Pathology of mitral stenosis

2021-01-28 12:00 AM

Strong T2 at the base of the heart due to increased pulmonary pressure due to the closure of the aortic valve and the pulmonary artery, resulting in split T2.

Outline

Mitral stenosis is a fairly common disease in our country, accounting for about 40.3% of all acquired heart diseases. The disease is born in humans from the time it started to live in populations due to poor living conditions, cramped and unsanitary, easily causing infection. From 1887 Bouillaud then Sokolski described the disease. By 1920 Duckett Jones (USA) had studied this disease and until 1944 he published seven diagnostic criteria. Also, in these years, Cutter and Levine Phillipe (USA) tried to simultaneously operate mitral stenosis. that year Souttar in England also had mitral stenosis. At this stage, mitral stenosis is the most common cardiovascular disease, causing disability and death.

However, in underdeveloped countries the disease is widespread. Common diseases in the working-age range from 20 to 30 years old, the rate of mitral stenosis is very high, about 60-70%, the mortality rate is 5%. The disease has many complicated complications and leads to disability. The disease is more common in women than men (3/1) and more infected in rural areas than in urban areas.

The cause and treatment of pathogenesis

Mainly due to rheumatism of 99%, the remainder is congenital, or malignant carcinoid, systemic lupus erythematosus, rheumatoid arthritis is also believed to be caused by Coxsackie virus. The main cause of the disease is group A haemolytic streptococcus, causing sore throat, causing low heart damage. The reason that streptococci in the throat cause rheumatic heart disease without entering other organs is due to the lymphatic passageways between the throat and heart. The fetal structure shows that there is a pathway connecting blood vessels and nerves between the heart and neck.

In 1976 Taranta (USA) demonstrated the direct pathogenesis of streptococcal toxin to the heart. Antibodies appear in rheumatoid patients with heart inflammation, including cross-antigenic reactions between heart structures and streptococci. In summary, the mechanism of pathogenesis is as follows:

Group A streptococcus enters the body causing sore throat and also produces toxins. In addition, in the heart tissue also found materials with an immune structure similar to M protein, so the antibodies formed are also against the heart valves.

The confusing autoimmune phenomenon causes heart inflammation and arthritis. Heart inflammation can go away on its own, but after 2 years it can leave sequelae in the heart valve, 1 out of 3 patients have a sequela in the heart valve such as thick and sticky fibres causing the narrowing of the heart valve.

Symptom

clinical

Body as a whole: If the patient is infected before puberty, the patient is physically underdeveloped called a "mitral dwarf" (nanism mitral). If it happens after puberty, the baby develops almost normally.

Function:

There are times when it is found by chance by a mass physical examination that the patient does not have any symptoms even during exertion.

Sometimes patients go to the doctor because of difficulty breathing, coughing and spitting blood, palpitations, choking due to the atrial compression in the oesophagus, especially during exertion.

Entity: Cardiac listening is essential, can be heard when lying on their back, lying on their left side or sometimes having to let the patient do strenuous movements. Typical mitral stenosis often hears the following signs, according to the frequency of occurrence.

The sound of T1 sharp at the tip (due to the thick fibrous valve beating together).

Diastolic fibrillation (RTTr) in the apical stenosis due to a narrow valve, blood flow being forcefully pushed down the left ventricle into the muscular column and the muscular bridge in the left ventricle are inflamed, calcified, or RTTr disappears when the stenosis valve closes, the valve and organization under the valve thick, calcified, stick together.

A strong T2 is at the base of the heart due to an increase in pulmonary pressure due to the closure of the aortic and pulmonary valves, creating a split T2 (the pulmonary valve closes later than the aortic valve).

A mid-heart or apical anterior systolic murmur is caused by blood flow through a narrow space if it lingers in the left atrium, the left atrium must squeeze again to push the nodule to the left ventricle; but when atrial fibrillation or left atrium is dilated, no systolic blow is heard.

The crack of the mitral valve opens at the tip or in the tip. This sound is only available when the valve is still soft.

When the pulmonary artery pressure is high, the right ventricle dilates much to dilate the pulmonary valve ring causing diastolic blowing in the pulmonary valve called Graham - Steel blow.

There are also cases of mitral stenosis when examination does not hear anything but complications and thanks to the most subclinical is an ultrasound called mitral stenosis "mute".

Subclinical

Photoelectric: There are 2 postures to probe in the mitral stenosis:

Straight posture:

Right: The enlarged left atrium usually has 3 stages.

Stage 1: The left atrium is large, forming 2 arcs parallel to the inside of the left atrium, the outer edge is the right atrium.

Stage 2: The left atrium is enlarged to cut the right atrium, forming two different arcs.

Stage 3: The left atrium is enlarged to form two parallel arcs where the outer arc is the left atrium and the inner arc is the right atrium (as opposed to stage 1).

Left: There are 4 arcs: the aortic arch, the pulmonary artery, the left atrial ureter, the left lower arc with the heart tip upturned (large right ventricle).

Umbilical cord: Dark, forming on both sides of the heart ball, two wide-open spaces and unknown boundaries. Two fields are blurred due to congestion, the Kerley B pattern can be seen. If there is an increase in active pulmonary arterial pressure, the hilum is dark and the edge of the lung is very bright.

Barite on the slant film: the oesophagus is pinched in the middle 1/3. Loss of light before the heart or the sternum (large right ventricle).

ECG:

The first stage is not narrow or has no effect on the heart cavities: the electrocardiogram is normal.

Later stage: Left atrial thickening with P (0.12s or P biphasic, the negative phase is greater than the (+) phase in V1. The electrocardiogram axis has deviated right and right ventricular thickening.

In addition, you can also see arrhythmias such as atrial extrasystole, atrial tachycardia, atrial fibrillation is the most common. There may be an incomplete right branch block.

Echocardiography:

A means of diagnosing accurately determining mitral stenosis, especially when the stenosis is not clinically detected. Ultrasound also allows us to evaluate the valve and the under-valve body is thick or not so that we can decide whether to replace the valve or separate the valve.

In simple narrow:

 Single-plane type: Front and rear valve leaf stick together, so they move in parallel in the same direction, the valves are thickened. The valve takes the form of a plateau or a ski shoe. The EF diastolic slope is reduced. If narrow, the diastolic slope can be reduced by <15 mm / s. Left atrial diameter increased. RV diameter increased; right ventricular septum thickened. Indirect pulmonary hypertension can be seen.

2-way ultrasound: Determine the movement of the valve, due to the size of the heart chamber and measure the valve hole area.

Doppler ultrasound can detect mitral stenosis associated with other lesions for appropriate management. Simultaneously measure pulmonary artery pressure, monitor pulmonary artery pressure before and after treatment.

Dynamic centre map:

Combined with an electrocardiogram to evaluate the degree of narrow of the valve based on about Q - T1 and about T2 - CM. If Q - T1 is longer and T2 - CM shorter, the stenosis of the mitral valve is tight, now this probe is of little use because of echocardiography

Heart catheterization:

A diastolic pressure deflection between the left atrium and left ventricle is seen, a characteristic sign of mitral stenosis. Currently, ultrasound is decisive, so this means is rarely used. Use only when mitral regurgitation or combined aortic valve disease is suspected (rare).

Diagnose

Implementing the quadrants

Based on clinical and subclinical standards, as described above. The most decisive is still the echocardiogram and echocardiography.

Differential diagnosis

Diastolic fibrillation in tricuspid stenosis: Intraaxillary RTTr, uncharacteristic T1

The electrocardiogram has right atrial thickening. Echocardiography is crucial.

Left atrial mucous tumour (Myxoma): hear diastolic fibrillation change with position. There is no T1. Patients often faint. Diagnosis is based on echocardiography.

Stage diagnosis

There are 4 stages of mitral stenosis:

Stage 1: No symptoms of muscle function even during exertion. Clinical examination found accidental.

Stage 2: Clear exertion syndrome: Shortness of breath, palpitations, palpitations, coughing or coughing up blood, no manifestations of heart failure.

Stage 3: Difficulty breathing, right heart failure, but recovery treatment.

Stage 4: mitral stenosis with severe heart failure, irreversible treatment.

Diagnose the form of the disease

Simple form: The body is well tolerated; the patient has no signs of muscle function and often discovers the disease by accident.

Typical: As described above and on clinical examination, radiographs, electrocardiograms can be diagnosed.

"Mute" leaf picking valve stenosis: The patient may or may not have symptoms of muscle function. Cardiac hearing does not see the characteristic signs of mitral stenosis. This form requires looking for complications of mitral stenosis and subclinical especially echocardiography helps diagnose.

Progressive form: Usually cases of compact or very tight mitral stenosis. The patient was admitted to the hospital with severe complications. Arrhythmia, cardiac asthma, acute pulmonary oedema, embolism, etc.

Combination:

Combined mitral stenosis combined with mitral regurgitation: Must differentiate mitral regurgitation as main, stenosis is secondary or vice versa. If mitral regurgitation is mainly: hear strong TTT in the heart muzzle loud, spread, palpable systolic cataract. Mild diastolic fibrillation, X-ray, ultrasound, electrocardiogram with thick left ventricular dilatation and left atrium. Mainly echocardiography assesses the degree of mitral regurgitation, especially with Doppler ultrasound.

Coordination with aortic valve disease.

Tricuspid stenosis combined with aortic regurgitation: In addition to mitral stenosis, a diastolic murmur in the left intercostal III and right intercostal II spread down the left sternum, left ventricular thickening, ultrasound Cardiac doppler allows diagnosis.

Aortic stenosis combined with aortic stenosis: In addition to symptoms of mitral stenosis, there is also a systolic murmur in the right intercostal III and the right intercostal II spreading to the two-carotid artery with palpation.

Diagnosis of ECG with systolic left ventricular thickening, X-ray and echocardiography allow diagnosis.

Mitral stenosis combined with tricuspid valve disease:

Bicuspid stenosis combined with 3-leaf openings: Hear TTT in the snout or at the sternum. TTT sounds stronger when inhaled deeply and held in a breath. You can feel your liver loudly and beat according to the heartbeat. Neck pulsation. The lungs are usually brighter.

Atrial fibrillation of mitral valve stenosis: A stenosis associated with an atrial septal defect is called the syndrome

Lautenbacher. The diagnosis is confirmed by echocardiography and cardiac catheterization.

Mitral stenosis may also be associated with other cardiovascular conditions such as hypertension, but rarely

Complications diagnosis

Mitral stenosis often has the following complications.

Heart rhythm disturbances:

Sinus arrhythmia is usually tachycardia. External atrial systole, supraventricular tachycardia.

Atrial flutter and atrial fibrillation are serious complications of HHL. Since these arrhythmias can now cause peripheral embolism complications and longer lead to right heart failure.

Blocking: There are 2 mechanisms of clogging.

Angioplasty in the great circulation: Because blood stasis in the left atrium slowly circulates to the left ventricle, so blood clots easily. If tachyarrhythmias such as atrial fibrillation, the supraventricular tachycardia favours blood clots. After the heart rate slows down, the blood clot is carried down to the left ventricle and into the major circulation, causing embolism of the brain, limbs, kidneys, mesenteric etc ...

Pulmonary artery occlusion: Because a blood clot is formed from the peripheral veins, entering the right ventricle causes pulmonary artery obstruction. Or it may be due to increased pulmonary pressure in the mitral stenosis, which may form a local clot that clogs the pulmonary artery.

Infection:

Lung infection due to pulmonary artery stasis is a growing environment for bacteria: diffuse pneumonia, localized pneumonia.

Infections in the heart can cause Osler subacute endocarditis. This complication is rare, but when it does, the prognosis is bad because treatment is difficult and may fail.

Heart failure:

There may be acute pulmonary oedema heart attack common with exercise or at night. Due to blood stagnation in the lungs at night, the parasympathetic nerve is active, so it dilates the vessels, draining plasma into the alveoli, causing pulmonary oedema.

Right heart failure. This is also a complication and also the last stage of the disease. If not treated completely. These complications can occur when the patient exerts mental and physical exertion and causes an infection of the skin or lungs. Especially in pregnant women, at labour or menstruation.

Treatment

Internally medical treatment

Only good for mild to moderate mitral stenosis. If the narrow is tight, with the valve hole area <1.5 cm2, then surgical treatment will be effective.

Treatment of heart failure:

Diet:

Limit heavy labour, eat less, treat low recurrence, prevent Osler.

Diuretic:

When the body gains about 2 kg compared to before. Furosemide 40 mg x 1-2 tablets / day.

In acute heart failure can use Lasix 20 mg by slow intravenous injection. Note when using diuretics need to use more potassium (should make organic K + salt better than inorganic, such as K +, Mg ++ aspartate, Panangin brand name) to prevent hypokalaemia, easy to poison Digital.

Digital:

Less effect in heart failure due to mitral stenosis, even in the presence of right heart failure. Digital has good effects in heart failure due to mitral stenosis with atrial fibrillation complications to prevent atrial fibrillation attacks with rapid ventricular rate, aggravating heart failure, can use a slow enough absorbed dose. Digital 0.25 mg x 1 tablet/day for 5 days, rest for 2 days and then use again. Or Digital 0.25 mg x 1 tablet/day for 3 days, rest for 3 days and then use again.

Digital treatment should note signs of Digital poisoning such as:

Patients with vomiting, abdominal pain, blurred vision, double vision, loose stools.

Dual or malignant ventricular extrasystoles.

Either the heart rate spikes (while on Digital) or slows down with acute atrioventricular block, or coupling rhythm.

If the above symptoms appear, then digital should be discontinued and potassium supplemented by intravenous or oral administration, pay attention to adding Mg ++.

Vasodilators:

Used a lot in recent years. Vasodilators can be treated continuously, for a long time. Vasodilators work to reduce pre-load, after-load to help heart failure recover.

For heart failure in mitral stenosis best is the nitrate group and the derivatives are especially when mitral stenosis has increased pulmonary arterial pressure, chronic and acute pulmonary oedema. Risordan LP 20 mg x 1-2 tablets / day, or Imdur (Isosorbide mononitrate) 60 mg x 1/2 - 1 tablet / day.

Treatment of systemic artery occlusion:

Clogging can be cerebral artery, mesenteric artery, peripheral artery, spleen artery, renal artery, coronary artery ...

Complications of embolism are increased in patients with mitral stenosis with complications of atrial fibrillation and heart failure, especially in the presence of atrial fibrillation.

Mitral stenosis has more obstructive complications than mitral regurgitation. 20-60% are blocked a second time after the first obstruction in 6-12 months if no effective prophylaxis with anticoagulants.

Treat embolism as soon as possible:

Heparin 10,000 - 20,000 UI / day x 5 - 10 days. Low molecular weight heparin may be used especially for cerebral embolism. Then use anti-coagulants with anti-Vitamin K such as Sintrom, Previscan, Dicoumarin 48-72 hours before stopping Heparin to maintain the rate of Prothrombin about 30-35% or IRN 2.5-3 is the best.

After returning atrial fibrillation to sinus rhythm with medication or electric shock, mitral dilatation is the best method of preventing recurrent embolism. Or in patients who are not able to dilate valves, bypass surgery, or replace valves, they can take preventive thromboembolism for many years at low doses of 100 - 500 mg/day with aspirin (aspegic 100mg), dipyridamole, etc. ..

Preventive treatment:

Prevention of recurrence by Benzathylpenixilin 1.2 million units every 15-20 days, deep intramuscular injection after testing.

In addition, preventing superinfection of the lung or Osler with fast penicillin or Erythromycin 0.5g antibiotic before interventions such as tooth extraction, cutaneous boils, etc., when there are signs of phlebitis of the lower extremities can prevent artery occlusion. lungs by placing a lower vena cava filter.

Surgical treatment

Treatment of mitral valve surgery has made many signs of progress. The mitral valve is dilated by hand or with a tool or a balloon (catheter balloon).

Ball valve mitosis:

Insert the tube through the femoral vein into the right atrium, through the atrial wall into the left atrium to dilate the mitral valve with a balloon. This technique has been carried out in Vietnam. This method is indicated for young patients <40 years old, simple mitral stenosis, soft valve, under-valve organization not much deterioration, no blood clots in the left atrium or atrium. The complication of this method is a puncture of the left atrial wall causing acute pericardial haemorrhage, causing acute heart compression.

Close mitral commissurotomy:

Manual or instrumental: performed in patients: with narrow mitral pore area <1.5 cm2, soft or fibrous valve, no sinus rhythm calcification or atrial fibrillation, but no history of embolism, no aortic valve disease, or mitral regurgitation (if mild mitral regurgitation <2/4 then no contraindications), age <40, no pulmonary superinfection or progressive rheumatism, no Osler.

Results after dilatation in 5-10% of cases of symptoms of mitral stenosis, symptoms of increased pulmonary artery pressure gradually decrease and return to normal. Some patients with unproductive mitral dilatation or recurrent rheumatic fever cause re-sticking of the valve edge for a second dilatation, but with lower success and 10 times higher mortality initially.

Complications with dilatation and after dilatation:

Heart failure and arrhythmia after surgery.

Fever.

Post-dilated valve syndrome.

Pericardial effusion.

Transient cerebral occlusion.

Dilation of the mitral valve after dilatation is common in patients with calcifications of the valvular dysplasia.

Cardiac arrest while dilating.

Cardiac asthma, acute pulmonary oedema.

Cardiac arrhythmias (ventricular extrasystoles, atrial fibrillation, atrial fibrillation, paroxysmal supraventricular and ventricular tachycardia, fibrillation most).

Osler causes ligament rupture, mitral valve prolapses.

Open-heart surgery:

Need an artificial heart lung.

Mitral valve repair: The surgeon can widen or narrow the mitral valve ring, remove the ulcerated part, calcify or remove a blood clot in the atria, ventricles, and holes in the leaf. The muscle column and ligament were broken. The patient does not have to replace the valve, so the immune risk of transplant rejection, the risk of calcification, and embolism is reduced, so the anticoagulant is simpler than replacing the valve, reducing the risk of calcification, embolism, so anticoagulant therapy is simpler. .

Valve replacement surgery: Indicated in cases.

The stenosis of the mitral valve holds the thick calcified fibrous valve.

Combined stenosis with severe mitral regurgitation or simple mitral regurgitation.

Valve ulcer caused by Osder

Commonly used valve instead of the mitral valve:

Van Starr-Edwards: There is a cage holding the ball when the ball is lost, the ball moves up to the atrium to close the atrioventricular valve.

The SCDT-Custer valve is an improved Starr valve.

The Magovevu-cromtè valve is a modified Starr valve.

Van Kuy-Suzuki replaces the ball with a flat disc, has many advantages in hemodynamic than the ball valve, when the valve replacement surgery is lower, reducing the process of clotting in the valve and around the valve, which is the valve. Latest artificially improved from van Starr. With different shapes and materials such as Titanium, Teflon, Pyrolytic-carbon, Silastic, Polyproline .... has created many different types of valves:

Cuged-ball.

Starr-Edwards: 7 loại. Smeloff-custer: 2 loại: Braưald-custer, Cuged-disc.

Beall có 5 loại: Kay-Shiley, Kay Suzuki, Starr-Edwards, Cooley-Cutter, Tilting disc.

Bjork-Shiley has 3 types.

Lalehei-kaster: 4 kinds

A total of 27 types of artificial valves

 Biological mitral valve: Basically, recovery of hemodynamic, no infection, no blood clots, no rupture of the valve ring after a long time of surgery, so it opens up prospects for development in the future.

Complications after valve replacement:

In addition to complications such as dilatation, there are additional complications.

Sudden death during surgery.

Sudden death due to impaired valve action.

Fibrin binding, then calcification at the valve and around the chronic valve.

Osler caused by bacteria and fungi.

An abscess around the valve ring.

Open around the mitral valve ring.

High-grade atrioventricular block or His bundle of the bloc (due to amputation of the muscles).

Aortic stenosis or openness is secondary to mitral valve replacement.

Reduced ability to compensate for circulation during exertion.

Difficult to treat with an electric shock method, pacing when necessary.

Treatment of mitral valve dilatation or open or closed heart surgery requires continued treatment for rheumatism, Osler's room, anticoagulant treatment, and heart failure to prolong the patient's life.