heart health

Mitral Stenosis

Generality

Mitral stenosis is a narrowing of the mitral or mitral valve of the heart. Due to this narrowing, the disease compromises the regular blood flow passing through the orifice located between the left atrium and the left ventricle, controlled, in fact, by the mitral valve.

The main cause of mitral stenosis is a rheumatic disease due to a bacterial infection. The manifestations are multiple: dyspnea, atrial fibrillation and chest pain are just some typical symptoms. Their identification is based on a stethoscopic examination and, obviously, on instrumental diagnostic investigations. The therapy differs according to the severity of the stenosis: if this heart disease is severe, surgery is required.

What is mitral stenosis. Pathological anatomy and pathophysiology

Mitral stenosis (from the Greek στενόω, restrict) is a narrowing of the mitral valve, such as to compromise its correct activity. The mitral valve is located at the level of the orifice which connects the left atrium to the left ventricle of the heart. Its function is to regulate the unidirectional passage of blood, rich in oxygen, between the two cardiac cavities, during the phases of diastole and systole. In other words, in the heart of an individual with mitral stenosis, blood is hindered in its passage from the left atrium to the left ventricle.

Before examining how a mitral valve affected by stenosis looks like and how it works, that is, analyzing its pathological anatomy and its pathophysiology, respectively, it is useful to mention some fundamental characteristics of the valve:

  • The valve ring . Circumferential structure that defines the valve orifice.
  • The valve orifice measures 30 mm in diameter and has a surface of 4 cm2.
  • Two flaps, front and back. It is said, for this reason, that the valve is bicuspid . Both flaps fit into the valve ring and look towards the ventricular cavity. The anterior leaflet looks towards the aortic orifice; the posterior flap faces, instead, on the wall of the left ventricle. The flaps are composed of connective tissue, rich in elastic fibers and collagen.
    To facilitate the closure of the orifice, the edges of the flaps have particular anatomical structures, called commissures. There are no direct controls, of the nervous or muscular type, on the flaps. Similarly, there is no vascularization.
  • The papillary muscles . They are two and are extensions of the ventricular musculature. They are sprayed by the coronary arteries and give stability to the tendinous cords.
  • Tendinous chords . They serve to join the flaps of the valve with the papillary muscles. As the shafts of an umbrella prevent it from turning to the outside in strong winds, the tendinous cords prevent the valve from being pushed into the atrium during the ventricular systole.

Mitral stenosis results from a fusion of the commissures. The fusion can be more or less accentuated and turns the orifice into a slit. In cases of minor stenosis, or at an early stage, the cusps may appear only thickened; vice versa, if the stenosis is severe, the limbs become rigid and calcium salts are placed there (calcification).

The greater the narrowing of the orifice, the more severe the form of stenosis:

  • Mild mitral stenosis, if the surface measures less than 4 cm2 but not less than 2
  • Moderate mitral stenosis, if the surface measures between 2 and 1 cm2.
  • Severe mitral stenosis, if the surface measures less than one cm2.

When the normal blood flow through the mitral valve is hindered, the blood tends to accumulate in the atrium, that is the first cavity that it goes through when it reaches the heart. It is oxygen-rich blood from the lungs. The effect of this forced stop translates into an increase in pressure inside the atrium and, in general, of everything that is upstream of the occlusion, including the lungs (it follows atrial and pulmonary hypertension). The situation reflects what happens to a dam that accumulates water relentlessly and fails to discharge it. From the anatomical point of view, the increase in pressure determines a hypertrophy of the walls of the left atrium. Hypertrophy consists of an increase in cell volume. In this case, it is due to the increased effort that the cells make to push the blood through a narrow orifice.

The accumulation of blood in the atrium, by reduction of the flow through the valve, and the consequent increase in pressure, generate a further change: the ventricular pressure, in fact, is lower than normal. This pressure is fundamental in the phase of ventricular systole, that is when the heart contracts to push blood into the vessel systems. If it is reduced, the range and flow of blood through the aorta are also lowered. Thus, during a mitral stenosis, the following consequential events occur:

  • The orifice of the mitral valve is restricted.
  • The blood is forced into the left atrium.
  • Atrial and pulmonary pressure increase
  • The walls of the atrium become hypertrophic.
  • The ventricular pressure is reduced compared to normal, because the blood reaches the ventricle with more difficulty.
  • The range of blood, caused by the ventricular systole, is compromised.
  • The flow of blood through the aorta is reduced.

Finally, two other typical anatomical aspects of mitral stenosis concern the left ventricle and the lungs. The left ventricle is deformed following a previous adaptation of the tendinous cords and papillary muscles. This adaptation is created by the occlusion of the valve.

In the lungs, instead, edema zones are created, due to the stagnation of blood in the atrium and to the increase in pressure that it produces in all upstream vessel systems, especially in the pulmonary capillary apparatus ( pulmonary hypertension ).

Causes of mitral stenosis

The main cause of mitral stenosis is due to rheumatic diseases .

The rheumatic origin of heart disease is attributable to a bacterial (streptococcus) infection of the airways. As a rule, following an infection, the human body responds with a production of antibodies, which eliminate the bacteria, without complications. In some subjects, however, the antibody defenses produced against the streptococcus also recognize valvular cells as foreign and attack them. An inflammatory state is therefore created, which leads to deformation of the mitral valve. The latter is thickened and with the cusps fused together.

Other causes of mitral stenosis are:

  • Senile degeneration, due to the progressive deposition of calcium salts (calcification) on the valve leaflets. Calcification creates tissue stiffness. It is an event that leads to the 5th-6th decade of life.
  • Congenital heart problems. Since birth, some structural elements of the valve are deformed.
  • Valvular infections due to endocarditis. An endocarditis is a bacterial infection typical of the internal cavities of the heart.

Symptoms and signs

When mitral stenosis is mild, the affected individual has no particular symptoms or problems.

When, on the other hand, the stricture worsens, the first symptoms appear, linked to the physiopathological aspects described above: above all, the increased pressure in the left atrium and in the upstream compartments prevails, including the lung. Therefore, the main symptoms are:

  • Atrial and pulmonary hypertension.
  • Dyspnea on exertion.
  • Atrial fibrillation.
  • Respiratory infections.
  • Hemoptysis.
  • Organic weakness, defined adinamia.
  • Chest pain due to angina pectoris.

Effortless dyspnea consists of difficult breathing. In the specific case, it arises following the lower outflow of blood towards the left ventricle and, subsequently, towards the aorta. The heart struggles to pump blood through the occluded mitral valve and the body's response to the consequent lack of oxygen is to increase the number of breaths; respiratory acts that increasingly engage the heart. Furthermore, as the circulatory flow is obstructed at the level of the left atrium, there is an accumulation of blood in all the upstream districts, including the pulmonary veins and the lungs. This stagnation has serious consequences: increased pulmonary pressure (pulmonary hypertension ), compression of the respiratory tract and, in the most serious cases, the leakage of fluids from the vessels to the alveoli. This last condition is the prelude to pulmonary edema: in these conditions, the oxygen-carbon dioxide exchange between alveoli and blood is compromised.

Atrial fibrillation is a cardiac arrhythmia, ie an alteration of the normal heartbeat rhythm. It is due to a disorder of the nerve impulse coming from the atrial sinus node. It results in fragmentary and ineffective haemodynamic atrial contractions (ie they do not ensure adequate blood flow). In fact, the left atrium works poorly and the flow of blood, which flows into the underlying ventricle, is less than normal. The result is that even the ventricular contraction, which serves to push the blood into the aorta, is insufficient to satisfy the body's oxygen requirements. Faced with this situation, the individual suffering from atrial fibrillation increases the respiratory acts, manifest palpitation, irregularity of the wrist and, in some cases, fainting due to lack of air. The picture can further degenerate: the slowing down of blood flow and the accumulation of blood in the vessel systems, especially if associated with an altered coagulation, give rise to the formation of thrombi (solid, non-mobile masses, composed of platelets) inside of the vessels. The thrombi can disintegrate and release particles, called emboli, which, traveling in the vessel system, can reach the brain, or the heart. In these locations, they become an obstacle to normal spraying and oxygenation of brain or cardiac tissues, causing the so-called ischemic stroke (cerebral or cardiac) situation. In the case of the heart, one also speaks of a heart attack .

Respiratory or thoracic infections are due to pulmonary edema.

Emoftoe is the so-called blood spit, due to the rupture of the bronchial venules, in the lungs. Also in this case, it is the triggering cause of pulmonary edema.

Chest pain, due to angina pectoris, is a rare event. Angina pectoris is due to left atrial hypertrophy, ie the left atrium. In fact, the hypertrophic myocardium needs more oxygen, but this request may not be adequately supported by the coronary implant. It is therefore not an occlusion of the coronary vessels, but an imbalance between consumption and oxygen supply to the tissues.

The most characteristic physical signs, however, are:

  • Mitral facies.
  • First and second tone, or snap, of opening of the mitral valve.
  • Diastolic breath.

The mitral facies is manifested by a cyanosis of the face, in particular of the lips.

The opening snap of the mitral valve is a noise, or tone, due to the sudden movement that the valve makes at the moment of the ventricular contraction of the heart. It is the consequence of the abnormal pressures inside the left atrial and ventricular cavities, as well as the altered morphology of the valve cusps. This noise is attenuated when the mitral valve has calcification on the leaflets, typical of old age.

The diastolic murmur is perceived when the mitral valve is open, in the diastole or presystolic phase.

Diagnosis

Mitral stenosis can be detected by the following diagnostic tests:

  • Stethoscopy.
  • Electrocardiogram (ECG).
  • Echocardiography.
  • Thoracic radiography.
  • Cardiac catheterization.

Stetoscopy . Detection of a diastolic and presystolic murmur may be a clue to diagnose mitral stenosis. The noise of a diastolic murmur occurs when the blood passes through the stenotic mitral valve. It is perceived in the diastolic phase, since it is at this time that the atrioventricular valves are open and the atrium has not yet contracted. The detection zone is in the V intercostal space, ie the one coinciding with the position of the mitral valve.

ECG . By measuring the electrical activity of the heart, the ECG shows hypertrophy, left atrium overload and atrial fibrillation, all due to valve occlusion. Diagnosis by ECG gives an idea of ​​the degree of severity of mitral stenosis: if the outcome is comparable to that of a healthy individual, it means that the stenosis is not severe; vice versa, the examination shows the three irregularities mentioned.

Echocardiography . Taking advantage of the ultrasound emission, this diagnostic tool shows, in a non-invasive way, the fundamental elements of the heart: atriums, ventricles, valves and surrounding structures. From echocardiography, the doctor can detect:

  • Calcification or rheumatic lesions of the elements that make up the mitral valve.
  • Anomalies in the movement of the cusps.
  • Increase in the size of the left atrium.
  • Possible presence of thrombus in the left atrium.
  • The maximum flow rate, through the use of the Doppler. From this measurement, the pressure values ​​between the left atrium and the left ventricle can be derived.

Chest x-ray . It is useful for observing the situation at the level of the lungs, verifying whether or not edemas are present. Moreover, it allows to see the increased volumes of the vessels upstream of the valvular stenosis, due to hypertrophy and blood stagnation.

Cardiac catheterization . It is an invasive hemodynamic technique. The purposes of this exam are as follows:

  • Confirm the clinical diagnosis
  • Evaluate the haemodynamic changes, ie the blood flow in vessels and cardiac cavities, in quantitative terms.
  • Define confidently if you can intervene surgically.
  • Evaluate the possible presence of other cardiac pathologies.

Therapy

The therapy depends on how severe the stricture is. A mild and asymptomatic stenosis, that is, that has no symptoms, requires simple measures to prevent a deterioration:

  • Clinical surveillance
  • General hygiene rules to prevent bacterial infections, such as endocarditis.

If, on the other hand, the stenosis, albeit slight, presents symptoms, the administration of some drugs is required:

  • Digital, Beta-blockers and antiarrhythmics, in the case of atrial fibrillation at the beginning.
  • Diuretics, to reduce pulmonary hypertension.
  • Anticoagulants, to prevent thrombus and emboli formation due to chronic atrial fibrillation.
  • Antibiotics, if an endocarditis is detected, that is, a bacterial infection that afflicts the internal cavities of the heart. In this regard, it is good practice to recommend a careful oral and dental hygiene, to avoid predisposition to bacteria infections.

The therapeutic approach for individuals with moderate or severe mitral stenosis is different. In this case, surgery is required. In particular, if the patient, after the opportune diagnostic tests, presents hypertension and pulmonary edema, the intervention becomes a priority.

The possible surgical operations are:

  • Mitral Commissurotomy . The commissurotomy consists in the separation of the flaps of the valve, which are fused together following a rheumatic disease determining the stenosis. It is a veritable incision of the unnatural welding created. It can be performed using a balloon catheter - in this case we speak of percutaneous commissurotomy - or after a thoracotomy (open heart commissurotomy). It is not a valid approach for patients who present calcifications at the level of the cusps.
  • Replacement of the valve with a prosthesis . It is the most implemented intervention for the valves of those individuals suffering from severe anatomical anomalies. A thoracotomy is performed and the patient is placed in extracorporeal circulation (CEC). Extracorporeal circulation is achieved through a biomedical device which consists of creating a cardio-pulmonary pathway that replaces the natural one. In this way, the patient is guaranteed an artificial and temporary blood circulation that allows surgeons to interrupt the flow of blood in the heart, diverting it to another equally effective path; at the same time, it allows you to operate freely on the valve apparatus. Prostheses can be mechanical or biological.
  • Valvuloplasty . Stenosis is reduced with the use of balloon catheters, thus adjusting the altered atrial pressure and ensuring a better blood flow. It is indicated when a mitral stenosis due to calcifications and stiffened flaps is ascertained. It is carried out in a similar way to an angioplasty.
  • Mitral valve repair . It is an approach indicated for stenoses due to a modification or a rupture of the tendinous cords, which are replaced by the cardiac surgeon. It is also a valid solution in the event of valve ring anomalies. Again, patients are placed in extracorporeal circulation. This method is not suitable for cases of mitral stenosis with rheumatic origin.