Diastolic dysfunction

Definition: impaired ventricular relaxation and/or increased chamber stiffness causing raised filling pressures at normal or near-normal ejection fraction. When symptomatic it manifests as heart failure with preserved ejection fraction (HFpEF).

Geriatric importance: Essentials states plainly that diastolic, not systolic, dysfunction is the primary cause of heart failure in older patients, and that it is associated with a marked increase in all-cause mortality (Redfield 2003; Bursi 2006).

Pathophysiology: age-related myocardial fibrosis and collagen deposition, LV hypertrophy from chronic hypertension and arterial stiffening, impaired active relaxation (delayed calcium re-uptake by SERCA), titin stiffening, subendocardial ischaemia and microvascular inflammation.

Consequences: small increases in volume produce large increases in filling pressure → pulmonary congestion, especially with tachycardia (loss of diastolic filling time) or loss of atrial systole in atrial fibrillation. This explains the classic presentation of flash pulmonary oedema with new AF or a hypertensive surge.

Causes: hypertension with LV hypertrophy (commonest), coronary disease, diabetes, obesity, aortic stenosis, hypertrophic cardiomyopathy, restrictive/infiltrative disease (amyloidosis, haemochromatosis), and constrictive pericarditis as a mimic.

Clinical features: exertional dyspnoea, fatigue, orthopnoea and congestion indistinguishable from systolic failure at the bedside; a fourth heart sound (S4) and a sustained apex are suggestive; typically an older woman with hypertension, obesity, diabetes and atrial fibrillation.

Diagnosis: preserved ejection fraction (≥50%) plus objective evidence of raised filling pressures — echocardiographic E/e′ >14–15, septal e′ <7 cm/s, left atrial volume index >34 mL/m², tricuspid regurgitant velocity >2.8 m/s, LV hypertrophy — with raised natriuretic peptides.

Management (textbook position): treat congestion with diuretics, control heart rate with beta blockers to prolong diastolic filling, and treat the comorbidities that drive it — hypertension, coronary disease, atrial fibrillation and diabetes. Trials of digoxin and ARBs showed minimal benefit.

Practical cautions: these patients are preload-dependent — over-diuresis causes hypotension and acute kidney injury; avoid excessive rate reduction (chronotropic incompetence worsens exercise capacity) and avoid drugs that shorten diastole.

Prognosis: mortality approaches that of HFrEF, with hospitalisation driven as much by non-cardiac comorbidity as by cardiac events. Latest Updates and Current Practice Update (concise) The therapeutic desert has ended. Contrary to the textbooks, HFpEF now has evidence-based drug therapy: SGLT2 inhibitors (EMPEROR-Preserved, DELIVER) reduce worsening HF events across the ejection fraction spectrum and are recommended for all; finerenone (FINEARTS-HF, 2024) reduced cardiovascular death and worsening HF events by 16%, including at EF ≥60%. 2026 ACC HFpEF Expert Consensus Decision Pathway: SGLT2 inhibitor for all, plus a non-steroidal MRA (finerenone preferred over spironolactone), plus semaglutide or tirzepatide when BMI ≥30 kg/m²; diagnosis by sequential H2FPEF and HFA-PEFF scoring with systematic exclusion of mimics. Amyloid must be excluded: up to about 13% of older HFpEF patients with marked LV hypertrophy have transthyretin cardiac amyloidosis, which now has specific disease-modifying therapy.