Conservative treatment of ventricular aneurysm?

Conservative treatment of ventricular aneurysm?

Ventricular aneurysm is a phenomenon of myocardial necrosis caused by myocardial infarction. Generally, as long as the tumor is not particularly large, it can be treated conservatively first. Most ventricular aneurysms are related to heart disease such as coronary atherosclerosis. If the tumor is relatively small, the body will not show any symptoms. If the tumor is slowly growing, it will cause left heart failure and cause embolism in the brain and kidneys.

The main methods for detecting ventricular aneurysms are:

(1) Judge based on symptoms. This complication should be considered in patients with persistent, uncontrollable left heart failure or peripheral arterial embolism, or refractory tachyarrhythmias after acute myocardial infarction.

(2) Electrocardiogram. Two weeks after acute myocardial infarction, if the ST segment continues to be elevated, ventricular aneurysm formation should be considered. However, it is currently believed that persistent ST segment elevation is a specific but not very sensitive indicator of severe left ventricular regional dysfunction.

(3) Echocardiography. It is a sensitive and reliable method for detecting ventricular aneurysm. Two-dimensional echocardiography can not only show the location of ventricular aneurysm and the size of the aneurysm cavity, but also measure the thickness and activity of various parts of the aneurysm wall. It can also evaluate the normal myocardium around the ventricular aneurysm and provide a basis for surgical removal of the aneurysm. The sensitivity, specificity and safety of echocardiography in diagnosing ventricular aneurysm are superior to surface electrocardiography, X-ray and ventriculography.

(4) Nuclides and nuclear magnetic resonance. This method has unique advantages in detecting ventricular aneurysms.

Clinical characteristics of ventricular aneurysm Due to different definition methods and diagnostic criteria, the incidence of ventricular aneurysm has been reported differently, and may account for 10% to 35% of myocardial infarction. Currently, with the development of thrombolytic therapy and early revascularization, the occurrence of ventricular aneurysm has a decreasing trend. During routine coronary angiography, ventricular aneurysms can be found in approximately 7.6% of patients. The 10-year survival rate of asymptomatic ventricular aneurysms with conservative medical treatment can reach 90%, and most patients can still remain asymptomatic, while the 5-year survival rate of symptomatic ventricular aneurysms with medical treatment is 47% to 70%. The main causes of death include arrhythmia, heart failure and recurrent myocardial infarction. Factors that affect the effectiveness of medical treatment include age, cardiac function status score, degree of coronary artery lesions, angina pectoris, previous history of myocardial infarction, mitral regurgitation, ventricular arrhythmia, size of ventricular aneurysm, residual ventricular function and left ventricular end-diastolic pressure.

The most common symptom of ventricular aneurysm is angina pectoris. Ventricular aneurysm itself may increase myocardial oxygen consumption, reduce oxygen supply, and cause angina pectoris. In addition, more than 60% of patients with ventricular aneurysm have triple-vessel disease, and angina pectoris is even more common. Secondly, a common symptom is dyspnea, which is mostly a manifestation of heart failure caused by impaired systolic and diastolic functions. Combined arrhythmia is not uncommon, which can lead to palpitations, syncope, sudden death, worsening angina pectoris and dyspnea, and some may even have fatal arrhythmias. Generally, the chance of thromboembolism is small, but it can cause stroke, recurrent myocardial infarction, and ischemic symptoms of limbs or organs. Therefore, if mural thrombus is found in patients with atrial fibrillation and large ventricular aneurysm, it should be taken seriously and long-term anticoagulant treatment and ultrasound follow-up are required. The electrocardiogram often shows pathological Q waves and persistent ST-T elevation in the precordial leads, which should be differentiated from acute myocardial infarction. Chest x-ray showed left ventricular dilatation and cardiac hypertrophy but was not specific for ventricular aneurysm. Echocardiography can not only observe ventricular wall motion disorders, but also help detect intracavitary thrombus and mitral regurgitation. It is more advantageous in distinguishing true from false ventricular aneurysms, and has good sensitivity and specificity. Left ventriculography is the most important diagnostic criterion. Large ventricular segmental motion abnormalities are usually found in the anterior septum and apex, and the presence of mural thrombus can occasionally be demonstrated. Angiography can also be divided into akinetic, dyskinetic and paradoxical movement types according to the different ventricular wall motion abnormalities, which is of guiding significance for the selection of treatment plans. Radionuclide scanning and positron emission tomography (PET) examinations are important for distinguishing true ventricular aneurysms in the early stages of myocardial infarction from hibernating myocardium with recoverable function. The recently adopted magnetic resonance imaging (MRI) can accurately detect ventricular aneurysms and is also a relatively reliable method for detecting thrombus. Patients with ventricular fibrillation and ventricular tachycardia should undergo electrophysiological examination before surgery to determine whether to treat them during surgery. Electrophysiologic studies may not be helpful in patients with multifocal VT within 6 weeks of myocardial infarction. There is controversy over the value of electrophysiological examination in patients without ventricular tachycardia and ventricular fibrillation before surgery, because the risk of arrhythmias after surgery is relatively small and endocardectomy cannot improve this result.

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