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Pathophysiology of Acute Coronary Syndrome

Acute coronary syndrome (ACS) is a type of coronary heart disease (CHD.) ACS is caused by any activity or circumstance that slows or impedes the delivery of oxygen to the heart. This category of heart disease is inclusive of myocardial infarction (MI) and unstable angina as they have similar signs and symptoms. Patients with myocardial infarction describe chest pain felt during an actual heart attack. In unstable angina, patients describe chest pain felt while performing light physical activity or while at rest. In either case, the syndrome is usually diagnosed during an emergency room visit.

The root cause of CHD is a buildup of fat plaques in the arteries. Fat buildup usually happens over time due to multiple factors including poor diet and heredity. According to Copstead and Banasik (2010), ACS occurs when there is sudden obstruction of coronary blood flow. Acute obstruction is usually associated with the formation of a clot in the coronary artery at the site of a vulnerable plaque.

A variety of factors contribute to the erosion of the endothelium. The erosive factors include hypertension, diabetes, tobacco, infections, oxidative stress, and shear stress. Endothelial injury leads to the appearance of surface adhesion molecules [P-selectin, Vascular Cell Adhesion Molecule -1 (VCAM-1)] and chemokines which encourage leukocyte adhesion and aggregation within the endothelium. The endothelium becomes more permeable to low-density lipoprotein (LDL) and monocytes. LDL and monocytes accumulate in the intima of coronary arteries where they undergo chemical and structural changes. Monocytes are transformed into macrophages which engulf LDL to form cells called form cells (Char, 2005). Collagen-forming cells migrate into the intima and secret collagen fibers on the lipid-containing macrophages. This process yields fatty plaques/fatty streaks. It is not clear when fatty streaks start forming but evidence has shown that it begins in infancy. Rupture of the plaque exposes a rough area comprised of collagen and other molecules that are thrombogenic. Clot formation begins with the adherence of platelets to the ruptured plaque (Copstead and Banasik, 2010). Platelet aggregation may be started by decreased levels of nitric oxide in the blood vessels (Joseph, 2001. The formation of clots and fatty streaks happens simultaneously. Clots may partially block or completely occlude coronary arteries. Complete occlusion causes the sudden ischemic syndrome.

ACS is managed both pharmacologically and non-pharmacologically. Drug therapy of ACS focuses on stopping further fatty streak formation and alleviating pain. Analgesics like morphine and aspirin are used to manage acute pain. Beta-blockers, angiotensin-converting enzyme inhibitors, clopidogrel, and nitroglycerin are used to reduce cardiac workload (Antman et al., 2007). Nitroglycerin can also be used to treat vascular pain. Bile acid-binding resins reduce the formation of fatty streaks. The formation of clots can be stopped using anticoagulants like heparin and glycoprotein IIb/IIIa inhibitors (Antman et al., 2007).

Non-pharmacological management of ACS focuses on lifestyle modification. However, during an acute episode oxygen therapy is instituted. Delivery of oxygen via a nasal cannula aims at raising arterial oxygen saturation above ninety percent (SaO2 > 90%). Lifestyle change needs the cooperation of the patient to achieve a good result. Behavior adjustment includes doing regular physical exercises and eating healthy food. Patients should be advised to eat a balanced diet containing little salt and saturated fat.

This paper discussed the pathophysiology of the acute coronary syndrome and its management. Management of ACS focuses on stopping clot formation and alleviation of pain. Anticoagulants are used to eliminate clots.

References

Antman, E. et al. (2007). Focused Update of the ACC/AHA 2004 guidelines for the management of patients with STelevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation, 117(2), 296-329.

Char, D. (2005). The pathophysiology of acute coronary syndromes. Web.

Copstead, L., & Banasik, J. (2010). Pathophysiology (4th ed.). St. Louis, Missouri: Saunders Elsevier.

Joseph, L. (2001). Nitric Oxide Insufficiency, Platelet Activation, and Arterial Thrombosis. Circ Res., 88(8), 756-62. Web.

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OctoStudy. (2022, May 25). Pathophysiology of Acute Coronary Syndrome. Retrieved from https://octostudy.com/pathophysiology-of-acute-coronary-syndrome/

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OctoStudy. (2022, May 25). Pathophysiology of Acute Coronary Syndrome. https://octostudy.com/pathophysiology-of-acute-coronary-syndrome/

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"Pathophysiology of Acute Coronary Syndrome." OctoStudy, 25 May 2022, octostudy.com/pathophysiology-of-acute-coronary-syndrome/.

1. OctoStudy. "Pathophysiology of Acute Coronary Syndrome." May 25, 2022. https://octostudy.com/pathophysiology-of-acute-coronary-syndrome/.


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OctoStudy. "Pathophysiology of Acute Coronary Syndrome." May 25, 2022. https://octostudy.com/pathophysiology-of-acute-coronary-syndrome/.

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OctoStudy. 2022. "Pathophysiology of Acute Coronary Syndrome." May 25, 2022. https://octostudy.com/pathophysiology-of-acute-coronary-syndrome/.

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OctoStudy. (2022) 'Pathophysiology of Acute Coronary Syndrome'. 25 May.

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