Acute Coronary Syndrome is a group of clinical symptoms compatible with myocardial ischemia and includes unstable angina, non-ST – segment elevation MI (NSTEMI) and ST elevation MI (STEMI). The manifestation of these symptoms often needs urgent medical care and hospitalisation (Kumar & Cannon, 2009).
ACS happens as a result of decreased blood flow to the coronary arteries. Coronary arteries are arteries which transports blood into the cardiac muscle. They are primarily composed of the left and the right arteries both of which branch off. The left coronary artery comes from the aorta above the cusp of the aortic valve and supplies blood to the left side of the heart, which is responsible for systemic perfusion. The right coronary arteries originate from above the right cusp of the aortic valve, it travels down the right coronary sulcus, towards the crux of the heart.
Role of Atherosclerosis in the development of ACS
Atherosclerosis is an ongoing formation of plaque involves the inner parts of the large and medium arteries. The condition progresses relentlessly throughout the person lifetime before it manifests its self as an acute ischemic event. Children as young as even have been shown to have atherosclerotic plaques.
Damage to the endothelial lining of the blood vessels results in endothelial dysfunction, which then plays a very important role in initiating the atherosclerotic process. Reduced bioavailability of endogenous nitric oxide characterizes endothelial dysfunction and excessive production of endothelin. Which impairs vascular hemostasis, increases the expression of adhesion molecules and increase thrombogenicity of blood through the secretion of several active substances. Several Risk factors such as hypercholesterolemia, hypertension, diabetes, and smoking contribute to the process.
Once the endothelium has been damaged, the inflammatory cells, mainly the monocytes, migrate into the area by binding to the endothelial adhesion molecules. Once in the area, they undergo differentiation and turn into macrophages.
Macrophages then digest oxidized low-density lipoprotein that has also penetrated the arterial wall, which transforms into foam cells which causes the emergence of fatty streaks. The activated macrophages release chemoattractants and cytokines that further perpetuates the process by recruiting more macrophages and vascular smooth muscle cells.
The pathogenesis of ACS involves an intricate interplay among the endothelium, inflammatory cells and the thrombogenicity of the blood. Factors such as blood flow to the area, lipid and tissue factor content of the plaque, the severity of the rapture, the degree of the inflammation at the site. Also, the patients own endogenous antithrombotic and prothrombotic balance are essential in controlling the degree of thrombus formation and determining whether the plaque will rapture and result in ACS.
- Older age
- High cholesterol
- Lack of physical activity
- Unhealthy diet
- Obesity or overweight
- The family history of chest pain, heart disease or stroke
- Chest pain (angina) or discomfort, often described as aching, pressure, tightness or burning
- Radiating pain from the chest to the shoulders, arms, upper abdomen, back, neck or jaw.
- Nausea or vomiting
- Shortness of breath
- Sudden, heavy sweating
- light-headedness, dizziness or fainting
- Unusual or unexplained fatigue
- Feeling restless or apprehensive
Management of ACS
- 12 lead ECG within five minutes of first acute contact, monitoring for signs of myocardial ischemia. The patient should be reviewed as within 10 minutes of ECG being carried out.
- Cardiac-specific monitoring should be measured for example troponin at the hospital and a clearly defined period after the presentation. Other diagnostic tests done include Coagulation profile, Biochemistry, Echocardiogram, Cardiac catheterisation and angiogram and Stress testing.
- In all patients presenting with suspected ACS and without contraindications, aspirin should be given as soon as possible after presentation. Aspirin is a competitive inhibitor of cyclooxygenase.
- Additional antiplatelets and anticoagulation therapy, or other therapies such as beta blockers, should be given to patients without a confirmed or probable diagnosis of ACS.
- Narcotic analgesia
- Smooth muscle relaxation
- Sense of euphoria
- Reduced central nervous system response to pain.
Nitrates – Glyceryl Trinitrate (GTN),
- Smooth muscle relaxation
- Reduces preload and afterload
- Reteplase, streptokinase activates plasmalogens
- Relaxes the heart muscle and slows down the heart rate, thereby reducing the demand on the heart and lowering blood pressure.
- Expands the blood vessels, there reducing the blood pressure which reduces the work rate of the heart.
Angiotensin receptor blockers
- Helps control the blood pressure
According to the heart foundation, routine use of oxygen among patients with blood oxygen of above 93 is not recommended. 8L via Hudson mask or venturi mask in the case of COPD if oxygen use is indicated.
- Angioplasty and stents are used on the artery that is affected; a stent is a tube that is inserted by the medical officer. They are designed to open the narrowed blood vessels thereby restoring blood flow to the area affected.
- Coronary Bypass Surgery. This is where the doctors take a piece of another vessel from another part of the body and create a new route for the blood.
Kumar, A., & Cannon, C. P. (2009). Acute Coronary Syndromes: Diagnosis and Management, Part I. Mayo Clinic Proceedings, 84(10), 917-938.
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