Myocardial infarction complicated with left ventricular aneurysm

Introduction of myocardial infarction complicated with left ventricular ventricular aneurysm After left ventricular myocardial infarction, the ventricular wall is completely necrotic. About 10 to 38% of cases of necrotic myocardium are gradually replaced by fibrous scar tissue, forming ventricular aneurysm, the ventricular wall of the thin layer of the lesion is bulging outward, and the heart loses its mobility or exhibits abnormal movement when it contracts. As early as 1881, the evolution of coronary artery obstruction, myocardial infarction, myocardial fibrosis and left ventricular ventricular aneurysm was fully recognized. The clinical diagnosis of left ventricular aneurysm was rapid in the 1960s. In 1955, Likoff and Bailey performed a closed ventricular aneurysm. In 1958, Cooley performed the first ventricular aneurysm resection under cardiopulmonary bypass. basic knowledge Sickness ratio: 0.05% Susceptible people: no specific population Mode of infection: non-infectious Complications: shock, hypertension, hemoptysis, pulmonary embolism

Myocardial infarction complicated with the cause of left ventricular aneurysm

After left ventricular myocardial infarction, ventricular wall full-thickness necrosis, about 10 to 38% of cases of necrotic myocardium are gradually replaced by fibrous scar tissue, forming ventricular aneurysm, thin layer of ventricular wall bulging outward, cardiac contraction Loss of mobility or abnormal movement, about 85% of left ventricular aneurysm is located in the anterior lateral approach to the apical region, a small number of cases can be located in the surface of the heart, the ventricular wall of the lesion is thinned, showing white fiber scars, clear boundaries, local heart The outer membrane is closely adhered to the pericardium. In about half of the cases, there is a wall thrombus in the endocardial surface, sometimes showing calcification. The coronary artery obstruction is limited to the left anterior descending artery, but it can also involve several vessels, and the left ventricular cavity volume increases. Normal part of the heart muscle hypertrophy.

Myocardial infarction complicated with left ventricular ventricular aneurysm prevention

The prognosis of left ventricular aneurysm is closely related to the extent of left ventricular myocardial involvement and the volume of ventricular aneurysm. The tumor is small, the left ventricular myocardial involvement is limited, clinically asymptomatic or only mild urgency, after acute myocardial infarction Still more than 10 years of survival, the extent of the lesion is large, so that the left ventricular systolic blood transfusion function is seriously affected, the ejection fraction is significantly reduced, clinically congestive heart failure, the 5-year survival rate is reduced to 10 to 20% about.

Myocardial infarction complicated with complications of left ventricular aneurysm Complications, shock, hypertension, hemoptysis, pulmonary embolism

Due to the damage of left ventricular blood discharge function leading to left heart failure and gradually worsening, once the thrombus in the ventricular aneurysm falls off, systemic embolism can be produced.

Pulmonary embolism is common in systemic embolism. Because the thrombus in the exfoliated ventricular aneurysm is prone to block in the branch of the lung, causing serious complications. When a severe blood supply disorder occurs after embolization, the lung tissue may be necrotic. Pulmonary infarction is a common cause of acute lung disease. Clinical symptoms and signs are often non-specific and vary greatly. It is difficult to distinguish from other cardiovascular diseases. Although the severity of symptoms is related to the size of embolism and the scope of embolization, it is not necessarily In direct proportion, it is closely related to the original heart and the compensatory ability of lung diseases.

(A) acute large-area pulmonary embolism: severe dyspnea manifested as a sudden onset, myocardial infarction-like sternal pain, syncope, cyanosis, right heart failure, shock, sweating, cold and convulsions of the extremities, and even cardiac arrest Or ventricular fibrillation and rapid death.

(B) medium-sized pulmonary embolism: often have post-sternal pain and hemoptysis, when the patient's original heart, lung disease compensation function is very poor, can produce syncope and high blood pressure.

(C) microembolism of the lung: can produce adult respiratory distress syndrome.

(D) pulmonary infarction: often have fever, mild jaundice.

Myocardial infarction complicated with left ventricular ventricular aneurysm symptoms Common symptoms Arrhythmia Myocardial hypertrophy Anxiety angina pectoris Myocardial infarction Left ventricular volume increase Reverse pulsation Left heart failure Calcified chest compression pain

About 85% of the left ventricular aneurysm is located in the anterior lateral approach to the apical region. A few cases can be located in the palpebral area of the heart. The ventricular wall of the lesion is thinned, showing a white fibrous scar with clear boundaries and a close adhesion of the local epicardium to the pericardium. About half of the cases have a wall thrombus in the endocardial surface, sometimes showing calcification. Most of the coronary artery obstruction lesions are confined to the left anterior descending artery, but several blood vessels may be involved. The left ventricular cavity volume increases, and the normal part of the heart muscle is thick.

Left ventricular ventricular aneurysm causes loss of myocardial contractility in the lesion area, and can produce reverse pulsation. When the ventricle contracts, the ventricular wall tumor bulges outward, retracts when dilated, causing a decrease in left ventricular outburst, normal myocardial contractility. Strengthen, tension increased, myocardial oxygen demand increased, ventricular aneurysm volume exceeded 15% of left ventricular end-diastolic volume, left ventricular end-diastolic pressure increased, left ventricular dysfunction caused by damage to left ventricular dysfunction and gradually worsened When the thrombus in the ventricular aneurysm falls off, systemic embolism can be produced.

Most patients with left ventricular aneurysm have a history of angina pectoris and myocardial infarction. Common clinical manifestations include shortness of breath, left heart failure, angina pectoris, arrhythmia and systemic arterial embolism. The severity of clinical symptoms and the size of ventricular aneurysm and the normal part of the left ventricle The number and function of myocardium are closely related.

Physical examination: The apical area can reach the systolic or double pulsation, and the third heart sound or the fourth heart sound may be heard in the auscultation examination.

Examination of myocardial infarction complicated with left ventricular aneurysm

Chest X-ray examination showed local bulging of the apex of the left margin of the heart, weakened pulsation or reverse pulsation, stagnation of the lung field, enlargement of the left atrium and left ventricle.

Electrocardiogram examination often showed old myocardial infarction in the anterior wall of the heart, bundle branch block and ST segment elevation.

The left ventricular long-axis section supercardiographic examination showed that the myocardial part of the lesion was bulged, and the wall of the heart and the normal left ventricle showed abnormal movement.

Selective left ventricular angiography can show the location of the ventricular aneurysm, volume and thrombus in the tumor, and can determine and calculate left ventricular end-diastolic pressure, blood ejection fraction and end-diastolic volume.

Selective coronary angiography can show the location and extent of coronary artery branching, providing important information for the development of surgical treatment options.

Diagnosis and differentiation of myocardial infarction complicated with left ventricular ventricular aneurysm

Need to distinguish from ventricular septal defect and mitral regurgitation.

1, ventricular septal defect

Ventricular septal defect is a common congenital heart malformation, most of which is a single malformation, accounting for about 20% of congenital heart disease; it can also be a component of complex cardiac malformation, as seen in tetralogy of Fallot, completely Sexual atrioventricular access.

When the defect diameter is small, the flow rate is less, generally no obvious symptoms, when the defect is large, the flow rate is higher, there may be developmental disorders, palpitations after the activity, shortness of breath, repeated lung infections, breathing may occur in severe cases Symptoms such as distress and left heart failure, when mild to moderate pulmonary hypertension occurs, and the left to right sub-flow decreases accordingly, pulmonary infections are alleviated, but symptoms such as palpitations, shortness of breath and restricted mobility still exist, or Obvious, severe pulmonary hypertension, bidirectional or reverse (right to left) shunt, purpura, the so-called Eisenmenger syndrome, physical activity and lung infection, purpura aggravation, and eventually right heart failure.

2, mitral regurgitation

The mitral valve consists of four components: the leaflets, the annulus, the chordae and the papillary muscles, any of which can cause structural abnormalities or dysfunction, which can lead to mitral regurgitation, usually from primary rheumatic carditis to Symptoms of apparent mitral regurgitation can be as long as 20 years; in the event of heart failure, rapid progression, mild mitral regurgitation may have no obvious symptoms or only mild discomfort, severe mitral regurgitation Common symptoms are: labor dyspnea, fatigue, sitting breathing, etc., activity endurance is significantly reduced, hemoptysis and embolism are less common, late hemorrhage can appear hepatic congestion, tenderness, ankle edema, pleural effusion Or ascites, acute acute heart failure or pulmonary edema can occur quickly.

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