Aortic stenosis represents a lesion that consists of narrowing the aortic orifice thus realizing an obstacle to emptying the left ventricle. The causes can be either congenital (lesion being present since birth) and acquired by calcification, sclerosis and interesting for Rheumatic valve.
The most common form of aortic stenosis is congenital bicuspid aortic valve, in which the foils that makes the aortic valve are fused to the periphery, so that the valve is turning into a diaphragm provided with a hole in its central area. Initially the valve is thickened and along with aging, it fibroses and gains limestone deposits, these entire phenomena further narrowing the orifice. Clinical manifestations will occur in case of bicuspid around the age of 40-50 years. Aortic stenosis acquired during life are either degenerative either from the rheumatic cause. The degenerative appear at over 60 years, unlike congenital stenosis; valvular foils are not fused, finding only a thickening of the valvular with a secondary deposition of calcium and fibrosis. Rheumatic aortic stenosis is associated quite frequently with other mitral lesion.
Because of the left ventricle must pump blood against the obstacle represented by aortic stenosis, while he develops the muscle mass hypertrophying. The degree of hypertrophy is directly proportional to the severity of aortic stenosis. This stage is compensated. In the final stages, the left ventricle cannot pump blood in the systole the entire amount of content and begins to dilate increasingly more to the stage of heart failure. Changes that installs retrograde are: dilated left atrium (because it increases pressure in the left ventricle diastolic) pressure increases in the pulmonary circulation and the right ventricle undergoes hypertrophy (increases muscle mass) and then dilate. Initial portion of the aorta shows changes in shape, dilating below the stenosis level.
The myocardial mass development of the left ventricle (LV hypertrophy) occurs as a compensatory mechanism to maintain normal systolic flow in spite of the trouble aortic orifice, due to the increase of contraction force. As ventricular hypertrophy is more pronounced, the more impaired ventricular relaxation in diastolic slowing down the filling of the left ventricle with blood coming from the left atrium. Thus ventricular diastolic function is impaired. The systolic function alteration of the left ventricle appears later, even after a few years, and is due to myocardial fibrosis and ischemia.
Ischemia, imbalance between oxygen supply to the myocardium and greatly increased oxygen demands of the myocardium is explained by the increase of myocardial mass of the left ventricle and contractility increase as compensatory mechanisms. Myocardial ischemia may underlie the generation of atrial fibrillation, once installed, quickly deteriorating hemodynamic status.
Obstacle to the flow of blood ejected from the left ventricle into the aorta causes an increase in pressure within the ventricle. Increased pressure in the left ventricle during diastole, makes it difficult for the left atrium to empty, incomplete, inducing retrograde an increased pressure in the pulmonary veins, pulmonary capillaries, and finally into the pulmonary artery. Therefore patients will present dyspnea, initially at high physical effort, because later on by lesion progression, at smaller efforts. In advanced stages of paroxysmal nocturnal dyspnea appears imminent choking sensation during the night, the patient adopting a sitting position with legs dangling from the edge of the bed. This position, called orthopnea position improves breathing.
In the early stages, of the left ventricle pump function is not altered because its fibers myocardial hypertrophy is compensatory. By hypertrophy is evident that the necessary (demand) of oxygen increases, but oxygen supply brought by coronary blood remains constant. Thus there is a discrepancy between supply and demand which is the very definition of myocardial ischemia. This pathological mechanism and the others of the left ventricle pump function deteriorate progressively decreasing systolic flow (volume of blood pumped by the ventricle in a systole) and cardiac output (amount of blood ejected per minute).
Reduced cardiac output produces the following symptoms:
increased heart rate;
increased respiratory rate;
feelings of fatigue;
angina-type pain (retrosternal pain induced by the effort that gives promptly to sublingual nitroglycerin or bed rest);
Loss of consciousness by reducing oxygen to the brain.
The pulse and the blood pressure are normal in most cases. Only in conditions of severe aortic stenosis, the pulse becomes weak perceptible to the touch.
Chest Radiography: in mild and medium, even in the presence of ventricular hypertrophy, the heart appears normal size. This is because of the left ventricle muscle growth occurs towards the inside of the ventricular cavity. It can detect an increased heart size in the time of the onset of the ventricular dilation. On the radiography can be observed calcification of the aortic valve, aortic dilatation.
Echocardiography: the most efficient method for investigating noninvasive providing reliable data on the location of the stenosis and the degree of stenosis. It highlights the fattening aortic valve, dilated ascending aorta, ventricular hypertrophy and is measured the area of the aortic stenosis.
Treatment of aortic stenosis
For patients with aortic stenosis that is installed as in the clinical picture previously described therapeutic indication is surgery. Surgical treatment is taken into account if the patient is asymptomatic but has severe aortic stenosis (determined by echocardiography).
There are two surgical methods:
Dilatation of the aortic orifice with a balloon inserted into the arterial system through the femoral artery. When the ball reached the aortic annulus, thereby causing dilation swell. This method is called balloon angioplasty.
Valvular prosthesis that is the injured aortic valve replacement with a biological prosthesis or metal.
Patients can resume their normal activities about three months after the intervention.