Anti-Aging Guide

peterhutch asked:

The key to preventing asthma attacks and better asthma control is to avoid your known asthma triggers. We have some basic tips on how to avoid your triggers. Keep your asthma symptoms at bay with these helpful asthma prevention techniques.

Mold Spores

Molds grow both indoors and outdoors and love damp, dark places. To control mold indoors, keep basements, kitchens, and bathrooms as clean and dry as possible. Avoid the use of humidifiers and vaporizers, which can become breeding grounds for mold. To avoid outdoor molds, stay inside in air conditioning on damp, windy days. Avoid playing or walking in fallen leaves and you may also have to avoid gardening.

Nuts also contain high levels of magnesium, which other research has suggested may protect against asthma and boost lung power.

Irritating fumes such as cigarette smoke should also be avoided. In some people with asthma, aspirin and other nonsteroidal anti-inflammatory drugs trigger attacks. Tartrazine, a yellow coloring used in some drug tablets and food, may also bring on an attack. Sulfites—commonly added to foods as a preservative—may trigger attacks after a susceptible person eats a certain food or drinks beer or red wine.

A daily diet of oranges, apples and tomatoes protected against wheezing and allergic rhinitis, as well as grapes.

If you feel even the slightest symptom, take the medication. Some asthmatics tend to do that. They cough more than once and they think they are having an attack and then they take the medicines and they prevent an attack. We are not saying you have to take the inhaler the second you cough but don’t dismiss the symptoms. Always keep your prescriptions filled at all times. The best thing you can do to prevent an attack when you are away or shopping or in a restaurant is to tell the people you are with, where you keep the inhaler in case they need to use it.

The group of children involved in the asthma intervention program avoided pets, secondhand smoke and dust mites, and were delayed the introduction to solid foods; the mothers were encouraged to breastfeed. The other group of children did not partake in the asthma intervention program.

Short-acting bronchodilator inhalers are used to quickly relieve the cough, wheeze, chest tightness, and shortness of breath caused by asthma (they dilate or widen the bronchial tubes). The most commonly prescribed short-acting bronchodilator is albuterol. However, albuterol only lasts for a few hours. If you need to use an asthma reliever more than twice a week, then your asthma is not optimally controlled. Ask your doctor about improving your asthma controller medication.

Early allergy injection treatment – Two studies in young children who became allergic to a single allergen such as house dust mites showed that allergy shots against that allergen prevented the development of allergy to other allergens. This suggests that allergy testing and injection treatment in children may be important to consider before the time when this is usually first done – i.e., under age 5 years. The cost-effectiveness of doing this is unknown at present.

J Seymour asked:

Your desire to stop stammering may be great but you might not know where to begin. Stammering self-help begins with an understanding of the condition and ways to quit your automatic responses. Your anti-stammer crusade can start with looking into stop stuttering hypnosis as a guide.

The Nature of a Stammer

Unfortunately, there is little information about the source of stammers. Your condition is relatively common whether you stammer or stutter but researchers have been unable to pinpoint a specific cause for this speech problem. This makes creating a viable treatment difficult.

We do know that the condition usually develops between three and five years and 90 percent of cases appear before the age of eight. Since some children are able to speak normally before the condition develops, many believe that there may be environmental factors that contribute to the problem.

A child may have a genetic predisposition to stammer and stress may be a factor in this condition. There is no evidence that pinpoints any specific causes and there seems to be no rhyme or reason for the occurrence. This condition is present in various cultures and among different demographics.

Stop Stammering Hypnosis

Using hypnosis to help stop stammering is a viable approach because it serves as a valuable complement to other interventions and therapies that are commonly used in the treatment of stammering. This approach uses the subconscious mind to reinforce fluency in speech while offering self-regulating techniques that you can do automatically to avoid stammering.

A stammer is diagnosed by a speech therapist who introduces interventions to treat the condition. Interventions include social and communication skills as well as assertiveness training. Other treatments include speech therapy and self-awareness. These approach vary according to your specific situation.

For example, you might be fluent when you speak with a group, when you are acting or when you are singing. This indicates that the focus of your treatment should be on assertiveness, self-awareness and social skills. Each plan of action should be catered to the individual.

Augmentation with Hypnosis

Hypnosis helps you slow down as you try to speak. Part of the problem is trying to speak as quickly as you think. When you try to speak along with your thoughts, you can easily trip over your words. The words become obstacles rather than a form of communication. You can address this and other problems in the subconscious mind.

You can find help in a self-hypnosis recording as in the one found here – Stop Stammering – by Joseph Clough. Joseph’s natural talent merges with his expertise to create a stellar composition guaranteed to get results. Another great selection found here – Stop Stuttering Hypnosis – is by renowned hypnotherapist, Duncan McColl who is well known for his legendary abilities. Other excellent options are available here – Stammering Self Help. Simply follow the links for more information.

Pushpa Latha asked:

“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, 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. 

Juliet Cohen asked:

Alzheimer’s disease is a progressive, irreversible brain disorder. Alzheimer’s disease (AD) is the most common form of dementia among older people. Alzheimer’ destroys a person’s memory and ability to learn, reason, make judgments, communicate and carry out daily activities. Genetic factors are suspected, and dominant mutations in three different genes have been identified that account for a much smaller number of cases of familial, early-onset AD. People with dementia often have trouble thinking and speaking clearly, remembering recent events, and learning new things. Over time, it becomes hard for them to handle everyday activities and take care of themselves. Age is the most important risk factor for AD; the number of people with the disease doubles every 5 years beyond age 65. Three genes have been discovered that cause early onset (familial) AD. Other genetic mutations that cause excessive accumulation of amyloid protein are associated with age-related (sporadic) AD. AD is part of an immune response that is attempting to contain the disease. The former may be more likely, since research indicates that anti-inflammatory drugs can prevent or retard AD development.

Alzheimer’s disease advances at widely different rates. Family history is another risk factor of Alzheimer’s. Several risk factor genes may interact with each other and with non-genetic factors to cause the disease. Cardiovascular Risk Factors The same factors that increase the risk for heart disease and stroke, such as high blood pressure, may also increase the risk for late-onset AD. Most people with mild forgetfulness do not have AD. In the early stage of AD, people may have trouble remembering recent events, activities, or the names of familiar people or things. Oxidative damage refers to cell damage caused by excess free radicals, which are highly reactive chemicals. Free radicals are often formed as a by-product of metabolism, or chemical processes within the cell. Excess free radicals may cause substantial neuronal damage, contributing to AD development. Type 2 Diabetes. A link between AD and type 2 diabetes, the form of diabetes in which insulin levels are high. One theory is that too much insulin in the blood promotes inflammation and oxidative damage in the brain, both of which contribute to AD development.

Symptoms of AD include memory loss, language deterioration, impaired ability to mentally manipulate visual information, poor judgment, confusion, restlessness, and mood swings. Alzheimer’s disease may also include behavioral changes, such as outbursts of violence or excessive passivity in people who have no previous history of such behavior. In the later stages, deterioration of musculature and mobility, leading to bedfastness, inability to feed oneself, and incontinence, will be seen if death from some external cause (e.g. heart attack or pneumonia) does not intervene. Moderate -As the disease progresses to the middle stage, the patient might still be able to perform tasks independently, but may need assistance with more complicated activities. Severe — As the disease progresses from the middle to late stage, the patient will undoubtedly not be able to perform even the simplest of tasks on their own and will need constant supervision. They may even lose the ability to walk or eat without assistance. They might forget to eat and starve.

Treatment Alzheimer’s Disease Tips

1. Acetylcholinesterase (AChE)-inhibitors reduce the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain (combatting the loss of ACh caused by the death of the cholinergin neurons).

2. Ginkgo for the treatment of “cognitive impairment and dementia,” a Cochrane Review concludes that “there is promising evidence of improvement in cognition and function associated with Ginkgo According to this review the two randomized controlled studies that focused on Alzheimer’s patients both showed significant improvement in these areas.

3. Tramiprosate (3APS or Alzhemed) is a GAG-mimetic molecule that is believed to act by binding to soluble amyloid beta to prevent the accumulation of the toxic plaques.

4. R-flurbiprofen (MPC-7869) is a gamma secretase modulator sometimes called a selective amyloid beta 42 lowering agent. It is believed to reduce the production of the toxic amyloid beta in favor of shorter forms of the peptide.

5. Leuprolide has also been studied for Alzheimer’s. It is hypothesized to work by reducing leutenizing hormone levels which may be causing damage in the brain as one ages.

6. Antihistamine drug Dimebon has also recently been found to show beneficial effects against Alzheimer’s disease in preliminary trials

7. Vaccines or immunotherapy for Alzheimer’s, unlike typical vaccines, would be used to treat diagnosed patients rather than for disease prevention.

8. Proposed alternative treatments for Alzheimer’s include a range of herbal compounds and dietary supplements.

9. Cognitive and behavioral interventions and rehabilitation strategies may be used as an adjunct to pharmacologic treatment, especially in the early to moderately advanced stages of disease.

10. DNA-based therapy is also Treating Alzheimer’s Disease.

Walter White asked:

Plaque Psoriasis is a chronic, non-contagious autoimmune skin disease, causing red, scaly patches due to rapid skin cell reproduction. It mainly harms elbow, knee or scalp, but can be spread to any other part. Up to 30% patients also suffer from inflammation of joints which is called as Psoriatic Arthritis. Several types of psoriatic arthritis include Symmetric arthritis, Asymmetric arthritis, Distal interphalangeal predominant, Spondylitis, Arthritis mutilans.

Though psoriasis can be genetic but it goes worse due to stress, alcohol consumption and smoking. It can occur at any age but mostly it is found in an age group of 15-20 in the beginning. But psoriatic arthritis occurs between ages of 30-50. It is found that, more than 9 million people suffer from these diseases. The psoriasis treatment takes place in three stages basically. If found in mild stage, i.e.- small areas of the body like less than 10% of the total skin surface, then topical (skin applied) creams, lotions, and sprays may be very effective and safe to use.

Occasionally, a small local injection of steroids directly into tough or resistant isolated plaque psoriasis may be helpful. For moderate to severe disease that involves much larger areas of the body (like 20% or more of the total skin surface), topical products may not be effective or practical to apply. So exposing the skin to ultraviolet (UV) radiation is done. This treatment is generally called as phototherapy. The third stage includes medication through pills or injection which is known as systemic treatment. The three basic traditional systemic medications are methotrexate, cyclosporine and retinoids.

While in Psoriatic arthritis, a localized form of psoriatic arthritis is very mild and usually will affect the two joints. A person may suffer for long time with absolutely no symptoms of disease at all. It normally causes less deformity and leads to long-term disability.

But in “Generalized” disabling psoriatic arthritis, people have 3 or more numbers of affected joints having a higher probability of joint destruction and further disability. When it is not cured by anti-inflammatory medicines, then more virile medications are needed. Some times surgery followed by rehabilitation is badly required to get well soon.

In the UK The Psoriasis and Psoriatic Arthritis Alliance (PAPAA) has funded research carried out to develop a symptom management programme called Electronic Targeted Intervention for Psoriasis) using a modified Cognitive Behavior Therapy model. This research is on psychological stress, distress and disability in patients with psoriasis. It is a condition for life time that is why called as chronic. Though there is no hundred percent guarantee regarding curability, but various treatments can help to control it. Severe psoriasis carries an increased risk of significant morbidity including skin cancers, lymphoma, liver disease, diabetes, heart disease, obesity and depression. A healthy lifestyle is basically important for people suffering from this disease. Regular exercises, healthy diet, stress reduction and a strong support network help the patients to develop mentally and physically a lot.

Juliet Cohen asked:

Alzheimer’s disease is a neurodegenerative disease. It is found in people over age 65. AD is also considered a tauopathy due to abnormal aggregation of the tau protein, a microtubule-associated protein expressed in neurons that normally acts to stabilize microtubules in the cell cytoskeleton. Alzheimer’s disease (AD) is a slowly progressive disease of the brain that is characterized by impairment of memory and eventually by disturbances in reasoning, planning, language, and perception. Alzheimer’s disease attacks the brain; it is not a normal part of aging. People with AD have a gradual memory loss and difficulties with language and emotions. The progressive loss of intellectual abilities is termed dementia. Several genetic factors have been identified that play a role with genes that are associated with Alzheimer’s Disease (AD). As the disease advances, the person may need help in all aspects of life: bathing, eating, and using the restroom. About 5-6% of the US population has AD or a related dementia.

Apolipoprotein E (ApoE) gene on chromosome 19. This is most interesting because it is both negative and positive. The e4-type is linked to significantly higher risk for AD, the e2-type is linked to significant protection from AD symptoms. Memory loss, especially of recent events and newly acquired information, is perhaps the most noticeable trait of AD. Alzheimer’s disease ranks fourth in the cause of death among adults. About 100,000 people die per year as a result of AD. It is estimated that by 2050, 14 million people in the US will suffer from AD. There are now more than 5 million people in the United States living with Alzheimer’s. Every 72 seconds, someone develops Alzheimer’s. Some changes in memory are a normal consequence of aging, but when changes in memory, spatial navigation, and concentration are affecting activities of daily living, then you may be experiencing some type of dementia. AD is just one form of dementia and dementia is just one reason for changes in memory.

There are treatments that can help with memory impairment and improve mental functioning and to help stabilize symptoms. Donepezil also appears to delay the onset of Alzheimer’s for about a year in people who have mild cognitive impairment (MCI). AChE-inhibitors reduce the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain. Proposed alternative treatments for Alzheimer’s include a range of herbal compounds and dietary supplements. Cognitive and behavioral interventions and rehabilitation strategies may be used as an adjunct to pharmacological treatment. Vitamin E (an antioxidant) and aspirin (an anti-inflammatory) are being considered as treatments. Risk factors are characteristics of the person, their lifestyle and environment that contribute to the likelihood of getting a disease.

Alzheimer’s Diseases Treatment Tips

1. Donepezil also appears to delay the onset of Alzheimer’s for about a year in people who have mild cognitive impairment (MCI).

2. AChE-inhibitors reduce the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain.

3. Cognitive and behavioral interventions and rehabilitation strategies may be used as an adjunct to pharmacological treatment.

4. Vitamin E (an antioxidant) and aspirin (an anti-inflammatory) are being considered as treatments.

Juliet Cohen asked:

Alexander disease is a set of genetic conditions called the leukodystrophies that affect development of the myelin sheath, the fatty covering, which acts as an insulator-on nerve fibers in the brain. Alexander disease is considered an autosomal dominant disorder, which means one copy of the altered gene in each cell is sufficient to cause the disease. Almost all cases result from new mutations in the gene and occur in people with no history of the disorder in their family. Children with hydrocephalus caused by Alexander disease usually have increased intracranial pressure and a more rapid progression of the disease. Generally, the earlier the age of onset of Alexander disease, the more severe and rapid the course. Therefore, unaffected parents of a child with ALX are at a low risk to have another affected child.

Alexander disease, which affects mostly males, usually begins at about 6 months of age. Signs and symptoms of the infantile form typically include an enlarged brain and head, seizures, stiffness in the arms and legs, mental retardation, and delayed physical development. Less frequently, onset occurs later in childhood (the juvenile form) or adulthood. Common problems in juvenile and adult forms of Alexander disease include speech abnormalities, swallowing difficulties, and poor coordination. Infantile Alexander Disease leads to symptoms in the first two years of life; while some children die in the first year of life, a larger number live to be 5-10 years old. Alexander disease belongs to leukodystrophies, a group of diseases which affect growth or development of the myelin sheath. In Alexander disease, the growth of the white matter of the brain, or myelin sheath, is affected.

Cerebellar disease also occurs in this disorder. In most cases, Alexander disease appears to occur randomly for unknown reasons, with no family history of the disease. In an extremely small number of cases, it is thought that the disorder may have affected more than one family member. Affected children survive a few weeks to several years. The juvenile form usually presents between four and ten years of age, occasionally in the mid-teens. Survival is variable, ranging from the early teens to the 20s-30s. Prior to the identification of the genetic features, other names were used to describe the clinical features and pathology of Alexander disease, such as hyaline panneuropathy and dysmyelinogenic leukodystrophy. These terms are no longer used.

Because the genetic defect in Alexander disease is known, genetic testing on a blood sample can be used to diagnose most cases of Alexander disease. There is no medication for Alexander disease. Treatment, which is symptomatic and supportive, primarily consists of attention to general care and nutritional needs, antibiotic therapy for infections, and management of associated complications such as anti-epileptic drug therapy for seizures. A suggestive diagnosis can also be made from the clinical symptoms, including enlarged head size, combined with radiological studies and negative tests for other leukodystrophies. Surgical interventions, including placement of a feeding tube and/or shunting for hydrocephalus, may also be required. Orthopedic surgery for scoliosis has been reported in a case of Alexander disease.

Peter Harris asked:

People of all ages suffer from shoulder pain. The causes are many and can range from an unknown onset to a traumatic event. Many people develop shoulder pain from performing repetitive type activities for prolonged times. Others will experience pain in the shoulder following a fall onto the shoulder or on the outstretched arm. Sometimes the reason for pain is not as obvious. I see many cases where a person cannot identify what caused the pain in the shoulder. Often times this pain for unknown reasons can occur when someone bumps their shoulder against the door jam in the middle of the night when going to the bathroom. This rather benign action sets off a chemical process in the shoulder that will build up over several days. Eventually this will cause pain in the shoulder. Since the “injury” occurred several days earlier the person cannot recall any event that started the process. Regardless of the cause of the pain in the shoulder the treatment is often similar from case to case.

Treatment of the shoulder can encompass several different areas. Conservative measures include medication (anti-inflammatories, pain medications), rest, cortisone injections, and/or physical therapy. All of these methods can be effective in helping relieve a painful shoulder especially when they are performed in combination with each other.

Often times when you present to your medical doctor with complaints of shoulder pain they will prescribe some medication as described above. Rest will also be advocated although this is not always easy for people to follow depending on their activity levels or their occupations. Injections for the painful shoulder are sometimes given right away depending on your medical doctor’s philosophy. Some MD’s would rather you attend physical therapy before considering injecting the painful shoulder. Injections are not the end all beat all and they do not offer relief to all patients that receive them. Often times a well rounded physical therapy program can alleviate shoulder pain and you won’t have to consider having an injection.

Physical therapy treatment can consist of the following interventions:

Therapeutic exercises – this will consist of range of motion, conditioning, and strengthening exercises. The goal here is to maximize and restore any loss of range of motion, improve the overall endurance of the shoulder blade and shoulder muscles and to improve the strength of these same muscles. The muscles surrounding the shoulder blade must be conditioned and strengthened just as the main shoulder muscles would be because the shoulder blade muscles have to work in conjunction with the shoulder muscles in order to restore normal motion and to prevent recurrence of pain.

Manual therapy – this will consist of hands on treatment that the physical therapist would perform on you. This might consist of joint mobilization (i.e. techniques designed to improve joint motion and relieve pain), or soft tissue massage (i.e. techniques designed to improve muscle and connective tissue flexibility and to relieve pain).

Modalities – this consists of machines that the physical therapist may apply to your painful shoulder to assist in pain relief and healing along with the other treatments mentioned above. Some of these machines are ultrasound, electrical stimulation, TENS, or iontophoresis.

All of these interventions can be used in the treatment of a painful shoulder. It is common in clinical practice to use a combination of these interventions. It has been my experience in treating hundreds of shoulder patients over the years that therapeutic exercise is an absolute in the treatment of the painful shoulder. Well rounded exercises that target the shoulder blade and shoulder muscles are the mainstay of any good physical therapy regimen for the treatment of shoulder pain.

SURESH U VATAKETHIL asked:

Heart Disease in Women: Women and Heart Disease

The risk of heart disease in women increases with age. Heart disease is the leading cause of death in women over 40 years old, especially after menopause. Menopause is a normal stage in a woman’s life; it comprises any of the changes a woman experiences either before or after she stops menstruating. As menopause nears, the ovaries gradually produce less estrogen (a female hormone), causing changes in the menstrual cycle and other physical changes. Every year, more than 500,000 U.S. women die of heart disease. This translates to approximately one death every minute.

Heart disease in women is preventable as per the latest guidelines from the American Heart Association. Reason to understand the cause of heart disease in women could not be stressed enough. Heart disease kills 1 in 3 American women, but it doesn’t have to be that way. 60% of U.S. women now know that heart disease is their No. 1 health threat.

Prevention is better than cure. Heart disease in women is preventable with a disease prevention strategy. The knowledge of heart disease occurs to a person when it is too late.

Here are some guide lines for a simple prevention plan for heart disease in women:

Women aged 20 and older should see a doctor to find out their heart disease risk.

Chnaces are that one in 10 women will learn that there is no real risk of heart disease. These women should continue their heart-healthy lifestyles.

Women who are at risk of heart disease, should think of preventing heart disease and stroke. These women must stop smoking, adopt a heart-healthy diet, get at least 30 minutes a day of exercise, and watch their weight. And under a medical supervision, some of these women may need blood pressure medications, cholesterol-lowering therapy, or regular aspirin.

Women who already have some existing condition making it more likely to suffer from heart disease or stroke, should additionaly to taking the measures advised above, go after some aggressive medical treatments or rehab.

Depression is very common in women with heart disease. All women with heart disease should be evaluated for depression.

Women should exercise a minimum of 30 minutes a day, and for those women who want to lose weight, 60 to 90 minutes of daily exercise is recommended.

The risk of heart disease in women is increased by activities such as, diabetes and obesity, smoking, high blood pressure, high cholesterol level and inactivity.

Heart disease in women though is on the increase, can be altered through some variations in life style. Clinical experience suggest the following general guidelines for preventing heart disease:

- Maintain blood pressure of less than 140/90 mmHg (120/80 is optimal)

- Maintain blood glucose of 80-120 mg/dL (less than 100 is optimal)

- Maintain total cholesterol of less than 200 mg/dL (and not less than 160) and LDL (low-density lipoprotein) of less than 130 mg/dL (less than 100 is optimal)

- Exercise regularly (30-60 minutes of aerobic exercise three to five times weekly is optimal).

However, there are certain factors that cannot be influenced to prevent heart disease in women. Factors such as age, family history and menopause cannot be controlled or prevented.

But there are other factors that could be influenced, through exercising the right option. This could prevent death from heart disease in women. As indicated earlier, introducing some changes to our life style, and carrying a positive out look towards the meaning and purpose of life, women can fight this terrible disease and live more healthier and meaningful lives. Meditation, yoga, prayers and religous activities can have huge impacts on our life and provide the necessary inner strength to cope with the pain and pressure of heart disease.

Diabetes and high cholesterol, homocysteine, and blood pressure can be improved through diet, exercise, medication, and supplements. High C-reactive protein (CRP), an inflammatory biomarker, may help to identify those who would benefit from anti-inflammatory intervention. Diet, lifestyle changes, positive adaptation to stress, and supplements can assist in weight loss and help decrease stress. Quitting smoking will also reduce risk of heart disease in women. The scientific data strongly suggest that modification of these multiple risk factors can help to lessen heart disease risk and thus total mortality in women.