This essay delves on the treatment of acute myocardial infarctions by heparin. Below will be described some examinations of use of heparin for treatment of the acute myocardial syndrome. Received outcomes show that use of low molecular weight heparin is more effective than the use of unfractionated heparin. Also, some researches state that heparin treatment can be replaced by the treatment of other medication in certain cases. Additionally, the nursing implications of acute myocardial infarction treatment by heparin will be described in this essay.
Acute Myocardial Infarction (AMI)
Myocardial infection is a part of an acute coronary syndrome. An acute myocardial infarction is caused by blockage of a coronary artery by a thrombus. (i.e. by necrosis of myocardial tissue). Michael Bolooki, in his article Acute Myocardial infarction, described this process as follows: ‘Myocardial infarction occurs when myocardial ischemia, a diminished blood supply to the heart, exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms designed to maintain normal operating function and homeostasis’.
Miocardial infarction can be diagnosed by a ‘detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least one value above the 99th percentile of the upper reference limit, together with evidence of myocardial ischemia’. Evidence of myocardial ischemia should include one of the factors mentioned below: electrocardiogram alterations indicative of a new ischemia; symptoms of ischemia; imaging evidence of the new abnormality of wall motion which can be regional or viable myocardium new loss; and pathological Q-wave development alterations in the electrocardiogram.
Nowadays, acute myocardial infarction is one of the main causes of mortality and morbidity.
Unfractionated heparin and low molecular weight heparin may be used for the treatment of acute myocardial infarction.
Unfractionated heparin is a special kind of anticoagulant. It is used for prevention and treatment of thrombosis. Unfractionated heparin leads to inhibition of the activity of coagulation factors in the blood. This medication is used till complete recovery of inciting thrombotic cause (ruptured plaque). It is also widely used for ‘treatment of extension of venous thrombosis, prevention of postoperative deep venous thrombosis and pulmonary embolism in patients with clotting in arterial and cardiac surgery’ (Heparin). Thus, forms of heparin are also used for prevention of embolism that can occur in people with atrial fibrillation. Health care providers prescribe treatment by unfractionated heparin for patients with non-Q wave myocardial infarctions (like non-ST elevated acute coronary artery syndrome) and for patients which suffer from unstable angina
Treatment should be held in accordance with specific guidelines. Unfractionated heparin can be administered in different ways: subcutaneously or intravenously. Duration of this treatment differs greatly for patients with different diagnoses.
Low molecular weight heparin is used for prevention of deep vein thrombosis, potentially fatal blood clots. This medication is derived from unfractionated heparin by depolymerization. Both unfractionated heparin and low molecular weight heparin inactivate coagulation enzymes by binding to AT (Unfractionated and Low Molecular Weight Heparins). At the same time low molecular weight heparin ‘has the lower affinity for binding to proteins other than AT and is, therefore, associated with a predictable dose response and fewer non-hemorrhagic side effects’ (Unfractionated and Low Molecular Weight Heparins). Nowadays low molecular weight heparin is presented by Delteparin, Enoxaparin, Nadroparin, Cetroparin, Tinzaparin, Ardeparin, Reviparin, Bemiparin and Panaparin.
Patients, who are not treated by fibrinolytic therapy, can use low molecular weight heparin instead of unfractionated heparin. This medication can be used for the treatment of patients who have no contraindications to heparin
The Effect of Heparin on Patients with Acute Myocardial infarction (AMI)
Yamamoto in his work ‘The effect on tissue factor and tissue factor pathway inhibitor in patients with acute myocardial infarction’ examined plasma TF and free TFPI levels. These examinations were held during the experiment on 26 patients who suffered from acute myocardial infarction; 25 people who suffered from chest pain syndrome and 26 patients with stable exertional angina. Test samples were taken during several periods of time. For example, test samples of blood from patients who suffered from acute myocardial infection were taken in 4 hours; 8 hours; 16 hours; 24 hours; 48 hours period after admission and on the 3d; 5th; 7th; and 14th day after commencement of reperfusion therapy. It should be mentioned that patients who suffered from acute myocardial infarction have higher admission than patients who suffered from pain in chest and stable exertional angina: 248.0 +/- 117.4 vs. 179.5 +/- 29,2 vs. 189.5 +/- 29.6 pg/ml, P < 0.01). Patients, which suffered from acute myocardial infarction, received heparin. This treatment caused a reduction of the level of plasma TF.
At the same time, Yamamoto stated that ‘plasma free TFPI levels in patients with AMI on admission were significantly higher than in the chest pain syndrome and stable exertional angina groups (33.5+/-12.4 vs. 26.0+/-7.6 ng/ml (P<0.01) vs. 27.5+/-6.3 ng/ml, P<0.05)’ After taking heparin, plasma TFPI level of patients with AMI reached its maximum after 4 hours of admission. In the next hours, this level decreased.
Based on these examinations, Yamamoto made the following conclusions ‘continuous administration of a low dose of heparin was effective in decreasing TF levels without affecting TFPI levels… administration of heparin is beneficial in AMI patients undergoing percutaneous revascularization.’.
Anticoagulant Therapy and the Effect of Heparin Treatment on Patients
There are different types of anticoagulant therapies for patients with different syndromes. For example, patients with non-ST elevation acute coronary syndrome should take other medicine in comparison with patients with the ST-elevation acute coronary syndrome.
Patients with a non-ST elevation acute coronary syndrome are treated by unfractionated heparin (UFH). This treatment takes at least 48 hours. The goal of unfractionated heparin treatment is to reduce the combined endpoint of death. Also, this treatment decreases myocardial infarction. A national clinical guide of Scotland provided the following figures: absolute RR 2.5 % relative RR 33 % (Acute Coronary Syndromes). According to this report ‘this is predominantly driven by a reduction of non-fatal myocardial infarction’ (Acute Coronary Syndromes).
Patients with ST-elevation acute coronary syndrome use combined treatment. This treatment includes use of fibrin-specific agents together with aspirin and thrombolysis. These patients use unfractionated heparin. Combination of these medication leads to the reduction of the rate of death and re-infarction. According to national clinical guide of Scotland, death rates decrease on 0.5 % absolute RR and rates of re-infection decrease on about 0.3 % absolute RR (Acute Coronary Syndromes).
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Low molecular weight heparin is prescribed for patients with different diseases. Below will be described the treatment of patients with Non-ST elevation acute coronary syndrome and for patients which suffer from ST-elevation acute coronary syndrome.
Treatment of patients with non-ST elevation acute coronary syndrome with low molecular weight heparin reduces myocardial infarction (Acute Coronary Syndromes). Also, this treatment decreases coronary revascularization procedure rates in comparison with the treatment by unfractionated heparin. At the same time, there were no differences in major bleeding and mortality episodes. According to national clinical guide of Scotland, ‘the number of patients needed to treat with low molecular weight heparin rather than unfractionated heparin to prevent one myocardial infarction was 125’(Acute Coronary Syndromes). It is also stated that the number of patients needed to treat with low molecular weight heparin rather than unfractionated heparin to prevent one extra revascularization procedure was 50 (Acute Coronary Syndromes).
Antaman in his work Enoxaparin prevents death and cardiac ischemic events in unstable angina/non-Q-wave myocardial infarction stated the following: ‘benefits from low molecular weight heparin remain evident well beyond the duration of treatment and in the TIMI IIB trial were still evident at one year’. Magee, in the book Low molecular weight heparins versus unfractionated heparin for acute coronary syndromes, supported this idea by the following ‘extended use of low molecular weight heparin beyond the inpatient stay or for more than eight days is of no value’ (Magee, 2004).
It should be mentioned that the use of low molecular weight heparin together with glycoprotein llb/llla receptor does not show any considerable changes in efficiency in comparison with the use of unfractionated heparin with glycoprotein llb/llla receptor. However, use of low molecular weight heparin does not change the condition of bleeding complications or even decreases these complications.
Therefore, use of low molecular weight heparin was more effective then use of unfractionated heparin for patients with ST elevating acute coronary syndrome. According to national clinical guide of Scotland ‘misanalysis confirms that, in patients treated with thrombolytic therapy, low molecular weight heparin (enoxaparin) is associated with better outcomes’ (Acute Coronary Syndromes). These positive outcomes include decreasing of myocardial infarction (absolute RR 2.3 % relative RR 41 %); decreasing of death (absolute RR 2.9 % to relative 26 %); considerable lowering of recurrent ischemia (absolute RR 2.0 % to relative RR 30 %) (Acute Coronary Syndromes). At the same time, the researches showed no changes in mortality in cases when patients take low molecular weight heparin in comparison with the cases when patients take unfractionated heparin.
Also, the combination of medication gives considerable effects in treatment. For example, use of Tenecteplase or Alteplase with enoxaparin leads to increasing in major bleeding. This leads to increasing of relative risks (on about 44 %) and growth of absolute risks (on about 1 %) (Acute Coronary Syndromes). Combination of medication has a strong effect on patients of the elder age. This is confirmed by the national clinical guide of Scotland ‘predominantly in patients over 75 years of age where the dose of enoxaparin may need to be reduced’ (Acute Coronary Syndromes). Hence, nurses and health care providers should pay much attention to the patient’s age during his or her medical treatment with using heparin. These researches were based on a treatment by unfractionated heparin and treatment by enoxaparin given throughout hospital admission. The duration of treatment was 48 hours. Use of enoxaparin leads to decreasing of recurrent myocardial infarction (absolute RR 2.1 % relative RR 17 %). At the same time, there were no changes in overall mortality. However, there was a considerable increase of major bleeding in cases of use of enoxaparin during a long period of time (30 days). In this case, relative risks increased by 53 % and absolute risk increased by 0.7 %. Antam, in his work Enoxaparin versus Unfractionated Heparin with Fibrinolysis for ST-Elevation Myocardial Infarction, stated that ‘although the superior efficiency of enoxaparin was apparent by 48 hours, this trial observed a rise in event rates after unfractionated heparin was discounted suggestion that 48 hours of anticoagulation is sufficient’ (Antman, 2006).
Treatment by heparin may be replaced by other medication. It should be mentioned that ‘direct thrombin inhibitors appear to have a similar magnitude of benefit over unfractionated heparin to that seen with low molecular weight heparin’ (Acute Coronary Syndromes). However, there were no comparative studies to support this idea.
Synthetic pentasaccharides can be used in the treatment of patients which suffer from ST-elevation acute coronary syndrome. This medication can replace use of unfractionated heparin. This is confirmed in clinical guide of Scotland: ‘intravenous bolus followed by daily subcutaneous fondaprinux injection (2.5 mg) reduced the primary endpoint of death or recurrent myocardial infarction at 30 days (absolute RR 1.5 % and relative RR 14 %) compared treatment with placebo or unfractionated heparin’ (Acute Coronary Syndromes). These tests were made during different time periods of 9 days, 30 days and 180 days. Rates of death decreased considerably within all time periods. For example, during 30 days time period the death rate reduced to absolute RR of 1.1 % and relative RR of 13 %. At the same time, there were no changes in the incidence of major bleeding during these time periods. However, these positive effects were seen only during the treatment of patients who were not related to primary percutaneous coronary intervention (Yusuf, 2006).
Michael Bolooki, in his work Acute Myocardial infarction, noted that heparin therapy may be replaced by taking of the direct thrombin inhibitor, Bivalirudin: ‘the 2007 American College of Cardiology (ACC) and the American Heart Association (AHA) guidelines recommend Bivalirudin as an alternative to heparin therapy for patients who cannot receive heparin for a variety of reasons (e.g., heparin-induced thrombocytopenia)’.
Nursing Actions and Related Consequences of Taking Heparin
Taking heparin can lead to considerable worsening of patients’ health conditions. Nurses should obtain a complete health history of the patient before giving heparin to the patient. This health history should contain information concerning the patient’s allergies, any possible drug interaction and drug history. It should be mentioned that the patient’s drug history should include use of over the counter medications that might affect coagulation and cause allergies.
Also, nurses should make several assessments. They should assess the history of GI bleeding, bleeding disorders, recent trauma and cerebral bleed. Nurses have to assess baseline coagulation studies and CBC.
Dr Haley Willacy, in his article Acute Myocardial infarction Management, noted the following: ‘for patients who cannot be offered PCI within 90 minutes of diagnosis, a thrombolytic drug should be administered along with either unfractionated heparin (for maximum two days), a low molecular weight heparin (eg, enoxaparin) or fondaparinux.’ . This is done because ‘thrombolytic drugs break down the thrombus so that the blood flow to the heart muscle can be restored to prevent further damage and assist healing’ .
These actions are necessary for the reduction of the possibility of numerous side effects of taking heparin. These side effects include injuries, risks for bleeding related to side effects of anticoagulant medication. Also, potential negative nursing diagnosis of taking heparin include tissue perfusion and risks of venous or hemorrhage thrombosis related to side effects of anticoagulant therapy.
Side effects of heparin treatment include: hematologic, cardiovascular, dermatologic, hypersensitivity, hepatic, endocrine, metabolic, musculoskeletal and local.
Hematologic side effects are represented by melena, hematuria, hematomas, ecchymosis, epistaxis and hematemesis. Cardiovascular side effects include new or recurrent venous and arterial thrombosis and thrombocytopenia. Necrotic lesions at subcutaneous injection sites, extensive skin necrosis, erythematous, nonnecrotic plaques at injection sites, generalized pruritic and erythematous rash compose dermatologic side effects. Hypersensitivity includes papular, and vesicular lesions, drug fever, asthma, rhinitis, urticaria, pruritic, and naphylaxis. Hepatic side effects are represented by aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The growth of free thyroxine levels causes endocrine side effects. Other side effects are netabiloc (hypertriglyceridemia, hyponatremia, and hyperkalemia), musculoskeletal (osteoporosis) and local (erythema, mild pain, injection site irritation, and hematomas) (Heparin).
Nurses should know about the expected outcomes of taking heparin. After taking this medication patient will remain free of unusual bleeding. Also, he will maintain effective tissue perfusion.
Therefore, taking of heparin should be precisely controlled by nurses or other medical staff. Special monitoring for bleeding is extremely necessary. They should check the color of the patient’s urine, any changes in vital signs and occult blood in the stool. Strict control should be performed over the patients, which have a history of alcoholism, peptic ulcer disease, liver or kidneys disease. These patients are at greatest risk of bleeding. Also, nurses should perform strict monitoring of the condition of patients of the elderly age.
They should give advises to patients in order to monitor and to improve their health conditions. For example, patients can use an electric shaver and soft toothbrush. People who are taking heparin should avoid any contact sports. Health care provider should receive information from the patient about any injures (even minor). In the case when patients receive SQ heparin outside hospitals, they should wear identification stating that these people are on anticoagulant therapy.
The effect of heparin can be decreased by nicotine. So, nurses should encourage the reduction of smoking in patients Hence, patients should stop smoking at least for the time of taking this medication.
Anticoagulation can lead to excessive blood loss during menstruation period. Therefore, nurses should monitor CBC in women who are menstruating in order to decrease this blood loss. Patients should know that taking heparin could lead to increased menstrual bleeding. Health care provider should know about any increasing in bleeding in order to make appropriate actions and avoid worsening of the patient’s condition.
It should be mentioned that PTT for therapeutic values baseline should be monitored. This figure has to be 1,5 – 2,5. Caregivers and patient should know the rationale for frequent lab test with IV heparin.
Nurses should perform an evaluation of the patient’s condition during drug therapy and upon its completion. The therapy is considered to be effective when the patient will remain free of unusual bleeding or will maintain effective tissue perfusion.
Conclusion
Above was given information about the use of heparin for treatment of acute myocardial infarction. Unfractionated heparin and low molecular weight heparin have different effects on the patient’s condition. So, health care providers should carefully examine the health condition of each particular patient in order to prescribe the most effective treatment. At the same time, nurses should pay much attention to the patient’s condition during heparin therapy in order to avoid and decrease any worsening.