Aortic and mitral valve disease

Key Takeaways

  • Symptomatic severe aortic stenosis needs specialist assessment for valve intervention.

  • Acute severe mitral regurgitation can cause shock despite a deceptively soft murmur.

  • Moderate-to-severe rheumatic mitral stenosis with AF generally requires warfarin rather than a DOAC.

Last updated: October 2026

Valvular Heart Disease, Infective Endocarditis & Pericarditis

Valvular heart disease, infective endocarditis, and pericardial disorders encompass structural, inflammatory, and infectious pathologies that frequently present to acute medical units across Australia. Mastering physical examination signs, echocardiographic thresholds, and emergency interventions is critical for timely medical stabilization and surgical referral.


Valvular Heart Disease: Aortic and Mitral Pathologies

Aortic Stenosis (AS)

  • Etiology: Calcific degeneration of a normal trileaflet valve in older adults (>70 years> 70\text{ years}) vs calcification of a congenital bicuspid aortic valve in younger patients (40 to 60 years40\text{ to }60\text{ years}). Bicuspid aortic valve is the most common congenital cardiac anomaly (1% to 2%1\%\text{ to }2\% prevalence) and is frequently associated with ascending aortic aneurysms.
  • Pathophysiology: Fixed left ventricular outflow tract (LVOT) obstruction leads to concentric left ventricular hypertrophy (LVH), reduced myocardial compliance, elevated diastolic filling pressures, and increased myocardial oxygen consumption.
  • Classic Symptom Triad:
    1. Angina: Historical untreated severe-AS cohorts had poor survival after symptoms; these figures are not an individual contemporary prognosis.
    2. Syncope on exertion: Caused by an inability to augment cardiac output across a fixed stenotic orifice in the face of exercise-induced peripheral skeletal muscle vasodilation. Historical untreated severe-AS cohorts had poor survival after symptoms; these figures are not an individual contemporary prognosis.
    3. Dyspnoea / Heart Failure: Indicates left ventricular decompensation. Historical untreated severe-AS cohorts had poor survival after symptoms; these figures are not an individual contemporary prognosis.
  • Physical Examination:
    • Pulse: Slow-rising, low-amplitude carotid pulse (pulsus parvus et tardus).
    • Auscultation: Harsh, crescendo-decrescendo ejection systolic murmur maximal at the right second intercostal space radiating to both carotid arteries. A late peak of the murmur correlates with greater severity.
    • Heart sounds: Soft or inaudible aortic component of the second heart sound (A2A_2), prominent S4S_4 gallop reflecting atrial contraction into a stiff hypertrophied ventricle, and reversed (paradoxical) splitting of S2S_2.
  • Echocardiographic Criteria for Severe AS:
    • Peak aortic jet velocity ≥4.0 m/s\ge 4.0\text{ m/s}
    • Mean transvalvular gradient ≥40 mmHg\ge 40\text{ mmHg}
    • Aortic Valve Area (AVA) ≤1.0 cm2\le 1.0\text{ cm}^2 (or indexed AVA ≤0.6 cm2/m2\le 0.6\text{ cm}^2\text{/m}^2)
  • Intervention Indications:
    • All symptomatic patients with severe AS.
    • Asymptomatic patients with severe AS who have LVEF<50%LVEF < 50\%, an abnormal exercise stress test (symptoms or blood pressure fall), or very severe stenosis (velocity >5.0 m/s> 5.0\text{ m/s}).
    • Modality selection: A Heart Team weighs age, life expectancy, anatomy, surgical risk, concomitant surgery and patient preference. The 2025 ESC/EACTS guideline supports TAVI for anatomically suitable patients aged at least 70 with tricuspid aortic stenosis. This is not an automatic Australian age-only rule: bicuspid anatomy, aortopathy, coronary surgery and durability can favour surgical replacement.

Aortic Regurgitation (AR)

  • Etiology: Aortic root dilatation (ascending aortic aneurysm, Marfan syndrome, aortic dissection) or primary valvular damage (infective endocarditis, bicuspid valve, rheumatic heart disease).
  • Physical Examination:
    • High-pitched, early diastolic decrescendo blowing murmur best heard at the left third/fourth intercostal space with the patient sitting upright, leaning forward in held expiration.
    • Marked widening of pulse pressure (SBP↑,DBP↓SBP \uparrow, DBP \downarrow, e.g., 160/45 mmHg160/45\text{ mmHg}).
    • Peripheral signs of hyperdynamic circulation: Rapidly rising and collapsing "water-hammer" pulse (Corrigan pulse), capillary pulsations in nailbeds (Quincke sign), head nodding with cardiac cycle (de Musset sign), systolic pistol-shot sounds over femoral arteries (Traube sign).
    • Austin Flint Murmur: Mid-to-late diastolic low-pitched rumbling murmur at the apex, caused by the regurgitant jet impinging on the anterior mitral leaflet.
  • Surgical Indications: Symptomatic severe AR; asymptomatic severe AR with LVEF≤50%LVEF \le 50\% or severe left ventricular dilatation (LV end-systolic diameter >50 mm> 50\text{ mm}).

Mitral Regurgitation (MR)

  • Primary (Organic): Degenerative mitral valve prolapse (myxomatous degeneration), infective endocarditis, ruptured chordae tendineae, rheumatic heart disease. Murmur is holosystolic (pansystolic) maximal at the apex radiating to the axilla, accompanied by a soft S1S_1 and laterally displaced hyperdynamic apex beat.
  • Secondary (Functional): Left ventricular dilatation and wall motion abnormalities displacing papillary muscles (ischaemic cardiomyopathy, dilated cardiomyopathy). Valve leaflets are structurally normal.
  • Acute Mitral Regurgitation: Rupture of chordae or papillary muscle (post-MI or trauma). Presents abruptly with flash pulmonary oedema and cardiogenic shock. Crucially, the murmur may be soft or deceptively short because left atrial pressure rises rapidly to equalize with left ventricular pressure in early systole. Emergent transoesophageal echocardiography and urgent surgical repair are required.

Mitral Stenosis (MS)

  • Etiology: Almost exclusively rheumatic heart disease secondary to childhood Group A streptococcal pharyngitis.
  • Physical Examination: Loud S1S_1, high-pitched opening snap (OS) in early diastole (a shorter A2–OSA_2\text{--}OS interval indicates more severe stenosis), and a low-pitched mid-diastolic rumbling murmur with presystolic accentuation heard best at the apex in the left lateral decubitus position.
  • Mitral stenosis and AF: Moderate-to-severe rheumatic MS with AF has high embolic risk and generally requires warfarin rather than a DOAC, independent of the usual AF score. Reassess the valve/rhythm context rather than describing every stenosis as an automatic lifelong anticoagulation indication.
  • Intervention: Percutaneous mitral balloon commissurotomy (PMBC) for pliable non-calcified valves without significant MR; surgical valve replacement for calcified valves.

Primary references (checked 7 October 2026): ESC/EACTS 2025 valve guideline.

Test Your Knowledge

A 76-year-old woman is referred after experiencing an episode of syncope while walking up a flight of stairs. She reports progressive exertional shortness of breath over the past six months. On examination, her pulse is slow-rising and of low volume (pulsus parvus et tardus). Blood pressure is 108/76 mmHg. Cardiac auscultation demonstrates a harsh, late-peaking crescendo-decrescendo ejection systolic murmur maximal at the right second intercostal space radiating to both carotids, with an inaudible aortic component of the second heart sound. Transthoracic echocardiography reveals an aortic valve area of 0.7 cm², peak aortic jet velocity of 4.5 m/s, and mean pressure gradient of 48 mmHg. Which of the following is the most appropriate management?

A

Refer to a structural heart team for evaluation and prompt aortic valve intervention

B

Reassure the patient and repeat clinical and echocardiographic surveillance in twelve months

C

Commence high-dose oral beta-blocker therapy to reduce left ventricular myocardial workload

D

Prescribe oral loop diuretics and recommend complete avoidance of moderate physical exertion

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