Heart Failure — Etiopathology, Clinical Presentation, Stages and Management

Heart failure (HF) is a clinical syndrome in which structural or functional cardiac abnormality causes reduced cardiac output and/or elevated intracardiac pressures, producing typical symptoms and signs.

Prevalence rises steeply with age — HF is present in 13–14% of people over 80 years.

Nearly one-third of HF patients have chronic kidney disease, and more than 50% of HF patients have atrial fibrillation (Framingham data).

Causes: hypertensive heart disease, coronary artery disease, cardiomyopathies, valvular heart disease, arrhythmias, pericardial disease, myocarditis, drugs (alcohol, NSAIDs, chemotherapy, biologics), nutritional causes (thiamine deficiency, anaemia), and primary right heart failure from pulmonary disease.

Hypertension increases the risk of HF two- to threefold and is the commonest underlying cause in older people; treating it significantly reduces incident HF.

Pathophysiology rests on neurohormonal activation — sympathetic nervous system and renin-angiotensin-aldosterone system activation initially compensate but ultimately drive adverse remodelling, fibrosis and apoptosis.

Contributing age-related changes: increased ventricular and arterial stiffness, impaired diastolic relaxation, reduced beta-adrenergic responsiveness, and mitochondrial dysfunction.

Precipitants of decompensation: acute coronary events, atrial fibrillation with rapid ventricular rate, medication non-adherence, infection, excess fluid or sodium intake, anaemia, renal impairment, thyroid disease, and drugs such as NSAIDs and glucocorticoids.

Left- versus right-sided, low-output versus high-output, and systolic versus diastolic heart failure.

NYHA functional classification: I — no limitation; II — slight limitation, symptoms on ordinary activity; III — marked limitation, symptoms on less-than-ordinary activity; IV — symptoms at rest or on any activity.

ESC classification by ejection fraction: HFrEF <40%, HFmrEF 41–49%, HFpEF ≥50%. HFpEF and HFmrEF additionally require elevated natriuretic peptides plus structural abnormality or diastolic dysfunction.

ACC/AHA stages describe progression: Stage A at risk without structural disease; Stage B structural disease without symptoms; Stage C structural disease with current or prior symptoms; Stage D refractory HF requiring advanced interventions.

Symptoms — exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, reduced exercise tolerance, ankle swelling.

Signs — raised JVP, displaced apex, third heart sound, basal crackles, hepatomegaly, ascites, pleural effusion, peripheral oedema.

One-third of older people with HF display none of these signs, and comorbidities confuse the picture; individual symptoms and signs have low sensitivity, but their combination supports the diagnosis.

In older people presentation is often atypical — confusion, falls, functional decline, or unexplained weight loss.

The ESC algorithm combines symptoms, signs, prevalent heart conditions and an abnormal ECG; the presence of any of these prompts natriuretic peptide measurement.

BNP >35 pg/ml or NT-proBNP >125 pg/ml should trigger echocardiography. Normal levels make HF unlikely. Levels are equally predictive in HFrEF and HFpEF and carry prognostic value.

Echocardiography is the key confirmatory test; chest X-ray helps exclude COPD and pulmonary fibrosis.

Smoking cessation (RR of HF is 1.75 in current smokers), alcohol counselling, sodium restriction to about 1500 mg/day, fluid restriction where there is dilutional hyponatraemia, patient education, medication review, vaccination, multidisciplinary input, and structured follow-up.

Exercise training reduces mortality (HR 0.65) and counteracts the deconditioning spiral; it should be offered to older HF patients.

All patients should receive an ACE inhibitor or ARB regardless of NYHA class, plus optimal diuretic therapy to maintain euvolaemia.

Symptomatic patients should also receive a beta blocker (carvedilol, bisoprolol, nebivolol, or modified-release metoprolol — benefit demonstrated up to age 80) and a mineralocorticoid receptor antagonist (spironolactone 12.5–50 mg reduced morbidity and mortality by 30% in NYHA III–IV; eplerenone benefits mild symptoms).

ARNI (sacubitril/valsartan) reduced cardiovascular death and HF admission (HR 0.80) versus enalapril; do not combine with an ACE inhibitor and wait 36 hours after the last ACE inhibitor dose.

Ivabradine is added if the patient remains symptomatic in sinus rhythm with heart rate >70/min (HR 0.82 for CV death and HF hospitalisation).

Digoxin reduces hospitalisation but not mortality (DIG trial); in those over 70 use 0.125 mg daily, targeting a plasma level of 0.5–0.9 ng/ml, with monitoring of potassium and renal function.

Hydralazine-isosorbide dinitrate is used in self-declared Black patients and as an alternative when ACE inhibitors/ARBs are contraindicated.

“Start low and go slow” is the governing principle in older people, with monitoring of BP, creatinine and potassium after each dose change.

CRT if QRS >130 ms; ICD for secondary prevention after cardiac arrest or ventricular arrhythmia, and for primary prevention in NYHA II–III HFrEF with ischaemic or dilated cardiomyopathy and expected survival >12 months. Mortality benefit is seen across all age groups including >75, though the effect attenuates with age.

HFpEF trials have been largely negative — CHARM-Preserved, I-PRESERVE, PEP-CHF, SENIORS, DIG-ancillary, TOPCAT and PARAGON-HF showed no mortality benefit, with some reduction in hospitalisation.

Prognosis remains poor despite therapy; multidisciplinary team involvement and advance care planning, including palliative care, are of paramount importance.