The aortic valve may show degeneration with advancing age, with increasing calcification and thickening of the leaflets. A mild form is called sclerosis. This can progress to reduced aortic valve opening and ultimately severe aortic stenosis (AS) if the valve orifice area (AVA) falls below 1.0 cm².

Aortic stenosis can both cause or contribute to heart failure. Initially this produces a picture of HFpEF with left ventricular hypertrophy. With further deterioration, the left ventricle will fail and progress to HFrEF.

Intervention is indicated in a symptomatic patient with severe aortic stenosis, regardless of the ejection fraction. All decisions in this regard must be made in the Heart Team.

The therapeutic options are:

1. PTAV (percutaneous transluminal aortic valve valvuloplasty): balloon dilation. Only as a bridge to definitive intervention or as palliation in advanced heart failure.

2. Surgical aortic valve replacement, if possible minimally invasive via ministernotomy or right anterior thoracotomy (RAT).

• This operation is preferred in patients < 75 years of age with a low surgical risk.
  There are 2 types of artificial valves:
  • Bioprosthesis :
    • Most commonly used.
    • Chronic low-dose aspirin recommended afterwards (AHA/ACC 2020).
    • Degeneration and dysfunction of the prosthetic valve may occur after several years.
  • Mechanical (metal) prosthesis :
    • Only used in young patients < 55-60 years.
    • Normally, no degeneration of the valve occurs.
    • Afterwards, there is a strict indication for life-long blood thinning with oral anticoagulants (coumarins, e.g. warfarin) to prevent valve thrombosis. DOACs are contraindicated in these patients!

3. Percutaneous aortic valve replacement (TAVI). The aortic valve bioprosthesis is inserted via the femoral artery and advanced to the aortic position where the valve is deployed. This intervention is increasingly preferred in patients > 75 years of age and/or with an increased surgical risk. Afterwards there is an indication for blood thinning with chronic low-dose aspirin.

In mitral regurgitation (MR), some of the content of the left ventricle leaks back into the left atrium and pulmonary circulation during systole. MR can both cause and/or contribute to heart failure.

A distinction is made between :

• Primary (organic) mitral regurgitation :
  • The valve leak is caused by an abnormality of the valve itself.
  • If severe and symptomatic, intervention is indicated: preferably surgical valve repair (mitral valvuloplasty), or a mitral valve replacement if repair is not possible.
    There are 2 types of artificial valves:

• • • Bioprosthesis :
      • Most commonly used.
      • Chronic blood thinning with low-dose aspirin
      • After several years, degeneration and recurrence of dysfunction of the prosthetic valve may occur.
    • Mechanical (metal) prosthesis :
      • Only used in young patients < 55-60 years.
      • Normally no degeneration of the valve occurs.
      • Afterwards, strict indication for life-long blood thinning with oral anticoagulants (coumarins, e.g. warfarin) to prevent valve thrombosis.
        DOACs are contraindicated in these patients!

• Secondary (functional) mitral regurgitation :
  •  Valve leak caused by an abnormality of the left ventricle.
  • Question of whether or not an intervention can help is more difficult than with primary MR.
  • First step is always an optimal heart failure treatment for a few weeks to months, including a CRT device if indicated.
  • If revascularization is necessary, CABG + mitral valve repair can be chosen.
  • If no revascularization is necessary, you can opt for :
    • Surgical mitral valve repair: in case of a low surgical risk.
    • Percutaneous mitral valve repair (edge-to-edge repair with MitraClip): in case of a higher surgical risk and when the patient meets the following criteria (the COAPT criteria) :
      • Appropriate anatomy of the mitral valve
      • LVEF 20-50%
      • LV end-systolic diameter (LVEDD) ≤ 70 mm
      • Systolic pulmonary arterial pressure (sPAP) ≤ 70 mmHg
      • Absence of severe RV dysfunction and/or tricuspid regurgitation
      • Hemodynamic stability

All therapeutic decisions should be made in the Heart Team.