Aortic valve insufficiency can be congenital or acquired, although the congenital form is very rare. As the heart develops very early during pregnancy, congenital aortic insufficiency often develops before the eighth week of pregnancy.
In addition to genetic factors, drug and alcohol consumption and an infection with the rubella virus can also contribute to a heart valve defect. However, aortic valve insufficiency can just as easily be caused by a bacterial inflammation of the heart, known as endocarditis. The bacteria attack the pocket valve and damage its structure so that it no longer closes properly. However, this form of valve defect has become rare in Europe, as bacterial infections are now treated early on with antibiotics.
Rheumatic valve defects also result from an infection. However, unlike bacterial endocarditis, rheumatic feveris a late and not a direct consequence of the disease. If there is an infection with certain bacteria (usually streptococci), the body forms antibodies against these pathogens. The surface structure of the bacteria is similar to that of some of the body's own structures, so that the antibodies formed also attack these and cause inflammation. If these inflammatory processes occur in the area of the heart, the heart valves can be irreversibly damaged.
Other diseases can cause aortic valve insufficiency in a similar way, such as Marfan syndrome or Ehlers-Danlos syndrome. Aortic valve insufficiency can also be caused by excessive stretching of the valve components. However, this phenomenon mainly occurs in people over the age of 60 or when the aorta is dilated as a result of an aneurysm. As the aorta expands, the aortic valve is pulled apart and thus loses its functionality.
Mild forms of valve insufficiency are compensated for by the body and are therefore not noticed by the patient. In severe forms, shortness of breath (dyspnoea) is the main symptom. Depending on the severity, the backflow volume is up to two thirds of the ejection volume. This means that two thirds of the blood that the left ventricle pumps into the aorta flows back again during the relaxation phase of the heart. On the one hand, this pendulum blood is missing in the blood circulation and, on the other hand, puts a strain on the left heart.
The result is an enlargement of the left heart, known as hypertrophy. After decades, this cardiac hypertrophy leads to a malfunction of the heart muscle, so that left heart failure gradually develops. The heart can no longer pump the amount of blood that the body needs. This manifests itself as:
- Shortness of breath on exertion and later also at rest,
- coughing fits at night,
- accumulation of water in the lungs (pulmonary edema).
If a heart valve defect is suspected, the doctor listens to the patient's chest with a stethoscope. He can recognize aortic valve insufficiency by the sound made by the backflow of blood into the left ventricle. This Austin-Flint sound is particularly audible above the apex of the heart.
Other important indications of aortic valve insufficiency are a low lower blood pressure value (diastolic blood pressure) and a high blood pressure amplitude. The blood pressure amplitude is the difference between the systolic (upper) and diastolic blood pressure values. The diastolic blood pressure is low due to the backflow of blood during the relaxation phase (diastole) of the heart. The systolic blood pressure, on the other hand, is normal, so that the amplitude is exceptionally high. The high blood pressure amplitude also leads to the characteristic Musset sign, a pulse-synchronized nodding of the patient's head.
However, instrumental procedures are required to confirm the diagnosis. An ultrasound examination of the heart, known as echocardiography, can be used to determine how much blood is flowing back into the ventricle. A cardiac catheterization as well as an electrocardiogram(ECG) or an X-ray examination of the chest can also be helpful in making a diagnosis.
In the early stages, the heart valve defect is treated with medication. ACE inhibitors, calcium antagonists and nitro preparations can relieve the heart by lowering the blood pressure. If the patient suffers from shortness of breath and/or the heart threatens to decompensate, an artificial heart valve should be implanted. A distinction is made between mechanical heart valves and biological prostheses.
Aortic valve reconstruction can also be attempted in some cases. In this procedure, the surgeon restores the patient's aortic valve to its original form and function without the use of foreign materials.
The prognosis for aortic valve insufficiency is generally good. Early surgery improves the prognosis and life expectancy of patients. However, to prevent vascular occlusion with blood clots, patients with a mechanical heart valve must take anticoagulants for the rest of their lives.
