Aortic Stenosis

Aortic Stenosis is a progressive disease most commonly caused by age-related calcification of a normal trileaflet valve or a congenital bicuspid valve. As the valve area decreases, the left ventricle must generate higher pressures to maintain stroke volume, resulting in concentric Left Ventricular Hypertrophy (LVH). AS is graded as mild, moderate, or severe based on echocardiographic findings (Valve area <1.0cm², Mean gradient >40mmHg, or Jet Velocity >4m/s). For many years, AS is asymptomatic, but the onset of symptoms (Syncope, Angina, Dyspnoea) signals a poor prognosis, with a median survival of 2-5 years without intervention. Clinical examination characteristically reveals an ejection systolic murmur radiating to the carotids and a slow-rising pulse. Management focuses on replacement of the valve, as medical therapy is ineffective. Decisions between surgical AVR and Transcatheter Aortic Valve Implantation (TAVI) are made by a multidisciplinary 'Heart Team' based on surgical risk (STS/EuroSCORE).

The pathophysiology of AS involves a chronic inflammatory process akin to atherosclerosis. Lipid insudation, oxidation, and myofibroblast differentiation into osteoblasts lead to calcium hydroxyapatite deposition on the valve leaflets. This stiffens the valve, restricting opening during systole. In bicuspid valves (found in 1-2% of the population), abnormal shear stress accelerates this calcification by 1-2 decades. To overcome the obstruction (increased afterload), the Left Ventricle (LV) undergoes concentric hypertrophy (Law of Laplace). While this maintains wall stress early on, it leads to decreased diastolic compliance, increased myocardial oxygen demand, and eventually LV systolic failure. Angina occurs even without coronary disease because the hypertrophied muscle outstrips its blood supply and the high LV pressure limits sub-endocardial perfusion.

SAD symptoms: 1. Syncope (usually on exertion as systemic vasodilation occurs but CO cannot increase). 2. Angina (myocardial oxygen supply/demand mismatch). 3. Dyspnoea (Heart failure due to diastolic/systolic dysfunction). Examination findings: 1. Pulse: Slow-rising (delayed peak) and small volume. 2. Palpation: Heaving (not displaced) apex beat due to LVH; systolic thrill in the aortic area. 3. Auscultation: Harsh ejection systolic murmur (ESM) following an ejection click (if valve is mobile). The S2 may be quiet or show reversed splitting. Complications: Sudden cardiac death, left heart failure, and Heyde’s syndrome (AS associated with GI angiodysplasia).

1. Bedside: 12-lead ECG (Signs of LVH: deep S in V1, tall R in V5-6, LAD, 'Strain' pattern/T-wave inversion).
2. Imaging: Chest X-ray (unremarkable early, later cardiomegaly; calcified aortic ring). Echocardiogram (Diagnostic: assesses valve area, pressure gradients, and LV function).
3. Special: Coronary Angiography (Required pre-op to rule out CAD); Dobutamine Stress Echo (for low-flow, low-gradient AS); Cardiac MRI.

1. Conservative: Asymptomatic patients need regular monitoring (Echo every 6-12 months). Avoid heavy exertion. Manage HTN/Statins (though they don't slow AS progression).
2. Medical: Limited. Diuretics can help HF symptoms but must be used cautiously (preload dependent). ACEi used with extreme caution.
3. Surgical: Surgical Aortic Valve Replacement (SAVR) is the treatment of choice in patients with low-to-intermediate surgical risk.
4. TAVI: Transcatheter Aortic Valve Implantation is preferred for elderly/frail patients or those at high surgical risk.
5. Balloon Valvuloplasty: Usually only a bridge to surgery in unstable patients or for palliative care.