Acute Myocardial Infarction

PATHOPHYSIOLOGICAL PROCESS TEMPLATE

DISEASE:

Acute Myocardial Infarction is a common disease with very grave consequences in morbidity, mortality and cost to the society (Boersma et.al, 2003) It has become the leading cause of death in the developed world. It has been estimated that about 450,000 people die from coronary disease per year in the United States.

Myocardial infarction primarily occurs when the blood supply to the heart is compromised. Just like all the cells of the body, the myocardial cells require a constant supply of blood and oxygen to keep working. Ischemia beyond a set threshold level exhausts the cells and causing them to be damaged. Authors have said that the word Myocardial Infarction should be used when there is evidence of necrosis of the myocardium in a clinical setting. There are five different types of MIs defined depending on the situation that occurs. Type 1 is primarily a spontaneous MI that is associated with a primary coronary event such as an occlusion by a thrombus due to plaque rupture. Type 2 is associated with ischemia from a mismatch due increased demand and reduced supply. Type 3 is a MI that is linked to sudden cardiac death. Type 4 and 5 are MI associated with percutaneous coronary intervention and coronary artery bypass surgery respectively.

AETIOLOGY:

There have been many risk factors identified to the development of atherosclerotic changes that lead to a MI. The six leader factors are increased cholesterol levels, hypertension, diabetes mellitus, the use of tobacco, family history of atherosclerotic disease and the male gender.

PATHOGENESIS:

Most of the Myocardial infractions are initiated by a disruption in the vascular endothelium. Ongoing atherosclerotic processes go on to stimulate the formation of intracoronary thrombus. The thrombus then lodges inside a coronary artery and ultimately causes the blood flow occlusion. If the blockage of the coronary artery persists for more than twenty minutes, irreversible damage to the muscle cells occur and ultimately cell death occurs (Kumar & Abbas et al., 2005)

CLINICAL FEATURES:

Chest Pain

Pain radiating to left arm, shoulder, back or neck

Nausea and vomiting

Sweating

Shortness of breath

(Bruyninckx et.al, 2008)

COURSE OF DISEASE:

The course of the disease depends on how well offending agent is treated. As stated before, irreversible damage occurs to the heart if the ischemia stays more than twenty minutes. The course of the disease, therefore, varies with the cause of the MI, the area of the heart involved and the treatment that is given to the patient.

COMPLICATIONS: The complications of Acute Myocardial Infarction are ventricular arrhythmias, cardiac rupture (Rosamond et.al, 1998), acute mitral insufficiency, heart failure and mural thrombosis (Keeley et.al, 1996)

PROGNOSIS:

The improvement in prognosis has occurred in the last decade mainly due to early treatment with reperfusion and thrombolytic agents (Hayashi et.al, 2005)

DIAGNOSIS:

The Diagnosis of MI is made by ECG, lab markers such as creatinine kinase, Troponin I and T. And myoglobin. There are two different types of MIs that can be distinguished by the ECG: one is ST elevation Myocardial infarction, and the other one is non-ST elevation MI.

TREATMENT:

Integration of antithrombotic therapy combined with timely reperfusion. For ST elevation, primary percutaneous coronary intervention or fibrinolysis is used. For non-ST elevation, invasive investigation and revascularization has been declared as a good treatment (White & Chew, 2008)

PREVENTION:

Acute Myocardial Infarction can be prevented by keeping all the risk factors under control. Anyone who has a positive family history should monitor their lipid levels, blood pressure and blood glucose levels very carefully. Besides, they should eat healthy and not have a sedentary lifestyle (Anderson et.al, 2011)

Question 1

Mr. White has a positive family history for atherosclerotic problems and heart disease. He is diagnosed with hypertension and high lipid levels yet he still has been smoking since a long time. In short, Mr. White has a lot of risk factors which were not controlled the way they should have been. Smoking and increased lipid levels have gone to cause the formation of plaque deposition in his arteries. Moreover, high blood pressure and smoking has also made his vessels very hard and prone to damage. All these insults and continuous blood pressure have been causing damage to his vessels slowly.

It is to be noted that the atherosclerotic plaques take a lot of time to develop and are present in the majority of elderly men and women today. However, it is the rupture of the plaque that initiates an acute myocardial infarction. The plaque that gets formed has a fibromusuclar cap and a core which is rich in lipids. The main reason that causes the rupture of the plaque is due to the actions of metalloproteases and collagenases. The enzymatic actions cause the thinning of the fibromuscular cap. Along with the hemodynamic forces acting on the plaque, the enzymatic actions combined go on to because disrupted of the endothelium and ultimately rupture of the cap. This disruption caused the activation of the coagulation cascade and increased platelet activation. This process ultimately leads to the formation of a thrombus. If the thrombus is significant enough to occlude the coronary circulation, then a myocardial infarction results.

The myocardial infarction that results renders the heart muscle weak and incapable of doing its function. As it would be known, the function of the heart muscle is pump blood throughout the body. When the heart is undergoing a myocardial infarction, it is unable to contract. The shortage of blood and oxygen to its own muscle causes it to either pump weakly or not pump at all. The Left Anterior descending artery supplies the left ventricle which includes the papillary muscles and mitral valve of the heart. One structural change could be rupture of the papillary muscle which would render the mitral valve insufficient. Furthermore, with the heart not being to pump blood in the proper way, it is likely that the enough blood does not reach the entire body and heart failure ensues.

Question 2

Mr. White had a crushing pain in the centre of his chest which is indicative of ischemic damage to the heart. When the heart’s blood supply is compromised, there is a decreased supply of oxygen to the heart. Due to this reason, there is an accumulation of lactic acid which subsequently causes pain. This, therefore, explains why Mr. White has a crushing pain in the centre of his chest.

Another clinical manifestation of Mr. White is that he felt sick and faint. This can be explained by the reduced contraction of the heart muscle and the decreased blood supply to the entire body. Despite being hypertensive, Mr. White’s blood pressure is 95/60 mmHg. This proves that the heart is not able to contract in the proper way and therefore the blood circulation of the entire body is compromised.

Question 3

Mr. White is given sublingual glyceryl trinitrate which primarily acts on the arteries in the body. Glyceryl trinitrate is a vasodilator meaning that it increases the diameter of the coronary arteries. This causes increased blood to flow through the artery which, therefore, increases the supply of blood and oxygen to the heart muscle. Mr. White’s symptoms do show that his heart muscle is being compromised of blood and oxygen, therefore, this would go on to increase the blood supply to the heart.

Aspirin and Heparin both go on to target the clotting function of the blood and reverse the processes that have already started in the body. As stated before, an acute Myocardial Infarction results due to the blockage of a coronary vessel by a thrombus. Heparin and Aspirin both work to reverse the clotting process so that the blockage can be reduced, and the blood circulation can be resumed back to normal.

References

Anderson, J.L., Adams, C.D., Antman, E.M., Bridges, C.R., Califf, R.M., Casey, D.E., Chavey, W.E., Fesmire, F.M., Hochman, J.S., Levin, T.N. & Others (2011). 2011 accf/aha focused update incorporated into the acc/aha 2007 guidelines for the management of patients with unstable angina/non — st-elevation myocardial infarction a report of the american college of cardiology foundation/american heart association task force on practice guidelines. Circulation, 123 (18), pp. 426 — 579.

Boersma, E., Mercado, N., Poldermans, D., Gardien, M., Vos, J. & Simoons, M.L. (2003). Acute myocardial infarction. The lancet, 361 (9360), pp. 847 — 858.

Bruyninckx, R., Aertgeerts, B., Bruyninckx, P. & Buntinx, F. (2008). Signs and symptoms in diagnosing acute myocardial infarction and acute coronary syndrome: a diagnostic meta-analysis. The british journal of general practice, 58 (547), p. 1.

Hayashi, T., Miyataka, M., Kimura, A., Taniguchi, M., Kurooka, A., Yabushita, H., Kiyoshima, T., Nakamura, H., Hirano, Y. & Ishikawa, K. (2005). Recent decline in hospital mortality among patients with acute myocardial infarction. Circulation journal: official journal of the japanese circulation society, 69 (4), p. 420.

Keeley, E.C. & David Hillis, L. (1996). Left ventricular mural thrombus after acute myocardial infarction.Clinical cardiology, 19 (2), pp. 83 — 86.

Kumar, V., Abbas, A.K., Fausto, N., Robbins, S.L. & Cotran, R.S. (2005). Robbins and cotran pathologic basis of disease. Philadelphia: Elsevier Saunders.

Rosamond, W.D., Chambless, L.E., Folsom, A.R., Cooper, L.S., Conwill, D.E., Clegg, L., Wang, C. & Heiss, G. (1998). Trends in the incidence of myocardial infarction and in mortality due to coronary heart disease, 1987 to 1994. New england journal of medicine, 339 (13), pp. 861 — 867.

White, H.D. & Chew, D.P. (2008). Acute myocardial infarction. The lancet, 372 (9638), pp. 570 — 584.