Coronary artery disease is the leading cause of death in the world, accounting for 6·26 million deaths (Murray and Lopez, 1997). In countries with a high incidence of coronary heart disease, the prevalence of angina is asmuch as 30 000-40 000 per million total population (European Society, 19970. The severity of anginal symptoms has an impact on a person’s quality of life. This may limit everyday activities and in some cases lead to early retirement. Even patients with stable angina experience more stressful events, have more sleep disturbance (nightmares, tiredness at work) and psychosomatic symptoms than their healthy counter-parts. Nursing care of an angina patient is not only limited to the in hospital care called as secondary treatment, but also counselling and life style modification in order to prevent further episodes.
Angina Pectoris is defined as a ‘chest discomfort due to myocardial ischaemia associated with coronary artery disease’ (Cunha, 2008). Typically, a patient with angina complains of central chest pain, usually described as heavy, gripping, or constricting, which is brought on by exertion or stress and is relieved by rest and glyceryl trinitrate. The pain may spread down the left arm, sometimes down both arms and may also spread up the neck to the jaw. The pain experienced often frightens the person involved, resulting in marked anxiety. Patients may even feel they are about to die.
Briefly atherosclerosis is the result of a complex interaction between blood elements, disturbed blood flow and vessel wall abnormality (Falk etal, 1995). A coronary artery must be narrowed by at least 50-70% in luminal diameter before coronary blood flow is inadequate to meet the metabolic demands of the heart during increased exercise or stress (European Society, 1997). The loss of blood supply to the heart muscle makes it unable to increase its work in response to demands made during exercise or stresswhich lead to progressive muscle dysfunction that causes heart failure. It disrupts the normal electrical conducting system in the heart, which produces ventricular fibrillation (VF), the major cause of sudden death.
Typical nursing interventions are taking a careful history and, if necessary, seeking supporting evidence from specific investigations is essential for making a diagnosis of angina. Physical examination of the patient may not reveal any diagnostic signs, however, there may be evidence of key risk factors for the development of CAD or of existing vascular disease. Thus, there may be evidence that the patient smokes, has or has had hypertension, has peripheral vascular disease or already has evidence of heart failure. At this stage it is essential that othersituations are ruled out, since some diseases may mimic an angina. These are pleuritis, pericarditis, pneumonia, dyspepsia, mitral valve prolapse, aortic dissection, herpes zoster, and it may be psychiatric in origin also. These may be distinguished both clinically as well as with the use of investigations (Cunha, 2008)
Patients suspected of having acute coronary syndrome should be referred to a hospital for observation, electrocardiography, and blood testing (cardiac markers). It is essential to understand that a normal electrocardiogram does not rule out acute coronary syndrome (although it does make it less likely), particularly if documented after relief of symptoms.however it is an essential first line investigation as it is able to point in the directoin of angina, and effectively rules out other differential diagnosis (Kendall, McMurray 1998). In addition, it may give indicators such as hypertension, cardiac failure also. Thus it has a great positive predictive value.
Cardiac enzymes are an essential investigation for the diagnosis of angina. It is an important to assess the levels as a baseline marker. However again normal concentrations of cardiac markers do not rule out acute coronary syndrome, particularly if measured shortly after the onset of complaints. Elevation of these markers takes four to six hours after myocardial necrosis, and six to eight hours are needed before markers of necrosis appear in peripheral blood. If an initial blood test is normal, and the history is highly suggestive, it is essential to repeat the test after eight to 12 hours (Ohman etal, 1996). If this is also normal, and the electrocardiogram is normal or shows little acute evolution, then the patient is at very low risk and may be discharged. However, such patients should have an early stress test to document whether provoked ischaemia is present. If the cardiac biomarkers are raised or the electrocardiogram shows evolutionary changes, admission to hospital is indicated. The in-hospital management of patients with chest pain is determined by the risk of complications and death. Indicators of high risk include typical complaints, documented coronary artery disease, and advanced age. On physical examination, new mitral regurgitation, hypotension, excessive sweating, pulmonary oedema, and rales are all associated with high risk (Norris,1998) On the electrocardiogram, new Q waves, new ST segment deviation, or new T wave inversion with symptoms indicate high risk. Raised cardiac troponin T, troponin I, or creatine kinase MB in the serum indicates myocardial necrosis and a high risk of an adverse outcome. In addition, markers of congestive heart failure, particularly plasma B-type natriuretic peptide, have been shown to be independent predictors of death in patients with non-ST segment elevation acute coronary syndrome (Kendall, McMurray , 1998).
Imaging techniques may support the diagnostic process by showing wall motion abnormalities (echo-cardiography, magnetic resonance imaging), ischaemia (nuclear perfusion scanning), or coronary pathology (multislice computed tomography scanning). When a coronary artery is significantly narrowed, the heart muscle supplied by this artery does not contract as well as the rest of the heart muscle during exercise. Abnormalities in muscle contraction can be detected by echocardiography. Stress echocardiography and thallium stress tests are both about 80% to 85% accurate in detecting significant coronary artery disease (Cunha, 2008). Thus they are combined in the initial assessment of the patient. There is a rapid emergence of the role of CT angio as a noninvasive investigation to assess the arterial blockade in the heart and the areas critically affected. However a conventional arteriography is the gold standard and all patients need to be worked up for this procedure (Peters etal, 2007).
The initial management
Therapy of the angina patient is directed at stabilizing the hemodynamics, relieving ischemic pain, using antithrombotic therapy to minimize myocardial damage and reducing the risk for recurrent ischemia. Subsequently, risk stratification should be utilized to assess the likelihood for failure of medical therapy and the need for revascularization. It has been estimated that 80% of ACS patients can be stabilized within 48 hours after being started on an intensive medical program for ischemia, while the rest require urgent catheterization and revascularization (Yeghiazarians 2000.)
Patients with hypertension, hyperlipipidemia, diabetes and clotting abnormalites, strong family history are take to be at a higher risk and receive greater attention. Predictors of death in patients with acute coronary syndromes, according to the GRACE registry are – Age, Killip class (heart failure), Heart rate, Blood pressure, ST deviation on electrocardiogram, Cardiac arrest, Raised creatinine,and Raised creatine kinase MB or troponin (Peters et al, 2007)
Initial therapy for patients presenting with chest pain has traditionally employed oxygen, aspirin, nitroglycerin and morphine. The main target in the treatment of angina is to reduce myocardial oxygen consumption and/or increase myocardial perfusion.
Morphine – Morphine may be useful to achieve analgesia and reduce anxiety.
Nitrates increase coronary blood flow, cause vasorelaxation of coronary arteries and reduce platelet adhesion and aggregation. The most commonly used nitrates are nitroglycerin (glyceryl trinitrate), isosorbide dinitrate and isosorbide mononitrate. Nitrates may be used to provide antianginal efficacy for 12-15 h a day.
Beta-blockers (Peter et al, 2008))- Beta-blockers slow the heart rate and reduce myocardial contractility and therefore decrease heart work and myocardial oxygen consumption. They also improve blood flow through myocardial blood vessels by reducing the frequency of the ventricular contractions that constrict coronary artery branches that pass through the myocardium. There is good evidence that beta1 selective drugs are better tolerated and that lipophilic drugs are the drugs for which there is more evidence that they are cardioprotective and reduce sudden death
Anticoagulants – Aspirin irreversibly blocks cyclooxygenase in platelets, rendering them incapable of synthesizing thromboxane A2 for the rest of their circulating lifetime. Aspirin is the mainstay of treatment. In an authoritative review by collaborating trialists, the use of aspirin was associated with a nearly 50% reduction in relative risk of vascular events compared with placebo. (Antithrombotic Trialists’ Collaboration. Collaborative 2002.)
Surgical intervention – angiography and or angioplasty/ CABG
In patients who are not responding to the conservative line of managemetn, coronary angiography is indicated. Often stenting is required at the initial stage itself. In patients who are unfit for angioplasty, a coronary bypass procedure is indicated. This procedure for myocardial revascularization has been the main effective coronary artery surgery for decades. It involves removing the affected section of the coronary artery (or arteries) and replacing them with a suitable graft. Percutaneous transluminal coronary angioplasty (PTCA) (Cunha, 2008)
Long term treatment from a nursing perspective
After discharge, management of patients with acute coronary syndromes consists of two main components. Firstly, prevention of recurrent ischaemia and death requires continued treatment with aspirin (indefinitely), anti cholestrol agents and [beta] blockers. Secondly, the underlying atherosclerotic process should be treated by tackling all modifiable risk factors. These include the strict treatment of hypertension and diabetes, cessation of smoking, achieving an optimal body weight, regular physical exercise, and healthy food choices.
1. Murray C, Lopez AD. (1997) Mortality by cause for eight regions of the world: Global Burden of Disease Study. Lancet, 349, 1269-1276.
2. Recommendations of the Task Force of the European Society of Cardiology. (1997) Management of stable angina pectoris. European Heart Journal, 18, 394-413.
3. Cunha JP (2008). Angina Accessed on 11 June, 2008 from http://www.medicinenet.com/angina/page4.htm#5whatare.
4. Falk E, Shah P, Fuster V. (1995) Coronary plaque disruption. Circulation, 92, 657-671.
5. Kendall M, McMurray J. (1998) Cardiovascular disease, hypertension and angina. In: Kendall MJ, Horton RC, eds. Preventing Coronary Artery Disease. Cardioprotective Therapeutics in Practice, 2nd edn. Martin Dunitz, Singapore
6. Ohman EM, Armstrong PW, Christenson RH, et al. Cardiac troponin T levels for risk stratification in acute myocardial ischemia. GUSTO IIA Investigators. N Engl J Med 1996;335:1333–1341.
7. Norris RM. (1998) Fatality outside hospital from acute coronary events in three British health districts. 1994-5. British Medical Journal, 316, 1065-1070.
8. Peters, R J G; Mehta S, Yusuf S. Acute coronary syndromes without ST segment elevation. BMJ. Volume 334(7606), 16 June 2007, pp 1265-1269
9. Yeghiazarians Y, Braunstein JB, Askari A, et al. Unstable angina pectoris. N Engl J Med 2000;342:101–114.
10. Antithrombotic Trialists’ Collaboration. Collaborative metaanalysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002;324:71–86.)