Acute Coronary Syndrome

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Original Editors - Students from Glasgow Caledonian University's Cardiorespiratory Therapeutics Project.

Top Contributors - Haseel Bhatt, Kim Jackson, Lucinda hampton, Adam Vallely Farrell, Michelle Lee, Admin, 127.0.0.1 and WikiSysop  

Definition/Description

Acute coronary syndrome (ACS) is a spectrum of disease ranging from undifferentiated chest pain to unstable angina to non-ST-segment elevation myocardial infarction (NSTEMI) to ST-segment elevation myocardial infarction (art 5).

Epidemiology

Background epidemiology to the disease or condition (to include prevalence and incidence as appropriate from a UK or Scottish perspective. (You may want to also look at the disease prevalence across different social economic groups).

Aetiology

Vascular injury and thrombus formation are key components in the initiation and progression of atherosclerosis and in pathogenesis of acute coronary syndrome (Epstein, 1992). Atherosclerotic plaque formation occurs as a result of damage to the endothelium of the blood vessel. The damaged endothelium stimulates a cascade of inflammatory events that causes macrophages to digest low-density lipoprotein (LDL) transforming into foam cells and causing formation of fatty streaks in the subendothelium (Kumar, 2009). Several coronary risk factors can influence this process, including hypercholesterolemia, hypertension, diabetes, and smoking (Kumar, 2009). ACS takes place when a disrupted atherosclerotic plaque in a coronary artery stimulates platelet aggregation and thrombus formation. Previous research has suggested that the narrowing of the coronary artery causes a decrease in blood flow and ultimately ischemia, however, recent studies have suggested that the rupture of an unstable atherosclerotic plaque is chiefly responsible for thrombus formation and infarction. Autopsy studies have shown that plaque rupture causes approximately 75% of fatal myocardial infarction in comparison to superficial endothelial erosions which account for only 25% (Davies, 1990).

Investigations

This may well include any investigations used to gain a diagnosis or that you might need to gain information about your patient assessment.

Clinical Manifestations

The extent to which a coronary artery is occluded often correlates with presenting symptoms and diagnostic findings. Angina or chest pain is considered the cardinal symptom of ACS. Other symptoms that are commonly associated with ACS include; pain with or without radiation to left arm, neck, back or epigastric area, shortness of breath (SOB), diaphoresis, nausea and light headedness. It is important to note that women often present with atypical symptoms which may ultimately delay diagnosis and treatment. These clinical manifestations include; fatigue, lethargy, indigestion, anxiety and pain radiating down the back.

Physiotherapy and Other Management

Anti-Platelet therapy is common management provided by other healthcare professionals. This generally involves the utilzation of medications, predominately in tablet form. These drugs can be aspirin, adenosine diphosphate (ADP)-receptor blockers and aglycoprotein IIb/IIIa inhibitors, among others(ART 2).

Asprin

"Aspirin (acetylsalicylic acid [ASA]) blocks the synthesis of TxA2 from arachadonic acid via its inhibition of the cyclooxygenase (COX) enzyme. It represents the oldest and most studied antiplatelet agent, with early clinical trials in ACS showing consistent benefit over placebo or untreated control for reducing the risk of death and recurrent MI." (ART 2)

Adenosine Diphosphate-Receptor Antagonists

"The joint interaction of ADP with its P2Y1 and P2Y12 receptors not only induces platelet aggregation but also amplifies the platelet response through enhanced secretion of, and response to, platelet agonists such as TxA2 and thrombin.15 Consequently, clopidogrel and other thienopyridines, which specifically and irreversibly inhibit the ADP P2Y12 receptor subtype, have become increasingly important in the management of ACS. Several newer antiplatelet agents also act via P2Y12 antagonism and show promise for assuming greater roles in ACS therapy." (ART2)

Ticlopidine

"Ticlopidine was developed as the original ADP P2Y12 receptor antagonist.16 Clinical trials have shown its superiority over control, and its equivalence to aspirin in the prevention of secondary vascular events in patients with ACS.17,18 The concept of combining ASA and a thienopyridine for ACS management was first assessed using ticlopidine, with several studies in patients with PCI demonstrating the benefit of dual antiplatelet therapy over ASA alone or ASA plus warfarin.19-23 However, ticlopidine is associated with elevated risks of neutropenia and thrombotic thrombocyptopenic purpura (TTP) and is poorly tolerated with associated increases in nausea and vomiting." (ART 2)

Clopidogrel

"Establishing the benefit of clopidogrel in UA/NSTEMI. The Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial was the first large randomized clinical trial to establish the benefit of clopidogrel in secondary prevention. The trial compared clopidogrel (75 mg/d) against ASA (325 mg/d) in 19 185 patients with recent MI, recent ischemic stroke, or established peripheral arterial disease (PAD). There was an observed 8.7% relative risk reduction in patients receiving clopidogrel versus ASA for the composite end point of vascular death, MI, or stroke (5.32% vs 5.83%, P ¼ .04).27 Subgroups of the CAPRIE trial with diabetes mellitus, prior coronary artery bypass graft (CABG) surgery, or prior history of MI or ischemic stroke showed particular benefit with clopidogrel as opposed to aspirin therapy." (ART 2)

Prevention

Brief consideration of how this pathology could be prevented and the physiotherapy role in health promotion in relation to prevention of disease or disease progression.

Resources

add appropriate resources here

Recent Related Research (from Pubmed)

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References

see adding references tutorial.