A Diagnosis On Chest Pain Case Summary Biology Essay

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Mrs X, a 59 years old lady was presented to the A&E department with chest pain and discomfort. She described the pain as pricking and it was felt at the retrosternal region and side. The pain radiated to her shoulder and back and was associated with palpitations. She also complained about nausea, sweating, shortness of breath as well as loss of appetite. Her legs were swollen and she had hyperglycaemia symptoms at home. (add History of presenting illness)

Her past medical history reveals that she has had Type 2 Diabetes Mellitus and hypertension for more than 10 years. She also suffers from hypercholesteremia and Ischemic Heart Disease. She had multiple admissions for IHD and undergone angiogram before. She neither smokes nor drinks alcohol, is independent and staying with her children. However, she avoids walking outside or leaving the house due to exertional chest pain.

Mrs X's father was hypertensive and he passed away due to stroke. Her mother is diabetic. Before admission, she was on Glicazide, Metformin, Humulin N for her diabetes, aspirin for prophylaxis of ischaemic heart disease (IHD), simvastatin for hyperlipidemia secondary to prevention of IHD as well as isosorbide dinitrate and perindopril for her hypertension.

Patient was diagnosed with Non-ST Elevated Myocardial Infarction (NSTEMI).

Disease overview

Acute coronary syndrome (ACS) is an umbrella term describing a broad spectrum of ischemic heart diseases. ACS can be categorised into Unstable Angina/Non ST Elevated Myocardial Infarction (UA/NSTEMI) and ST- Elevated Myocardial Infarction (STEMI) based on the ST-elevation of the electrocardiogram. NSTEMI occur due to partial occlusion of the coronary artery whereas in STEMI the coronary artery is completely blocked. Blockage of coronary arteries lead to myocardial tissue necrosis and cardiac enzyme would subsequently be detected in the blood. Unstable angina occurs when there is no significant myocardial tissue death whereas in NSTEMI and STEMI patients, there is an elevation of cardiac enzymes due to tissue damage.

An estimated 7.2 million people die each year from CHD worldwide and it is currently the most common cause of death in Europe. Unstable angina and NSTEMI heart attacks account for approximately 2.5 million hospital admissions worldwide and about 40% to 75% of all heart attack victims die before reaching the hospital. From 2000-2005, 20-25% of all deaths in government hospitals from were due to CVD. Mortality rate following an acute myocardial infarction (AMI) is high and was about 20% in 2004.

Pathophysiology

NSTEMI is characterised by an imbalance of oxygen supply and demand. It is usually caused by the narrowing of coronary arteries due to thrombus formation on a disrupted atherosclerotic plaque. This disrupted atherosclerotic plaque is in turn, most commonly caused by inflammation of the arteries due to non-infectious caused by noninfectious (e.g., oxidized lipids) and, possibly, infectious stimuli. This can destabilize the plaque, causing it to rupture or erode, and lead to thrombogenesis. Although less likely, coronary spasm may also cause dynamic obstruction and reduce oxygen supply to the heart. The imbalance of oxygen supply and demand is not always limited to the arterial bed. It can also be precipitated by other conditions, such as the increase in myocardial oxygen demand which is secondary to unstable angina.

NSTEMI can be diagnosed by physical investigations, looking at the Clinical history of ischaemic type chest pain and investigation of ECG changes as well as evidence of myocardial injury or necrosis as indicated by

elevated serum cardiac biomarkers

Drug pharmacology

S/L Nitrate

Aspirin : It is an anti-inflammatory and anti-platelet agent which act by formation of thromboxane A2 and platelet aggregation through inhibition of the cyclooxygenase-1 (COX-1) pathway.

Clopidogrel/ Ticlopidine

Inhibits platelet aggregation mediated by adenosine diphosphate

UFH and LMWH

inhibit the inactivation of thrombin and factor Xa by antithrombin III

Statins

Inhibit the activity of HMG CoA reductase, which is responsible for the synthesis of cholesterol.

ACE Inhibitors

ACE I blocks the conversion of angiotensin I to angiotensin II, which is facilitated by Angiotensin Converting Enzyme.

Beta blockers : Act on beta 1 receptors to reduce myocardial oxygen consumption via reduction in myocardial contractility, sinus rate, AV node conduction and SBP

Trimetazidine

Selectively inhibit mitochondrial long chain 3- Ketoacyl co- enzyme A thiolase, the last enzyme involved in beta- oxidation. Affects myocardial substrate utilization by inhibitrng fatty acid oxidation and shifting ATP production with less 02 consumption from FFA to glucose oxidation

Evidence for treatment of the condition (s)

Management

Alogrithm for the management of UA/NSTEMI

Early management

In- Hospital Management

Antiplatelets

ASPIRIN

The use of aspirin in treating NSTEMI has been strongly recommended by guidelines1,2,3 and its effectiveness over placebo is well demonstrated.4,5,6,7 Lewis JR et al has shown a statistically significant decrease of 51% in the incidence of death or acute myocardial infarction in patients who received aspirin instead of placebo.7 A meta-analysis of 287 studies involving 135 000 patients showed that aspirin is effective in reducing the risk of myocardial infarction, unstable or stable angina and other cardiovascular disease. 9 However, aspirin is associated with the risk of GI bleeding. 10 Aspirin is usually given in a dose range of 81- to 100-mg/d and low dose aspirin (≤100 mg/d)was less likely to cause a major bleeding event in comparison with standard-dose aspirin. 11 This supports the use of low dose aspirin in the recommended guidelines. In my case study, aspirin was initially on 150mg of aspirin OD which was appropriate management for NSTEMI. Nevertheless, aspirin was then stopped on 8/4. The reason for stopping aspirin was not known and could possibly be to due to aspirin allergy or GI bleeding. In the absence of any contraindications, aspirin should be restarted. Clopidogrel is recommended for patients who are intolerant to aspirin. 1

Adenosine diphosphate antagonist

CLOPIDOGREL

APatient was not on clopidogrel. According to the guidelines, clopidogrel should be added to aspirin if a non-interventional approach is planned. 1 This recommendation was supported by AAA large randomised trial involving 12,563 patients called Clopidogrel for the Reduction of Events During Observation (CURE), which showed that combination of clopidogrel and aspirin was superior over aspirin alone. 11(from aspirin). Incidence of mortality due to cardiovascular causes, non fatal myocardial infarction or stroke, was found to be significantly lower in the group of patients who were on clopidogrel in a 9 months follow up. Besides in-hospital severe ischemia and revascularization was reduced. (AHA guideline) However, the risk of intracranial bleeding was increased in this group and this was especially so for patients who undergone coronary artery bypass graft. Therefore, clopidogrel is only recommended if a non-intervnetional approach was planned. Hence, clopidogrel is suitable for my patient and should be recommended. (Eric H. et al)

TICLOPIDINE

Patient is on ticlopidine. Reason why patient should be on clopidogrel.

Ticlopidine associated with neutropenia. Although ticlopidine and clopidogrel were both shown to be effective in treating UA/NSTEMI, Clopidogrel has a much better safety profile (Pietro Di Pasquale et al and AHA)

HEPARIN

Low Molecular Weight Heparin (LMWH)

Enoxaparin and dalteparin are currently approved for the treatment of UA/NSTEMI. Tinzaparin, nadroparin and ardeparin are also available for the management of UA/NSTEMI whereas fondaparinux is a new member of the LMWH which also has potential benefits. Properties between members of the LMWH differ, is associated with distinct clinical efficacy and hence their use is non-interchangable.

Enoxaparin

LMWH vs Unfractionated Heaparin (UH)

The ESSENCE (Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q Wave Coronary Events) showed that the efficacy of enoxaparin was superior over UH as the risk of developing ischemic cardiovascular events as well as the need for diagnostic catheterization or coronary revasculation in patients was reduced. This findings was supported by a similar large trial, TIMI 11B (Thrombolysis in Myocardial Infarction 11B)13 E.M. Antman, C.H. McCabe and E.P. Gurfinkel et al., Enoxaparin prevents death and cardiac ischemic events in unstable angina/non-Q-wave myocardial infarction. Results of the Thrombolysis in Myocardial Infarction (TIMI) 11B trial, Circulation 100 (1999), pp. 1593-1601. View Record in Scopus | Cited By in Scopus (723) studies. Although enoxaparin was more likely to cause minor bleeding, the risk of major bleeding was similar to that of UFH. (Mukherjee D the use of) LMWH is also found to be more resistant to inhibition by activated platelets, has a more predictable anticoagulant effect with less need for monitoring and lower incidence of side effects. Apart from this clinical advantage, LMWH also appear to be more cost-effective. (cost effectiveness enoxaparin ref.) Hence, LMWH is recommended for NSTEMI patients.

Risk stratification

Why patient don't need GPIII AT

Early invasive vs early conservative therapy

Although previous studies have shown similar outcomes between early invasive and conservative approaches in treating NSTEMI, it has been increasingly demonstrated that high-risk patients with myocardial marker proteins would benefit from an early invasive approach. This was tested by Randomised Intervention Treatment of Angina (RITA-3), which was a large randomised multicentred trial involving 1810 patients. My patient had….. elevated troponin levels.. and thus was considered as a high risk patient. An early invasive strategy might be considered in this patient.

Post Hospital Management

Alert

This article is not included in your organization's subscription. However, you may be able to access this article under your organization's agreement with Elsevier.

Jeffrey S. Low-Dose Aspirin in Patients with Stable Cardiovascular Disease: A Meta-analysis

Statins

There is good evidence for the use of statins. Statins reduces mortality rate.

ACE(I)

Beta-blocker

Treatment with early BBs may have a beneficial impact on hospital and 6-month mortality in all patients, including those who are presented with heart failure. (Michael Emery et al.)

Lifestyle Modification

Trimetazidine

Clinical Evidence

The value of trimetazidine in symptomatic relief and functional outcomes in patients with angina has been shown in several studies. In one study, H. Szwed et al. reported that trimetazidine significantly increased exercise capacity in a group of patients who were over 65 years old. H. Szwed also reported that anginal episodes and weekly nitrate consumption were significantly reduced in this group of patients. Hence, this study demonstrates that trimetazidine when added to current anti-anginal therapy, is beneficial and well-tolerated for the treatment of angina pectoris in the elderly population. Also, trimetazidine was reported to increase cell tolerance to ischemia and has it is suggested to be cytoprotective of ischemia. Hence, the use of trimetazidine in my patient is supported, even though its use is not included in the current guideline recommendations for UA/NSTEMI.

Close adherence to guidelines improves patient outcomes. Evidence based guidelines.

Conclusion:

My patient is managed according to the evidence based guidelines, except for the use of ticlopidine in this patient. The use of clopidogrel instead of ticlopidine is recommended. This is because clopidogrel has fewer incidences of adverse effects and its effectiveness is more established. Management of this patient should closely adhere to the guidelines as management according to these guidelines have significantly improved patient outcomes. Although trimetazidine was not included in the recommendation, its use in this patient is appropriate and substantiated by clinical studies

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