Clinically can be divided into acute and old myocardial infarction
Acute myocardial infarction: is due to coronary artery occlusion, resulting in a sharp reduction in coronary artery blood supply interruption, so that the corresponding myocardial due to severe and persistent ischemia, hypoxia, part of the myocardial degeneration, necrosis. Clinical manifestations of posterior sternal pain and myocardial necrosis caused by systemic reactions and ECG progressive changes, may be associated with arrhythmia, shock, heart failure, and even sudden death and other clinical manifestations, is a serious type of coronary heart disease.
Aura About 1/2 to 1/3 of patients in the AMI before or several weeks before the occurrence of unstable angina symptoms.Angina pectoris duration is longer than usual, the incentive is not obvious, nitroglycerin ineffective, angina attack accompanied by nausea, vomiting, sweating, bradycardia, acute cardiac dysfunction, severe arrhythmia or blood pressure increased volatility, etc. There may be a precursor to myocardial infarction.
2. chest pain. 70% to 80% of patients with chest pain, pain, the same nature and angina, but the degree of aggravation, longer duration, generally more than 30 minutes or hours or days, no obvious incentive, rest or contain nitroglycerin often Can not be relieved, accompanied by irritability, sweating, fear or dying.
3. Gastrointestinal symptoms. Some patients have nausea, vomiting, abdominal pain, hiccups and other symptoms, the reasons may be associated with necrotic myocardium stimulation and cardiac output decreased tissue perfusion related.
4. Cardiovascular system performance: arrhythmia, heart failure, shock
5. fever. On the second day after the disease began to rise, usually around 38 ℃, 1 week after recovery. For the absorption of myocardial necrosis caused by the reaction.
1. Blood tests: white blood cells often in the 10.0 ~ 20.0 × 109 / liter, ESR faster.
2. Serum myocardial enzyme examination: increased enzyme activity, manifested as creatine phosphokinase, aspartate aminotransferase and lactate dehydrogenase increased, and a certain evolution.
3. ECG examination: may have necrosis Q wave, injury ST segment elevation and ischemia type T wave inversion and so on, there is evolution.
1. typical history of chest tightness.
2. ECG characteristic changes.
3. Serum enzyme changes, consistent with the enzyme sequence changes.
Two of the above three can be diagnosed with typical myocardial infarction.
Old myocardial infarction:
Old myocardial infarction can be based on previous history, positive ECG changes, but not associated with acute myocardial infarction and clinical manifestations of serum and other changes in the diagnosis of serum. If there is no left ventricular electrocardiogram change, according to the previous typical ECG changes or in accordance with past changes in the positive serum enzyme diagnosis.