What're the symptoms of aortic stenosis?
Most children with aortic valve stenosis have no symptoms, so it’s difficult to detect. In general, many patients will be easily fatigued, but show no other symptoms until their thirties to fifties. A small number of children may be prone to dizziness and fainting (syncope) within the first ten years of life. If the obstruction is great, infants may suffer from severe heart failure. Sudden death is uncommon, but possible. Adolescents with hypertrophic cardiomyopathy, a type of aortic stenosis where the left ventricle is noticeably enlarged, have the greatest risk of sudden heart failure. How is it diagnosed? Children with
aortic valve stenosis usually have a heart murmur that can be heard with a stethoscope. A doctor can also detect pulse abnormalities and will see irregularities on an electrocardiogram (ECG). A chest x-ray may also show an enlarged left ventricle. An echocardiogram may also be ordered. This technique uses ultrasound waves to create an image of the heart and its function. In cases where severe blockage is suspected and surgery most likely, doctors may do a left heart cardiac catheritization. In this procedure, a thin tube (catheter) is inserted through an artery and moved into the heart chambers. This procedure will measure the pressure difference between the left ventricle and the aorta.
Most patients with aortic stenosis develop one or more of these three classic symptoms: shortness of breath (dyspnea), passing out (syncope), and chest pain (angina pectoris). Thickening of the walls of the left ventricle causes the ventricle to become stiff and unable to relax between contractions. When this happens, the pressure in the left ventricle rises and blood can "back up" into the lungs, interfering with normal absorption of oxygen from the lungs into the bloodstream. This may cause shortness of breath, which worsens as the left ventricle becomes increasingly impaired. The aortic valve may become so constricted (stenotic) that it can open only slightly, drastically reducing the amount of blood that flows into the aorta and throughout the body. In some cases, the flow of oxygen-rich blood to the brain may not be enough to sustain normal brain function. When this occurs, patients may briefly lose consciousness, or pass out. Losing consciousness is called syncope.
Patients with aortic stenosis may also experience chest pain, pressure, or discomfort (called angina or angina pectoris), caused by an insufficient supply of oxygen to the heart. As the left ventricle thickens and works harder to expel blood through the stenotic aortic valve, its demand for oxygen increases. To compound the problem, aortic stenosis reduces blood flow to the heart itself as well as to the rest of the body (the coronary arteries and other arteries of the body originate from the aorta). Thus, while the heart's demand for oxygen increases, its supply of oxygen-rich blood decreases, causing angina.
Syncope in the setting of heart failure increases the risk of death. In patients with syncope, the 3 year mortality rate is 50%, if the aortic valve is not replaced. While it is unclear why aortic stenosis would cause syncope, the most popular theory is that severe AS produces a fixed cardiac output. When the patient exercises, their peripheral vascular resistance will decrease as the blood vesels of the skeletal muscles dilate to allow the muscles to receive more blood to allow them to do more work. This decrease in peripheral vascular resistance is normally compensated for by an increase in the cardiac output. Since patients with severe AS cannot increase their cardiac output, the blood pressure falls and the patient wil syncopize due to decreased blood persufion to the brain. A second theory as to why syncope may occur in AS is that during exercise, the high pressures generated in the hypertrophied LV causes a vasodepressor response, which causes a secondary peripheral vasodilatation that will then cause decreased perfusion to the brain.
Angina in the setting of heart failure also increases the risk of death. In patients with angina, the 5 year mortality rate is 50%, if the aortic valve is not replaced. Angina in the setting of AS is secondary to the left ventricular hypertrophy (LVH) that is caused by the constant production of increased pressure required to overcome the pressure gradient caused by the AS. While the myocardium of the LV gets thicker, the arteries that supply the muscle does not get significantly longer or bigger, so the muscle may become ischemic. The ischemia may first be evident during exercise, when the muscle requires increased blood supply to compensate for the increased workload. The individual may complain of exertional angina. At this stage, a stress test with imaging may be suggestive of ischemia. Eventually, however, the muscle will require more blood supply at rest than can be supplied by the coronary artery branches. At this point there may be signs of ventricular strain pattern on the EKG, suggesting subendocardial ischemia. The subendocardium is the region that becomes ischemic because it is the most distant from the epicardial coronary arteries.
In Heyde's syndrome, aortic stenosis is associated with angiodysplasia of the colon. Recent research has shown that the stenosis causes a form of von Willebrand disease by breaking down its associated coagulation factor (factor VIII-associated antigen, also called von Willebrand factor), due to increased turbulence around the stenosed valve.