Cardiovascular Pathology Case Studies



CASE 2: Acute Myocardial Infarction


Clinical History:

This is a 51-year-old executive for a shipping company. He has been feeling some chest pains over the last year, particularly after climbing up the stairs to the accounting office. He had cholesterol screening done, which showed a total cholesterol of 250 and HDL component of 25. His fasting glucose is 145 mg/dl. He smokes half a pack of cigarettes a day. He is overweight. He is admitted to hospital after onset of severe chest pain that was substernal and described as "crushing".
  1. What is the diagnosis in this man?
  2. He has an acute myocardial infarction.

  3. What are the risk factors for his disease?
  4. He has quite a few: male sex, older age, sedentary lifestyle, smoking, probable diabetes mellitus, high total cholesterol with low HDL cholesterol, obesity.

  5. Explain the symptomatology.
  6. The coronary atherosclerosis leads to narrowing of the arterial lumens. This can lead to ischemia with anginal pain. Nitroglycerin may help to dilate the coronaries and relieve such pain. However, in this case the pain is more characteristic of infarction. Sometimes the pain radiates into the arm or up into the neck.

  7. What is the lesion in the coronary artery?
  8. An acute coronary thrombosis is evident.

  9. Describe and date the pathologic findings seen in images 2.3 to 2.9.
  10. In image 2.3 contraction bands are seen in the first day and also with reperfusion following use of thrombolytic agents. Image 2.4 depicts early acute myocardial infarction with loss of nuclei, loss of cross striations, and PMN infiltration beginning in the first day and peaking at 2 to 3 days. Image 2.5 demonstrates an acute myocardial infarction with central pale yellow zone of necrosis surrounded by a hyperemic border that could be anywhere from 3 to 7 days old. In image 2.6 there has been a rupture of the left ventricular wall, typically when the myocardium is softest at 3 to 5 days. In image 2.7 the infarction is now "intermediate" in age with capillaries, macrophages, and fibroblasts depositing collagen which begins at day 3 but is most prominent at the end of the first week and continuing for another couple of weeks. At 7 weeks, there is only fibrosis to signify a remote infarct. In image 2.8 the infarction is healed (remote in age) and a large ventricular aneurysm has formed with focal mural thrombosis. In image 2.9 there is a fibrinous pericarditis with strands of pink fibrin jut from the pericardial surface, and this could produce a friction rub in the first week.

  11. How would you use laboratory findings to help diagnose his condition?
  12. CK-MB begins to rise in a couple of hours following an MI, peaks at 6 to 8 hours, and then diminishes over 1 to 3 days. Total CKBegins to rise a little later than the MB fraction and peaks toward the end of the first day, but diminishes in the same time frame (remember that skeletal muscle injury can increase the total CK).

    LDH-1 appears and peaks similarly to total CK, but takes 5 to 14 days to disappear. Total LDH begins to rise in 12 to 24 hours, peaks at 2 to 4 days, and then disappears in 5 to 14 days.

  13. How could his disease be treated?
  14. Thrombolytic agents can be given right in the emergency room. Coronary catetherization can be done to determine the coronary lesions present and do angioplasty if needed. About 1/2 million Americans get a coronary artery bypass grafting procedure each year. With the severity of narrowing and calcification, angioplasty is less of an option than bypass surgery. Other options: stop smoking, decrease dietary fat, control hypertension, begin to gradually increase exercise level.

  15. What are possible complications?
  16. This process could result in sudden death, arrhythmias, congestive heart failure, rupture of the myocardium, and ventricular aneurysm on healing.

  17. What are etiologies for the complication seen in image 2.9?
  18. The major etiologies for fibrinous pericarditis are: uremia, myocardial infarction, radiation therapy, rheumatic fever, collagen vascular diseases (e.g., SLE), or cardiac surgery. The patient may have chest pain and fever. A friction rub may be present.

  19. What pharmacologic therapy would be useful in view of his total serum cholesterol?
  20. The use of "statin" drugs such as lovastatin and pravastatin could be useful in lowering his cholesterol and his risk for subsequent complications of atherosclerosis. These drugs inhibit HMG-CoA reductase in the pathway of endogenous cholesterol synthesis.

    Alternative cholesterol-lowering therapies to consider include the use of resins, such as cholestyramine, and niacin.

    This patient should be strongly encouraged to adopt lifestyle changes as well, and not just rely on drug therapy to try and solve his problems. Weight reduction can help treat diabetes mellitus. Smoking cessation should be strongly urged. A graduated increase in exercise is important.

  21. What dysrhythmias would most likely be seen as a result of the anterior descending lesion? What mechanisms would underlie these arrhythmias?
  22. Early in the lesion, ischemia would cause depolarization and excitation (secondary to catechols and loss of potassium into the extracellular space). This would result in premature beats and tachycardia. Following the infarction, the excitable focus would be silenced, but the ischemic zone around the infracted area would be prime for re-entrant tachycardias.