Myocardial infarction complicated by mitral regurgitation

Brief introduction of myocardial infarction complicated with mitral regurgitation Myocardial infarction involving the papillary muscle can produce varying degrees of mitral regurgitation, and coronary atherosclerotic heart disease is about 3% with mitral regurgitation. A mitral regurgitation caused by coronary heart disease can be caused by acute or chronic papillary muscle ischemia. In the case of myocardial infarction, the papillary muscle can be completely broken within a few hours due to acute ischemic necrosis. Although there are no abnormal lesions in the chordae and valve leaflets, the mitral valve leaflets in the corresponding site lose the function of opening and closing, and severe mitral regurgitation occurs in the early stage after the infarction. In the case of acute myocardial infarction, the sudden death of the mitral regurgitation due to rupture of the papillary muscle accounts for about 0.4 to 5%. In some patients, myocardial infarction causes avascular necrosis of the papillary muscle, but does not completely break immediately, or Due to long-term ischemia, necrotic myocardial tissue is gradually replaced by fibrous tissue. The papillary muscles become thinner and longer, and the contractile function is weakened or lost. The mitral regurgitation is more than 2 months after myocardial embolization. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific population Mode of infection: non-infectious Complications: hemoptysis pulmonary edema infective endocarditis sepsis

Myocardial infarction complicated with mitral regurgitation

Cause:

This disease is one of the complications of myocardial infarction, so myocardial infarction is the only cause of this disease.

Myocardial infarction complicated by mitral regurgitation prevention

This disease is one of the complications of myocardial infarction, so active treatment of induced disease is the only measure to prevent this disease, no other effective preventive measures.

Patients with myocardial infarction due to decreased cardiac output, plus absolute bed rest, weakened gastrointestinal motility, digestive function, so should give a light, digestible diet, ensure energy supply, avoid eating fat, high cholesterol food, so as not to further increase arteriosclerosis. Avoid eating a meal and increase the burden on the heart. Drinking and smoking are prohibited. Eat more fruits and vegetables, stay in bed, take fruit guide or soak in the sun or other laxatives or laxatives to ensure smooth stool.

Acute myocardial infarction should be absolutely bed rest in the first 1 to 2 weeks of onset. However, due to pain in the precordial area, the patient is unbearable, some are restless, and some patients feel that everything is normal after the pain, do not listen to the advice of medical staff, and get out of bed at will. The patient should be made aware that the activity will lead to a worsening of the condition. In the recovery period, it should be gradual and should not be rushed.

Myocardial infarction complicated with mitral regurgitation Complications hemoptysis pulmonary edema infectious endocarditis sepsis

1. The complications of chronic patients are similar to those of mitral stenosis, but they appear later. The earliest symptoms of mitral stenosis are paroxysmal dyspnea at night, and severe sitting breathing. Very severe cases can produce pulmonary edema and cough. Cough pink foamy sputum, more than sleep or increased after exercise, may be accompanied by cough, blood in the sputum, hemoptysis, as the disease progresses, the lower extremity edema, when the urine is low, the breathing difficulties can be alleviated.

2, infective endocarditis is more common, embolism is rare, the patient's main performance is:

1 sepsis performance, acute onset, rapid progress, high fever, chills, fatigue and other symptoms of poisoning;

2 skin bleeding points and embolism;

3 heart performance, early no noise, new murmurs appear in short-term after a few onset and quickly become high-profile, rough, and heart failure.

3, acute patients and chronic patients with chordae rupture, short-term acute left heart failure or even acute pulmonary edema, poor prognosis, patients with rapid onset, severe breathing difficulties, sitting breathing, frequent cough, white or pink The foam is sullen, restless, gray, sweaty, and weak.

Myocardial infarction complicated with mitral regurgitation symptoms common symptoms systolic murmur edema heart failure hypotension left heart failure shock

The anterior and posterior anterior papillary muscles each have a chordae, which is connected to the edge of the mitral valve leaflet. Each papillary muscle is responsible for the chordae function of the anterior or posterior half of the mitral valve. When the mitral valve is tightened, the edge of the leaflet is prevented from turning to the left atrium, resulting in a regurgitation. The blood supply to the anterior and external papillary muscles comes from the diagonal branch of the left anterior descending artery and the marginal branch of the circumflex artery, while the blood supply to the posterior papillary muscle is only From the posterior descending branch of the right coronary artery, therefore, in the coronary heart disease, the posterior papillary muscle is more prone to ischemic lesions than the previous external papillary muscle. About 80% of the acute papillary muscle rupture occurs in the posterior papillary muscle, caused by myocardial infarction. Papillary muscle necrosis, due to sudden mitral regurgitation, a large amount of blood from the left ventricle to the left atrium when the ventricle contracts, the left ventricle discharge decreased, blood pressure decreased, severe cases of shock, pulmonary vascular congestion, pulmonary edema .

Acute myocardial infarction only causes partial fracture of the papillary muscle. Although the papillary muscle is stretched and stretched, part of the mitral valve leaflets prolapse into the left atrium when the ventricle contracts, resulting in mitral regurgitation, but to a lesser extent, return flow Not much, the impact on hemodynamics is small, in some cases, the ischemic papillary muscles are not broken during myocardial infarction, and are gradually replaced by fibrous scar tissue, the contractility is lost, and the weak papillary muscles are elongated, although the scorpion Still connected with the papillary muscles, but due to dysfunction of the papillary muscles, the mitral valve leaflets can still sag into the left atrium when the ventricle contracts. However, the mitral regurgitation flow is generally not too much, the disease progresses slowly, but can develop to Left heart failure is present, which is more common in patients who have undergone surgery for mitral regurgitation more than 2 months after myocardial infarction.

Cases of mitral regurgitation caused by rupture or dysfunction of the papillary muscles, often accompanied by ventricular free wall myocardial infarction, the extent of infarction and the thickness of the affected myocardium are quite different, which may be due to transmural infarction or infarct lesions limited to subendocardial In the area, mitral regurgitation caused by severe papillary muscle rupture may be interspersed with ventricular septal rupture, ventricular free wall perforation or ventricular aneurysm.

Papillary muscle rupture can suddenly present acute pulmonary edema and / or hypotension and shock symptoms within a few hours to 2 weeks after the onset of acute myocardial infarction. The general condition deteriorates rapidly, and the systolic murmur can be heard in the apical region. In the ankle, the partial rupture of the papillary muscle is more audible, the third heart sound is often heard in the apical region, and the chest X-ray shows pulmonary edema, but the heart and left atrium are not common, and the right heart Swan-Ganz floating catheter is examined. The left atrial pressure is increased, the pressure curve is high and sharp V waves, but there is no left to right shunt at the ventricular level, which can rule out ventricular septal perforation.

Segmental echocardiography can show abnormal movement of the mitral valve leaflets. When the ventricles contract, the edges of the two leaflets fail to meet; and the papillary muscle rupture and papillary muscle dysfunction can be distinguished. When the ventricle contracts, the lesion area And some of the mitral valve leaflets turned into the left atrium, the anterior and posterior leaflets failed to align, and the ventricular diastolic returned to the left ventricle with blood flow, and sometimes the distal papillary muscle of the fracture was attached to the chordae, along with When the leaflets are turned up and down, the dysfunction of the papillary muscles shows that the contraction function of the papillary muscles is reduced. When the ventricles contract, the edge of the mitral valve leaflets is poorly aligned, and the free wall of the myocardium also shows movement disorders.

Selective left ventricular angiography can confirm the diagnosis, determine the severity of mitral regurgitation, understand the location and extent of left ventricular wall dysfunction, and find out whether there is ventricular aneurysm and can exclude ventricular septal perforation, but critically ill. Cases should be taken with caution and should not be routinely performed.

Selective coronary angiography can help identify sites that require concurrent coronary artery bypass grafting.

The mitral regurgitation caused by chronic papillary muscle ischemia often presents symptoms and signs of mitral regurgitation several months after the occurrence of myocardial infarction. The early symptoms of the lesion may appear intermittently, and then the degree of mitral regurgitation gradually increases. The ventricle and left atrium are significantly enlarged, with cardiac dysfunction and heart failure.

Myocardial infarction complicated with mitral regurgitation

(1) X-ray examination of mild mitral regurgitation, no obvious abnormal findings, severe left atrium and left ventricle increased significantly, significantly increased left atrium can be displaced and oppressed esophagus, pulmonary hypertension or right heart failure At the time, the right ventricle is enlarged, pulmonary stagnation, pulmonary interstitial edema, and Kerley B line are often seen. Calcification of the mitral valve leaflets and annulus is often present. Left ventricular angiography can quantify mitral regurgitation.

(2) ECG examination of patients with mild mitral regurgitation may be normal, severe cases may have left ventricular hypertrophy and strain; pulmonary hypertension may show left and right ventricular hypertrophy, chronic mitral regurgitation with left atrial enlargement Most of the patients had atrial fibrillation, and the sinus rhythm P-wave broadened and showed a double-peak shape, suggesting an increase in the left atrium.

(3) Echocardiography is the most accurate non-invasive diagnostic method for detecting and quantifying mitral regurgitation. On the two-dimensional echocardiography, the anterior and posterior lobes of the mitral valve are enhanced and thickened, and the valve is closed during systole. Poor combination; when the chordae rupture, the mitral valve can be changed in a sacral manner. On the long axis of the left ventricle, the leaflet is seen in the systolic phase with a gooseneck-like hook to the left atrium, and the diastolic phase is whip-like to the left ventricle. M-mode ultrasound showed diastolic anterior mitral EF slope increased, valve leaf activity increased; left atrial enlargement, systolic over-expansion; left atrial enlargement and ventricular septal hyperactivity, Doppler ultrasound showed left atrial contraction Period of reflux, left heart echocardiography, see contrast agent returned to the left atrium by the left ventricle during systole.

(IV) Radionuclide examination Radionuclide blood pool imaging showed enlargement of the left atrium and left ventricle, increased left ventricular end-diastolic volume, pulmonary artery hypertension and right ventricular enlargement.

(5) Right heart catheter examination of the right ventricle, pulmonary artery and pulmonary capillary pressure increased, pulmonary circulation resistance increased, left atrial catheter examination of left atrial pressure increased, pressure curve v wave significantly, and cardiac output decreased.

Diagnosis and diagnosis of myocardial infarction complicated with mitral regurgitation

The murmur of mitral regurgitation should be identified by systolic murmur in the apical region of the following conditions:

(1) Relative mitral regurgitation may occur in hypertensive heart disease, aortic regurgitation or myocarditis caused by various causes, dilated cardiomyopathy, anemia, etc. due to left ventricle or apex The annulus is significantly enlarged, causing the mitral valve to be relatively closed and the apical systolic murmur.

(B) functional apical systolic murmur about half of normal children and adolescents can hear systolic murmur in the anterior region, loudness is 1 ~ 2 / 6 level, short, soft, do not cover the first heart sound, no atrium And the enlargement of the ventricle can also be seen in the high-power circulation state such as fever, anemia, hyperthyroidism, etc., and the noise disappears after the cause is eliminated.

(C) ventricular septal defect can be heard in the third to fourth intercostal space of the sternal border and rough full systolic murmur, often accompanied by systolic tremor, murmur to the apical region, apical beats are lifted, ECG and X-ray examination The left and right ventricles increased, echocardiography showed continuous interruption of ventricular septum, and echocardiography confirmed the presence of left-to-right shunt at the level of the ventricle.

(4) Tricuspid regurgitation The lower left rim of the sternum is smear and the localized squeaky squeak of the localized squeaky squeak. When the inhalation is increased, the murmur is enhanced by the increase of the blood volume. When the pulmonary artery is high, the pulmonary heart valve is the second heart sound. Hyperthyroidism, v-wave of the jugular vein increases, there may be liver pulsation, swelling, right ventricular hypertrophy can be seen by electrocardiogram and X-ray examination, and echocardiography can confirm the diagnosis.

(5) Aortic valve stenosis The aortic valve area or apical area of the heart can hear loud and rough systolic murmur, which is transmitted to the neck, accompanied by systolic tremor, and may have early contraction, and the apex beat is lifted. ECG and X-ray examination showed left ventricular hypertrophy and enlargement, and echocardiography can confirm the diagnosis.

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