The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”

Published May 20, 2010

“The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”.

MYOCARDIAL INFARCTION

Myocardial infarction refers to a dynamic process by which one or more regions of the heart muscle experience a severe and prolonged decrease in oxygen supply because of insufficient coronary blood of subsequently, necrosis or death to the myocardial tissue occurs.

The onset of the myocardial infarction process may be sudden or gradual and the progression of the event to complete takes approximately 3 to 6 hours.

PREVALENCE

Myocardial infarction is the leading cause of death in the United States (US) as well as in most industrialized nations throughout the world. Approximately 800,000 people in the US are affected and in spite of a better awareness of presenting symptoms, 250,000 die prior to presentation to a hospital.4 The survival rate for US patients hospitalized with MI is approximately 90% to 95%. This represents a significant improvement in survival and is related to improvements in emergency medical response and treatment strategies.

In general, MI can occur at any age, but its incidence rises with age. The actual incidence is dependent upon predisposing risk factors for atherosclerosis, which are discussed below. Approximately 50% of all MI’s in the US occur in people younger than 65 years of age. However, in the future, as demographics shift and the mean age of the population increases, a larger percentage of patients presenting with MI will be older than 65 years.

Men are more susceptible than women, but the risk is more in female than in male after menopause.

CORONARY ARTERIES

The coronary arteries supply the capillaries of the myocardium with blood

The right coronary artery (RCA) supplies the right atrium and ventricle, the inferior portion of the left ventricle, the posterior septal wall and the SA and AV nodes

The left coronary artery (LCA) consists of two major branchiate left anterior descending (LAD) and the circumflex (LCX).

The LAD artery supplies below the anterior wall of the left ventricle, anterior ventricular septum and the apex of the left ventricle.

The LCX artery supplies blood to the lateral and posterior surfaces of the left ventricle.

CARDIAC ENZYMES

Levels of cardiac markers rise overtime. Hence, enzymes are drawn in a serial pattern usually on admission and over 6-24 hrs until 3 samples are obtained.

Enzymes commonly evaluated include CK, CKMB, LDH, TroponinT & I.

CK-MB ratio indicates the extent of damage of the cardiac muscle. The more the ratio, the more the damage of the cardiac muscle. Troponins are preferred markers of myocardial injury or they are very cardiac specific & are thought to rise before permanent injury develops.

Increased troponin concentrations should not be used by themselves to rule out a heart attack. Troponin will remain high for 1–2 weeks following MI allowing easy diagnosis if patient presents late with an old MI as other CE’s will not be raised unless reinfarction occurs.

Elevation of Cardiac Enzymes in Myocardial Infarction

Enzyme Rises in Peaks in Normalizes in Normal Value CKMB ratio

CK 12 hrs 16-30hrs 3-5 days 35-232IU/L

CKMB 4-8 hrs 24 hrs 72 hrs < 51IU/L <6%

Troponin I 3-6 hrs 20 hrs 14 days 0.0-0.4 ng/ml

Troponin T 2-4 hrs 8-12 hrs 14 days 0.0-0.1 ng/ml

LDH 12 hrs 12-24 hrs 10 days 100-190 IU/L

PATHOPHYSIOLOGY

The most common sites of MI are in the left ventricle, the chamber of heart which has the greatest work load. Tissue changes that occur in the myocardium are related to the extent to which the cells have been deprived of oxygen. Total deprivation results in an area of infarction in which the cells die and the tissue become necrotic.

Necrosis in this area is evident with in 5 to 6 hours after the occlusion. In response to this necrosis the body increases its products of leukocytes, which aid in the removal of dead cells. As collateral circulation enlarges, it brings fibroblasts, which form a connective tissue scar with in the area of infarction. Usually, the formation of fibrous scar tissue is complete with in 2 to 3 months.

Immediately surrounding the area of infarction is a less seriously damaged area of injury. It may deteriorate and thus extend the area of infarction or with adequate collateral circulation; it may regain its function with in 2 weeks.

The outer most area of damage is the zone of ischemia which borders the area of injury. The cells in this area are weakened by decreased oxygen supply, but function can return usually with in 2 to 3 weeks after the onset of occlusion.

RISK FACTORS

There are two types of risk factors for heart attack, including

Inherited factors
Acquired factors

Inherited factors

These are risk factors you are born with that cannot be changed, but can be improved with medical management and life style changes. Following are most at risk-

persons with inherited hypertension
persons with inherited low levels of HDL or high levels of LDL
persons with a family history of heart disease aging men and women
persons with diabetes mellitus [ type 1 diabetes ]
women, after the onset of menopause- generally, men are at risk, at an earlier age than women, but after the onset women are equally at risk

Acquired factors

These are risk factors that are caused by activities that we choose to include in our lives that can be managed through life style changes and clinical care. Following are most at risk-

Persons with acquired hypertension
persons with acquired low level of HDL or high level of LDL
cigarette smokers
people who are under a lot of stress
individual who lives a sedentary life
persons overweight by 30 % or more

TYPE OF MYOCARDIAL INFARCTION

1. Different degrees of damage occurs to the heart muscle-

Zone of necrosis: death to the heart muscle caused by extensive and complete oxygen deprivation that is, irreversible damage

Zone of injury: region of heart muscle surrounding the area of necrosis; inflamed and injured, but still viable if adequate oxygen can be restored.

Zone of ischemia: region of the heart muscle surrounding the area of injury, which is ischemic and viable; not endangered unless extension of the infarction occurs.

2. According to the layers of the heart muscle involved, MI can be classified as-

Transmural or Q wave infarction; area of necrosis occurs throughout the thickness of the heart muscle. Subendocardial or non transmural infarction; area of necrosis is confined to the innermost layer of the heart muscle.

3. Location of the MI is identified as location of the damaged heart muscle within the left ventricle inferior, anterior, lateral and posterior-

Left ventricle is the most common and dangerous location for MI, as it is the main pumping chamber of the heart

Right ventricular infarction commonly occurs I junction with damage to the inferior and or posterior wall of the left ventricle

4. Region of the heart muscle that becomes damaged determine by the coronary artery that becomes obstructed

Left main coronary artery

Circumflex branch

Anterior ascending branch

Great cardiac vein

Middle cardiac vein

Right cardiac vein

CLINICAL MANIFESTATIONS

1) Chest pain

not relieved by the rest over sublingual vasodilator therapy
severe steady sub sternal chest pain of a crushing and squeezing nature
may radiate to the arms, neck, jaw and shoulders
continuous more than 15 minutes
may produce anxiety and fear

2) Diaphoresis

3) Hypertension or hypotension

4) Bradycardia or tachycardia

5) Palpitation, severe anxiety, dyspnea

6) Disorientation, confusion and restlessness

7) Fainting, marked weakness

8) Nausea, vomiting, hiccoughs

9) Atypical symptoms such as epigastric pain abdominal distress, dull aching or tingling sensation, shortness of breath, extensive fatigue

DIGNOSTIC EVALUATION

1. ECG changes

Generally occur within 2 – 12 hours, but may take 72 – 96 hours.

Necrotic, injured and ischemic tissue alter ventricular depolarization and repolarization

ST segment depression and T wave inversion indicate a pattern of ischemia

ST elevation indicates an injury pattern

Anterior small           V3 – V4 leads
Anterior extensive   V2 – V5 leads
Anteroseptal            V1- V3 leads
Posterior                  V1 – V2 leads, progressive R wave and ST depression
Anterolateral          V4 – V6, I, Avl leads
Apical                       V5 – V6 leads
Inferior                     lead ii, iii and avf [ reciprocal ]

2. Elevation of serum enzymes and isoenzymes:

Enzymes are drawn in a serial pattern usually on admission and every 6 – 24 hours until 3 samples are obtained. Enzyme activity then is correlated to the extent of heart muscle damage

Enzymes commonly evaluated include are CK, LDH, CK-MB, AST, Troponin I, Troponin T. [Fig.4 ]

LDH 2 is normally greater than LDH 1 except when the heart muscle is damaged a reversal occurs

3. Other findings:

White blood cell count and sedimentation rate elevates due to inflammatory process associated with damaged heart muscle.

Radionuclide imaging allows recognition of areas of decreased perfusion

Position emission tomography determines the presence of reversible heart muscle injury and irreversible or necrotic tissue, extends to which the injured heart muscle has responded to treatment also can be determined

MANAGEMENT

Therapy is aimed at the protection of ischemic and injured heart tissue to preserve muscle function, reduce the infarct size, and prevent death. Innovative modalities provide early restoration of coronary blood flow , and the use of pharmacologic agents improve oxygen supply and demand, reduce and/or prevent disarrhythmias, and inhibit the progression of coronary artery disease.

1. Opiate analgesic therapy: Morphine is used to relieve pain, improve cardiac hemodynamics by reducing preload and after load and to relieve anxiety.

Meperidine [Demerol] is useful for pain management in those patients contraindicated to morphine or sensitivity to respiratory depression.

2. Anxiolytic agents: Benzodiazepines are used with analgesics when anxiety complicates chest pain and its relief

3. Antiplatelet agents: Aspirin interfere with the function of the enzyme cyclooxygenase and inhibits the formation of thromboxane A2. Within minutes aspirin prevents additional platelet activation and interferes with platelet adhesion and cohesion

Other antiplatelet agents are, Clopidogrel, Ticlopidine, Dipyridamole, these agents, specifically Clopidogrel may be useful for patients who have a true allergy to aspirin and some times can be used with combination with Aspirin.

4. Supplemental oxygen: Supplemental oxygen should be administered. The rationale for use is the assurance that erythrocytes will be saturated to maximum carrying capacity. Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and by other tissue may be diminished.

5. Nitrates: Intravenous Nitrates should be administered in MI, persistent ischemia, hypertension or large anterior wall MI. Nitrates are metabolized to nitric oxide in the vascular endothelium. Nitric oxide relaxes vascular smooth muscle and dilates the blood vessel lumen. Vasodilatation reduces both cardiac preload and after load, and decreases the myocardial oxygen requirements. Vasodilatation of the coronary arteries improves the blood flow through the partially obstructed vessels as well as through collateral vessels. When administered sublingually or intravenously, Nitroglycerin has a rapid onset of action.

6. Beta adrenergic blocking agents: Beta blockers are recommended within 12 hours of MI symptoms and are continued indefinitely. Beta blockers decrease the rate and force of myocardial contraction and decreases overall myocardial oxygen demand. During the acute phase of MI beta blockers may be initiated intravenously

7. Heparin: Unfractionated Heparin: intravenous unfractionated Heparin is recommended who undergo percutaneous revascularization. It is also recommended in patients who receive fibrinolytic therapy and non selective fibrinolytic agents such as urokinase, streptokinase and anistreplace. Heparin inhibits the additional formation and propagation of thrombi, effective when administered intravenous or subcutaneously.

Low-molecular-weight-Heparin: can be administered to MI clients not treated with fibrinolytic therapy

8. Fibrinolytic or Thrombolytic agents: Fibrinolytic therapy is indicated with ST segment elevation. Plasminogen activators restore coronary vessels by dissolving obstructing thrombus. The plasminogen activators have been shown to restore coronary blood flow in 50% to 80% of MI patients. The successful use of fibrinolytic agents provides a definite survival benefit that is maintained for years. Reteplase has been shown to produce slightly higher 60- and 90-minute angiographic patency rates than accelerated alteplase, while adverse-event rates were equal.

However, the better early patency rate did not translate into any survival advantage at 30 days follow-up. The most critical variable in achieving successful fibrinolysis is time from symptom onset to drug administration. A fibrinolytic is most effective when the “door-to-needle” time is 30 minutes or less.

9. Angiotensin converting enzyme inhibitors: Oral ACEI are recommended within the first 24 hours of the onset of the MI symptoms, decreases myocardial after load through vasodilatation.

10. Anti dysarrhythmic agents: Lidocaine decreases ventricular irritability, which commonly occurs post MI.

11. Calcium channel blockers: Improves the balance between the oxygen supply and demand by decreasing heart rate, blood pressure and dilating coronary vessels.

Diltiazem has been shown to decrease the incidence of reinfarction in patients with non-Q-Wave MIs.

12. Percutaneous Coronary Intervention [Fig-15]: Mechanical opening of the coronary vessel can be performed during an evolving infarction. A balloon tipped catheter is introduced through a guide wire into a coronary vessel with a non calcified atheromatous lesion. The balloon of the catheter is the inflated, causing disruption of the intima and changes in the atheroma. The result is an increase in the diameter of the lumen of the coronary vessel and improvement of blood flow below the lesion.

Percutaneous coronary intervention is an alternative therapy to fibrinolysis Restoration of coronary blood flow in a MI can be accomplished mechanically by percutaneous coronary intervention (PCI). Mechanical revascularization by PCI is used as a primary therapy as an alternative to fibrinolysis when fibrinolysis is not clearly indicated or contraindicated. PCI can successfully restore coronary blood flow in 90% to 95% of MI patients.

13. Surgical Revascularization: Emergent or urgent coronary artery bypass graft surgery is warranted in the setting of failed percutaneous intervention in patients with hemodynamic instability and coronary anatomy amenable to surgical grafting. Surgical revascularization is also indicated in the setting of mechanical complications of MI such as ventricular septal defect, free wall rupture, or acute mitral regurgitation. Restoration of coronary blood flow with emergency Coronary Artery Bypass Grafting (CABG) can limit myocardial injury and cell death if it is performed within 2 or 3 hours of symptom onset. Emergency CABG carries a higher risk of perioperative morbidity (bleeding and MI extension) and mortality than elective CABG. The risk of operative mortality during emergency CABG is increased in patients, who are in cardiogenic shock, those with previous CABG surgery, and with multi-vessel disease. On the other hand, urgent CABG confers a survival benefit in patients with recurrent ischemia post-MI whose coronary anatomy is unsuitable for complete revascularization with PCI. Elective CABG improves survival in post-MI patients who have left main artery disease, three-vessel disease, or two-vessel disease that is not amenable to PCI. The timing of elective CABG post-MI is controversial, but retrospective studies indicate that when CABG is performed as early as 3 to 7 days post-MI, operative mortality is equivalent to CABG performed on non-MI patients.

14. Cardiac Stress Testing: Cardiac stress testing post-MI has established value in risk stratification and assessment of functional capacity. Stress testing is not recommended within several days post-MI. Only sub-maximal stress tests should be performed in stable patients 4 to 7 days after MI. Exercise testing identifies patients with residual ischemia for additional efforts at revascularization. Exercise testing also provides prognostic information and acts as a guide for post-MI exercise prescription and cardiac rehabilitation.

15. Lipid Management: All post-MI patients should be on an American Heart Association Step II diet (< 200 mg cholesterol/day, < 7% of total calories from saturated fats). Post-MI patients with LDL-cholesterol levels > 100 mg/dL on a Step II diet are recommended to be on drug therapy to lower LDL-cholesterol levels < 100 mg/dL. Post-MI patients with HDL-cholesterol levels < 35 mg/dL on a Step II diet are recommended to participate in a regular exercise program and on drug therapy designed to increase HDL-cholesterol levels.4 Recent data indicate the all MI patients should be on statin therapy, regardless of lipid levels or diet

16. Long-term Medications: Most oral medications instituted in the hospital at the time of MI will be continued long-term. Therapy with aspirin and beta-blockade is continued indefinitely in all patients. ACEI is continued indefinitely in patients with congestive heart failure, left ventricular dysfunction (ejection fraction < 0.40), hypertension, or diabetes. A lipid-lowering agent, specifically a statin, in addition to dietary modification is continued indefinitely

17. Cardiac Rehabilitation: Cardiac rehabilitation provides a venue for continued education, re-enforcement of lifestyle modification, and adherence to a comprehensive prescription of therapies for recovery from MI, which includes exercise training. Participation in cardiac rehabilitation programs post-MI is associated with a decrease in subsequent cardiac morbidity and mortality. Other benefits include improvement in quality of life, functional capacity and social support. A minority of post-MI patients actually participate in formal cardiac rehabilitation programs due to either lack of structured programs, physician referrals, low patient motivation, non-compliance, or financial constraints.

NEED FOR THE STUDY

Reperfusion therapy, within which we include thrombolytic therapy and percutaneous coronary intervention (PCI), which includes angioplasty and stent placement, is the greatest advance in the treatment of acute myocardial infarction

Studies have shown that many patients with AMI who are eligible for reperfusion therapy do not receive it. Moreover, of those who do receive it, the time to administration of thrombolytic therapy, or “door-to-needle time” is often delayed, jeopardizing myocardium and leading to greater morbidity and mortality.

Clinical criteria and simple ECG parameters have limited value for the non-invasive diagnosis of myocardial reperfusion. Other methods, such as ST segment monitoring and kinetic analysis of biochemical markers, may also be value of in early identification of IRA {Infarct Related Artery}, total CK activity, CK-MB isoenzymes appear to be the most promising biochemical markers.

In addition, the thresholds suggested for the diagnosis of reperfusion were generally derived from “time-to-peak” values. This rules out early diagnosis because peak CK plasma values are reached, on averages 9 -+ 6 hours after thrombolysis.

Determination of plasma total and MB CK concentration provides accuracy superior to any other currently available method for the diagnosis of acute MI.

In addition to providing precise diagnosis of acute MI, quantitative MB CK assays can also be used to obtain an accurate estimate of infarct size. In recent years, accuracy in the diagnosis of acute MI has assumed even greater importance, since the choice and timing of a variety of diagnostic and therapeutic options following coronary care unit admission hinge on whether infarction has occurred. Furthermore, the advent of thrombolytic therapy of acute MI has emphasized the need for more sensitive biochemical markers of necrosis in the first hours. The eventual realization that the reestablishment of blood flow was the dominant mechanism for the diminution of infarct size led to a therapeutic approach dominated by thrombolysis and more literally by the use of interventions to open vessels and maintain them open.

The key observation is that benefit by the use of a drug could be demonstrated if the drug was given prior to the period of ischemia.

Nevertheless, the greatest benefit in the management of patients with myocardial infarction ha unquestionably been the reestablishment of blood flow as early as possible after occlusion

The aim of this study is to determine the reperfusion of injury exacerbated by thrombolytic drugs in Myocardial Infarction through the process of elevation of cardiac enzymes which peaks and comes to normal levels within 24 hours, preventing prolonged injury and ischemia of myocardial tissue.

However, the aim was to evaluate prospectively biochemical markers for the diagnosis of coronary patency early after IV thrombolysis for Acute Myocardial Infarction.

STATEMENT OF THE PROBLEM

“The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”.

OBJECTIVES

To evaluate the effect of thrombolytic drugs on cardiac enzymes.
To compare the effect of thrombolytic drugs and non thrombolytic drugs on cardiac enzymes
To determine the importance of thrombolytics for a patient with myocardial infarction
To suggest teaching guidelines to public regarding early seeking of medical help at the onset of chest pain.

OPERATIONAL DEFIITIONS

Effect: Result or produce a result

Thrombolytic drugs: medications used to dissolve blood clots

CPK: A cardiac isoenzyme which releases into the blood in high levels when an injury occurs to the heart. It is also known as Creatine Kinase or Creatine Phophokinase.

CK-MB: It is also a cardiac isoenzyme releases into the blood from the heart muscle during an injury of the heart

Myocardial infarction: Necrosis of a region of the myocardium caused by an interruption in the supply of blood to the heart, usually as a result of occlusion of a coronary artery.

HYPOTHESIS

“Thrombolytic agents has effect on fall in peak levels on cardiac enzymes, CK and CK-MB”

LIMITATIONS

Coronary care unit: The data of this research is applicable in the settings of coronary care unit.

Age: Clients are selected only between 35 to 65 yrs of age.

Myocardial infarction: This is also applicable to the clients who were admitted in the hospital within 6 hours of the onset of the chest pain with myocardial infarction who received Inj. Metalyse.

Acute coronary syndrome: The clients who are admitted after 6 hours of the onset of the chest pain with acute coronary syndrome are included in the control group.

METHODOLOGY:

This study was done by an experimental method of research design in the settings of Coronary Care Unit in Dubai Hospital, U.A.E. A consecutive series of patients receiving IV Metalyse [ Tenecteplase ] for MI from May 2006 to November 2006 were included in this study.

RESEARCH DESIGN:

This study uses the comparative design.

THE SETTINGS:

This study was conducted in patients irrespective of age, sex and nationality, who were admitted in Coronary Care Unit through Emergency Department in Dubai Hospital, U.A.E.

SAMPLE SIZE:

This study included 60 clients, men and women, irrespective of nationalities, between 35 years to 65 years of age. Among 60 clients 30 were taken as experimental group and another 30 considered as control group.

SAMPLING TECHNIQUE:

The samples are selected as convenient sample, into two groups, the experimental and control groups. The clients who received thrombolytic agents within 6 hours of the onset of the chest pain are selected as an experimental group, and the clients who were presented late after 6 hours of the onset of the chest pain and not received thrombolytics, are selected as control group. All patients treated had the diagnosis of myocardial infarction confirmed by subsequent elevation of both Creatine Kinase [CK] and CK-MB isoenzymes levels. IV Metalyse is administered at a dose of 6000 units to 9000 units according to the weight of the patients. Patients with acute MI who were admitted to CCU more than 6 hours of onset of pain were also included.

DATA COLLECTION PROCEDURE:

Data for the study is collected by an instrument, which consists of 22 items including sample number, age, and sex. Religion, nationality, occupation, food habits, life style onset of chest pain, date and time of admission, signs and symptoms, vital signs, type of MI, protocol of thrombolytic therapy, levels of cardiac enzymes, post thrombolytic treatment, drugs received and date of discharge.

Study reveals that, majority of the clients who had MI was from the Indian subcontinents, constituting 63.3 % and the minority constituting just 1.6 %, from Great Briton and Turkey. 3.3 % of the clients were Egyptians and Syrians. Bangladeshis comprised, 6.6 % and Pakistanis were about 21.6 %. Only 9.9 % of the clients who had MI were Dubai Nationals. Among them 46.6% of the clients were aged between 46 – 55 years and 41.6 % of the clients were between 36 – 45 years and the remaining 11.6 % of the clients are between 56 – 65 years of age.

36.2 % of the clients had acute coronary syndrome and were not given thrombolytics. Remaining of the clients was with true MI and most of them were thrombolysed. However, all clients have undergone coronary angioplasty. Out of these clients only one client had normal coronary vessels, two were with mild coronary stenosis for conservative medical treatment and 4 clients with major triple vessel block were posted for CABG. Rest of the clients was treated with Percutaneous Coronary Angioplasty to LAD [50%], RCA [21.6%] and Circumflex [13.5%].

It is also evident from the study that most of the Indians are affected with MI and the major contributing factors are smoking, stress and lack of knowledge about the disease condition.

Based on Chi-Square deviation the association between normalization of cardiac enzymes levels in the study groups are as follows-

In Experimental group, 30 clients have received Inj. Metalyse . among them except 4 clients, remaining 26 clients reports seen that cardiac enzymes are normalized within 24 hours after the admission and administration of thrombolytic agent.

In control group, 30 clients blood reports for normalization of cardiac enzymes were anlysed, where we found 27 clients reports shown the higher levels of cardiac enzymes after 24 hours of the admission.

Critical Value 14.56, P value < 0.05 and Null hypothesis rejected

Inj. Metalyse has a good effect on the cardiac muscle provided with Critical Value- 14.56, Probability Value- < 0.05, as evidenced by fall in peak levels of cardiac enzymes CK and CK-MB within 24 hours after received thrombolytic agent.

DISCUSSION

Tenecteplase [ Metalyse] is a recombinant fibrin-specific plasminogen activator. It binds to the fibrin component of the thrombus and selectively converts thrombus-bound plasminogen to plasmin, which degrades the fibrin matrix of the thrombus. Tenecteplase is cleared from the circulation by binding to specific receptors in the liver followed by catabolism to small peptides.

After single intravenous bolus injection of tenecteplase in patients with acute myocardial infarction, tenecteplase antigen exhibits biphasic elimination from plasma. There is no dose dependence of tenecteplase clearance in the therapeutic dose range.

The initial dominant half-life is 24+_5.5 [mean=/-SD] min. the terminal half-life is 129+_87 minutes, and plasma clearance is 119+_49 ml/min

The main finding of this study is the early peaking of the total CPK level and CK-MB

isoenzymes have identified with successful reperfusion after Metalyse therapy. The peak CPK levels reached in 12 hours and CK-MB levels were shifted in 6 hours. The study reveals that the cardiac enzymes levels peaked and normalized within 24 hours time in the experimental group who received Thrombolytic agents within 6 hours of the onset of the chest pain. Where as it took 3- 5 days for the enzyme levels to peak for clients in the control group, who did not receive thrombolytic agents due to late arrival to the hospital, resulting in more damage to the myocardium.

Thus, it is evident that the extent of injury to the myocardium as well as the oxygen demand is less in the experimental group of the clients.

Finally, it may be used as a surrogate end point for angiographic demonstration of

patency in future clinical studies of reperfusion therapy. Diagnostic performance improved when the analysis was restricted to patients treated >6 hours after the onset of symptoms.

CONCLUSION

Clinical studies of fibrinolytic therapy in myocardial infarction show, that early thrombolytic treatment starting within 6 hours of the onset of the chest pain, significantly decreases the risk of further damage of the myocardium and oxygen demand, by the process of fall in peak levels of cardiac enzyme levels within 24 hours.

Inj. Metalyse has early peaking of cardiac enzymes in experimental group reflect the Infarction Related Artery opened, the clot has dissolved by Inj. Metalyse which means we have good thrombolytic effect, that is why we have early peaking levels.

Early identification of patients with persistent occlusion after thrombolyis during

Acute Myocardial Infarction also is important because it can pave the way for rescue interventions such as rescue Percutaneous Transluminal Coronary Angioplasty or repeated thrombolysis.

NURSING IMPLICATIONS:

SERVICE

Determine intensity of client’s angina

Observe for signs and symptoms

Place patient in a comfortable position

Administer oxygen if required

Obtain vital signs every 15 minutes for 2 hours, every half an hour for one hour and

every hour for two hours then as required

Obtain a 12 lead ECG

Monitor for relief of pain

Monitor patient’s response to drug therapy

Institute continuous cardiac monitoring and observe for- reperfusion, arrhythmias, rhythm changes, bradycardia and tachycardia

Interpret rhythm strips

Watch for complaints of headache with use of nitrates

Watch for recurrences of pain. Reinforce the importance of notifying nursing staff whenever pain is experienced.

Administer medications to relieve patient’s anxiety as directed such as sedatives and tranquilizers

Provide complete bed rest for 24 hours

Determine level of activity that precipitated anginal pain occurs.

Identify specific activities patient may engage in that are below the level at which anginal pain occurs

Prepare for the diagnostic and treatment procedures such as coronary angiogram and PTCA [ Percutaneous Transluminal Coronary Angioplasty]

EDUCATION

Counsel on risk factors and life style changes such as-

Methods of stress reduction such as biofeedback and relaxation techniques

Low fat and low cholesterol diet

Avoid excessive caffeine intake

Do not use diet pills, nasal decongestants

Follow up visits to control diabetes and hypertension

Educate patient and family members regarding-

Prevention of recurrence of pain

Regular use of medications

Hazards of smoking

Prevention of other contributing factors

Regular follow up

Importance of dietary modifications

Avoiding activities which cause anginal pain such as sudden exertion, walking against the wind, extremes of temperature, emotionally stressful situations, refraining from engaging in physical activity for 2 hours after meals, reduce weight etc.

Appropriate use of medications

Side effects of medications

ADMINISTARTION

Lead interdisciplinary intervention programs

Education of nursing students and staff

Provide in-service nursing education

Maintenance of records and reports

Maintenance of statistics

Making of policies and procedures

Supervision and evaluation of staff performance

Recommendations for further study

A majority of post MI patients actually not participating in formal cardiac rehabilitation programs due to either lack of structured programs, physician

referrals, low patient motivation, non compliance and financial constraints.

Cardiac rehabilitation provides a venue for continued education, reinforcement

of life style modification and adherence to comprehensive prescriptions of

therapies for recovery for MI, which includes exercise training.

Participation in cardiac rehabilitation programs, post MI with a decrease in

subsequent cardiac morbidity and mortality.

Adequate education in the hospitals and work places on causative and contributing factors, preventive measures of heart attacks and re heart attacks, is necessary.

All forms of reperfusion, depending on local facilities, need to be available to patients. Protocols must be written and agreed for the strategy of reperfusion to be applied within a network. Early diagnosis of ST Elevation Myocardial Infarction is essential and is best achieved by rapid ECG recording and interpretation at first medical contact, wherever this contact takes place.

Pushpa Latha, MSN, Vinayaka Missions University, Selam, Madras, India E-Mail [email protected] Ph- 00971504277926

The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”

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