Is anterior wall myocardial infarction serious?

Heart disease is very familiar to many people, and myocardial infarction is a relatively common heart disease. Myocardial infarction is divided into many types. Anterior wall myocardial infarction is also a heart disease, and anterior wall myocardial infarction is relatively a disease of higher severity. Anterior wall myocardial infarction can easily lead to insufficient blood supply to the heart and cause cardiac arrest, which is very harmful to the human body.

Is anterior myocardial infarction serious?

Anterior myocardial infarction has a higher mortality rate than inferior myocardial infarction, and a permanent pacemaker may be required after anterior myocardial infarction. Myocardium cannot regenerate after myocardial infarction and can only be repaired by hypertrophy of adjacent myocardial cells and interstitial fibrous scars. Fiber scars have no contractile function. Since anterior myocardial infarctions mostly involve the left ventricle and ventricular septum, and inferior myocardial infarctions mostly involve the right ventricle, anterior myocardial infarctions have a great impact on left ventricular ejection function. The pressure of the pulmonary artery is one sixth of the aortic pressure, so the right ventricular ejection function is not greatly affected.

Laboratory tests

1. Electrocardiogram

Characteristic changes are the emergence of new Q waves, ST segment elevation, and dynamic evolution of ST-T.

2. Elevated serum biomarkers of myocardial necrosis

Elevated creatine kinase isoenzyme (CK-MB) and troponin (T or I) are important indicators for diagnosing acute myocardial infarction. It may begin to increase 3 to 6 hours after onset of the disease, CK-MB returns to normal in 3 to 4 days, and troponin returns to normal in 11 to 14 days. GOT and LDH have poor diagnostic specificity and are rarely used nowadays.

3. Detection of serum biomarkers of myocardial necrosis

The rapid diagnostic reagent using cardiac troponin I/myoglobin/creatine kinase isoenzyme (CK-MB) can be used as a rapid auxiliary diagnosis for sudden myocardial infarction and is being increasingly used.

4. Others

The number of white blood cells and neutrophils increased, the number of eosinophils decreased or disappeared, the erythrocyte sedimentation rate accelerated, and the serum myosin light chain increased.

Diagnosis and differential diagnosis

The correct diagnosis can be made based on typical clinical manifestations, characteristic electrocardiogram changes and dynamic changes in serum biomarkers. Patients with ST-segment elevation on the electrocardiogram are diagnosed with ST-segment elevation myocardial infarction; patients without ST-segment elevation on the electrocardiogram are diagnosed with non-ST-segment elevation myocardial infarction (formerly known as non-Q wave infarction). Elderly people who suffer sudden heart failure, shock or severe arrhythmia should also consider the possibility of this disease. Atypical manifestations often need to be differentiated from acute abdomen, pulmonary infarction, dissecting aneurysm, etc.

complication

1. Heart rupture

It often occurs within 1 to 2 weeks after myocardial infarction, and is more common in the lower 1/3 of the anterior wall of the left ventricle. The reason is that the infarct focus loses its elasticity, myocardial necrosis, and enzymatic dissolution caused by the release of hydrolases by neutrophils and monocytes leads to rupture of the heart wall, and the blood in the ventricles enters the pericardium, causing pericardial tamponade and sudden death. In addition, if the ventricular septum ruptures, blood from the left ventricle flows into the right ventricle, which can cause cardiogenic shock and acute left heart failure. Rupture of the left ventricular papillary muscle can cause acute mitral regurgitation and lead to acute left heart failure.

2. Ventricular aneurysm can occur in the early stage of myocardial infarction or in the healing stage of infarct fibrosis.

Ventricular aneurysm is formed by the localized outward bulging of infarcted myocardium or scar tissue under the action of intraventricular pressure. Ventricular aneurysm may be followed by mural thrombus, arrhythmia and heart failure.

3. Mural thrombosis

More common in the left ventricle. Thrombosis is induced due to the roughness of the intimal membrane in the infarct area and the occurrence of vortexes in the ventricular aneurysm. Thrombi may become organized, and a few thrombi may break off due to cardiac contraction and cause embolism in the arterial system.