Chronic Heart Failure

Cardiovascular

Description

Chronic heart failure is a progressive clinical syndrome in which the heart cannot pump blood at a rate commensurate with metabolic demand or can do so only at the cost of elevated filling pressures, leading to congestion, impaired organ perfusion and neuro-hormonal activation. It is phenotyped by left-ventricular ejection fraction into heart failure with reduced EF (HFrEF < 40 %), mildly reduced EF (HFmrEF 40–49 %) and preserved EF (HFpEF ≥ 50 %). The prevalence in industrialised nations now exceeds 2 % of the adult population and rises steeply with age, making heart failure the leading reason for hospital admission in patients ≥ 65 years.

Symptoms

Typical manifestations include exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, reduced exercise tolerance, ankle oedema, abdominal distension, early satiety and nocturia. Physical findings encompass elevated jugular venous pressure, displaced apical impulse, S₃ gallop, pulmonary crackles, hepatomegaly and peripheral pitting oedema. In HFpEF patients may present predominantly with exercise intolerance and pulmonary congestion despite normal EF.

Risk Factors

Coronary artery disease, prior myocardial infarction, uncontrolled hypertension, valvular heart disease, atrial fibrillation, diabetes mellitus, obesity, metabolic syndrome, obstructive sleep apnoea, chronic kidney disease, chronic obstructive pulmonary disease, excessive alcohol intake, cardiotoxic chemotherapy, familial dilated or hypertrophic cardiomyopathy, congenital heart disease and advancing age all increase the likelihood of developing chronic heart failure. Smoking and sedentary lifestyle potentiate risk, whereas regular aerobic exercise and optimal blood-pressure control mitigate it.

Diagnosis

Diagnosis integrates symptoms with objective evidence of cardiac structural or functional abnormality. Natriuretic peptides (BNP > 35 pg/mL or NT-proBNP > 125 pg/mL in out-patients) support the diagnosis. Transthoracic echocardiography quantifies EF, wall thickness, chamber volumes and diastolic indices. ECG screens for ischaemia and arrhythmia; coronary CT or angiography assesses obstructive CAD. Cardiac MRI delineates fibrosis via late-gadolinium enhancement. Laboratory tests evaluate renal, hepatic and thyroid function, ferritin, transferrin saturation and A1AT when indicated. In uncertain cases invasive haemodynamics or exercise right-heart catheterisation confirm elevated filling pressures.

Treatment

Guideline-directed medical therapy (GDMT) for HFrEF consists of four foundational classes started as early as tolerated: an angiotensin-receptor/neprilysin inhibitor (sacubitril-valsartan), a β-blocker (carvedilol, metoprolol succinate or bisoprolol), a mineralocorticoid-receptor antagonist (spironolactone or eplerenone) and an SGLT2 inhibitor (dapagliflozin or empagliflozin); together these reduce mortality by > 70 % compared with placebo regimens. Additional agents for selected symptomatic patients include ivabradine for heart rates ≥ 70 bpm in sinus rhythm, vericiguat and omecamtiv mecarbil after recent decompensation, and hydralazine–isosorbide dinitrate in self-identified Black patients or those intolerant of RAAS blockers. Loop diuretics relieve congestion; thiazide-type agents may augment natriuresis. For HFpEF/HFmrEF, SGLT2 inhibitors are now first-line based on EMPEROR-Preserved and DELIVER trials, complemented by diuretics, mineralocorticoid antagonists and risk-factor control. CRT is indicated for LVEF ≤ 35 % with LBBB ≥ 150 ms; ICD prevents sudden death when LVEF ≤ 35 % despite GDMT. Refractory cases advance to transcatheter edge-to-edge repair for secondary MR, ventricular-assist devices or cardiac transplantation. Pulmonary rehabilitation, vaccination, and meticulous management of comorbidities complement pharmacotherapy.

Outlook

With optimal GDMT, five-year survival has improved to ~75 % in HFrEF, yet prognosis remains worse than many malignancies, particularly after repeated hospitalisations. Each admission accelerates ventricular remodelling and heightens 60-day mortality to 6–10 %. HFpEF confers similar hospitalisation rates but slightly better survival. SGLT2 inhibitors and comprehensive disease-management programmes have reduced all-cause admissions and lengthened time to first decompensation.

Complications

Recurrent decompensated heart failure, cardiogenic shock, ventricular arrhythmias, thrombo-embolic stroke, progressive renal dysfunction, cachexia, hepatic congestion (“cardiac cirrhosis”), pulmonary hypertension, secondary mitral regurgitation and sudden cardiac death are major sequelae.

Prevention

Primordial prevention targets hypertension, hyperlipidaemia, diabetes and obesity through Mediterranean-style diet, regular aerobic activity, avoidance of tobacco and moderation of alcohol. Prompt reperfusion of myocardial infarction, guideline-level treatment of valvular diseases and cardiotoxicity surveillance during cancer therapy forestall progression to heart failure.

Support

Daily weight monitoring, sodium intake < 2 g, fluid restriction 1.5–2 L in hyponatraemia, adherence to GDMT, home blood pressure and heart-rate tracking, influenza and pneumococcal vaccination, smoking cessation, moderated alcohol, structured cardiac-rehabilitation exercise and advance-care planning enhance symptom control and reduce readmissions. Caregivers should learn to titrate diuretics per action plans and recognise early congestion.