug therapy.