Diagnosis of Acute Myocardial Infarction (AMI)

What sample is needed for the diagnosis of Acute Myocardial Infarction (AMI)?

1. The best sample is Venous blood to get a clear serum.
2. Heparinized plasma can be used.
3. Rapid Troponin-T can be performed on whole blood (using some available methods).
4. Current recommendation on admission with the possibility of acute MI, a blood sample should be taken at intervals of:
   1. Blood sample at admission.
   2. Second sample at 2 to 4 hours.
   3. Third sample at 6 to 8 hours.
   4. Fourth sample at 12 hours.
5. The serum can be stored at room temperature for 4 to 8 hours.
   1. At 4 °C, the serum is stable for  1 to 2 days.
   2. The serum is stable for 24 hours at 2 to 8 °C for troponin-T.

What are the precautions for the diagnosis of  Acute Myocardial Infarction (AMI)?

1. I/M injection may raise the level of CPK.
2. Strenuous exercise and recent surgery may raise the CPK level.
3. Early pregnancy may decrease the CPK level.

How will you define Acute Myocardial Infarction (AMI)?

1. This is characterized by the ischemia of the myocardial muscles. Also, this myocardial ischemia results in irreversible myocardial cell damage or death (necrosis).
   1. Or when there is obstruction of the blood supply to any part of the heart and necrosis of the muscles, or massive cell death occurs.
   2. It is almost always caused by atherosclerosis of the coronary arteries, followed by thrombosis.

How will you diagnose AMI?

1. Clinical S/S is very important in both suspicious and diagnosed cases of AMI.
2. Diagnosis depends upon the type of pain, its distribution, and its response to nitroglycerine.
3. The pain characteristics are typical, and the pain will respond to nitroglycerine.
   1. 20% to 30% of Acute Myocardial Infarctions (AMI) are painless.
4. Acute Coronary Syndrome includes:
   1. Silent ischemia.
   2. Stable angina.
   3. Unstable angina.
   4. Non-ST wave elevation.
   5. Non-Q wave.
   6. Infarction to typical acute myocardial infarction (AMI).

What are the types of acute myocardial infarction (AMI)?

1. Silent myocardial infarction occurs 40% to 50% of patients, who do not notice the typical signs and symptoms of acute myocardial infarction.
   1. These are diagnosed on the ECG.
   2. This is usually seen in diabetic patients and those with hypertension.
2. The AMI is classified based on anatomic, morphologic, and diagnostic clinical data:
   1. Nontransmural AMI is when there is the involvement of only the endocardium or both endo and myocardium.
   2. Transmural MI occurs when all three endo, myo, and epicardium layers are involved.

3. Another classification is:
   1. Non-Q wave subendocardial infarction.
   2. Q-wave was transmural infarction.

How will you discuss the pathophysiology of acute myocardial infarction?

1. There is an increased risk of AMI with increasing age.
   1. There is a 4 to 5 times higher risk in men between the ages of 45 and 54 years than in women.
   2. The risk is the same for both sexes (men and women) after the age of 80.
2. Before an acute myocardial infarction occurs, there is transient ischemia, where the oxygen supply to the muscle is deprived, which is called an Anginal attack.
3. In angina, there is no necrosis.
4. The major cause of AMI is atherosclerotic plaques and thrombus formation.
5. Ischemia begins in the endocardium and then spreads outward.
6. Irreversible muscle damage occurs during ischemia for at least 15 to 20 minutes.
   1. Vasospasm and platelet aggregation may contribute to coronary occlusion.

6. Myocardial necrosis starts:
   1. The necrosis process typically begins within 20 to 30 minutes.
   2. Infarcts start in the subendocardial area.
   3. After several hours, a mid and subepicardial area of the myocardium is involved.
   4. After 3 to 6 hours, full infarct formation occurs.
      1. Streptokinase injection can limit the infarct.

What are the changes in the myocardial infarction?

What will be the distribution of the infarct in the heart?

1. The ischemic necrosis involvement of the heart muscle depends upon the involvement of the anatomical blood vessel occlusion.
   1. The anterior left descending coronary artery involves the Anterior and apical part of the left ventricle and the adjacent interventricular septum.
   2. The left circumflex coronary artery involves the Lateral wall of the left ventricle.
   3. The right coronary artery involves the Posterior and basal portion of the left ventricle.

What are the risk factors for Acute myocardial infarction (AMI)?

1. Family history is a very important factor.
2. Physical inactivity, including walking or exercise.
3. Lifestyle.
4. Hypertension.
5. Tobacco use.
6. Weight (obesity), diet, and nutrition.
7. Diabetes mellitus.
8. Hyperlipidemia.
   1. High cholesterol.
9. Sex is more common in males.
10. More common in the case of family history.

What are the signs and symptoms of Acute myocardial infarction (AMI)?

1. Chest pain in the mid-thorax, accompanied by crushing substernal pain.
2. Pain may radiate to the teeth, jaw, shoulder, arm, or back.
3. There may be dyspnea or shortness of breath.
4. There may be sweating.
5. There may be epigastric discomfort, accompanied by nausea and vomiting.
6. The patient may go into syncope.
   1. In 50% of patients, the AMI is preceded by angina pectoris.
7. The pain of AMI is not relieved by nitroglycerin.

What are the characteristics of an Acute Myocardial infarction?

1. The typical rise of CK-MB. The more rapid rise and fall of CK-MB.
2. Raised level of Troponins. The more rapid rise and fall of Troponins.
3. ECG changes.
   1. Development of Q-wave.
   2. ST-segment elevation.
4. A coronary angiogram shows a coronary artery abnormality.

How will you diagnose acute Myocardial infarction (AMI)?

H/O chest pain:

1. Chest pain may be typical in the case of AMI. This may be present in the left arm and may radiate to the mandible.
2. This pain may be in the interscapular area, mimicking gallbladder pain.
3. In some patients, there is silent AMI, which is most common in people with diabetes.

What are the changes in AMI on the ECG?

1. The initial ECG is diagnostic in more than 50% of cases.
2. 15% of the cases show no initial changes in ECG.
3. Follow-up for 24 hours shows a positive ECG in 75% of the cases.
   1. These changes are reflected in the ST-segment, T-wave, and enlarged Q-wave.
   2. Initially, there is an elevation of the ST segment.
   3. Later on, the Q-wave becomes prominent.
   4. After weeks to months, the ST segment becomes normal.
   5. T-wave also comes back to its original position.
   6. But the Q-wave remains abnormal.

What are the abnormal cardiac enzymes?

1. CK.
2. CK-MB.
3. LDH.
4. Myoglobin.
5. Troponin T and I.
6. SGOT.

What is the value of CK and CK-MB in AMI?

1. CK is found in the heart muscles, skeletal muscles, and brain.
2. CK can reflect the timing, quantity, and resolution of MI.
3. CK has isoenzymes:
   1. CK-1 =BB = Found predominantly in the brain and lung.
   2. CK-2 =MB = Found predominantly in the cardiac muscles.
   3. CK-3 =MM = Found predominantly in the skeletal muscles.
4. CK-MB is more specific for cardiac muscle injury.

How will you interpret CK-MB?

1. This also helps in quantifying and giving a degree of myocardial injury.
2. If there is no further myocardial damage, then:
   1. CK-MB was detected in the first 3 to 6 hours.
   2. The peak level is at 20 to 24 hours.
   3. This returns to normal in 12 to 48 hours (another reference becomes normal in 72 hours).
   4. By 72 hours, 2/3 of the patients still show some increase in CK-MB.
   5. Sampling every 6 hours is more likely to find peak levels.
   6. Diagnosis of AMI is confirmed within 8 to 12 hours.
   7. Sampling beyond 24 hours is not advised.
   8. The single sample value is not diagnostic; serial estimation at least 4 hours apart shows ≥a 50% increase.
   9. Serial measurement is more important, as it enables a diagnosis with 100% accuracy.
3. Total CK may be normal, but CK-MB will be raised.
4. Raised CK-MB with normal total CK will represent patients with non-Q-wave AMI.

What are the disadvantages of CK-MB?

1. A rapid return to normal makes it a poor marker.
2. CK-MB is not as specific as Troponin, and there are false-positive reports of non-ischemic cardiac injuries like pericarditis and myocarditis.
   1. CK-MB is also positive in muscular dystrophy, exercise, and rhabdomyolysis.
3. CK-MB usually does not arise in the case of angina, pulmonary embolism, or congestive heart failure.
   1. CK-MB may rise in case of shock, malignant hyperthermia, myopathy, or myocarditis.
4. There is a small amount of CK-MB in the skeletal muscles.
   1. A case of severe skeletal muscle injury may give rise to a significantly high level of CK-MB.
5. CK-MB is more helpful and more specific than Myoglobin when the patient comes with chest pain after 10 to 12 hours.

What is the CK-MB relative index?

1. This is done to avoid skeletal muscle injury with myocardial muscle damage.
2. Calculation:
   1. CK-MB/total CPK
   2. Normal CK-MB/Total CPK index = <2.5.
3. Examples:
   1. If CK-MB = 3.0 ng/mL
      1. Relative index = ≥2.5
      2. This is highly suggestive of myocardial injury.
   2. If CPK-MB = >3.0 ng/mL
      1. Relative index = <2.5
      2. Not diagnostic for myocardial injury.