by Wootang01

Treating Hypertension

In most cases, high blood pressure is usually present long before its complications developed and shows some of its symptoms. In order to treat high blood pressure it is important to detect it in its earliest stage before it can do severe damages to the critical organs in the body. In addition, the increases in public awareness as well as the promotion of some screening programs that are aimed towards the detection of hypertension in its earliest stage are some of the keys that lead to successful treatment of hypertension.

The essence of treating high blood pressure in its earliest stage can decrease significantly the risk of stroke, heart attack and even kidney failure. Moreover, life style changes in patients which are pre-hypertensive are advised since it is not yet well proven that treatment by means of medication are beneficial for patients with pre-hypertension.

In treating high blood pressure, it is important to note the blood pressure reading. For blood pressure that is consistently higher than 140/90 mm Hg, the treatments consist of lifestyle modifications coupled with an appropriate medication. However, for cases wherein the diastolic pressure remains at a borderline level which is usually under 90 mm HG and steadily remains above 85 mm Hg, a more aggressive treatment may be advised.

Furthermore, there are instances wherein the borderline diastolic pressures are associated with end-organ damage, this kind of problem is usually associated with systolic hypertension as well as some factors that may have increase the risk of cardiovascular diseases especially on patients that are 65 years and over who are smoking and has hyperlipemia and diabetes.

Regardless of the stage of hypertension, any patient can start with any one of the several classes of medication except of course the alpha-blocker medications. The reason for this is that alpha-blockers are usually used only in combination with another anti-hypertensive medication and only in specific medical situations.

There are some particular situations wherein certain classes of anti-hypertensive drugs are preferable compared to others as the first choice of drugs. An example of which is the angiotensin converting enzyme (ACE) which are inhibitors or the angiotensin receptor blocking (ARB) drugs which are some of the first prescribed medicines especially for patients with heart failure, chronic kidney failure, for diabetics as well as for patients with weak heart muscles.

Moreover, some patients with hypertension sometimes have coexisting medical conditions in which case a particular class of anti-hypertensive medication or a combination of which may be chosen as the initial approach in treating hypertension. The rationale behind this is to control the hypertension at the same time curing the coexisting medical condition.

A British man is preparing to leave the hospital after pioneering surgery to install an artificial heart implant. The implant is powered by a portable device and is designed to keep him alive while he waits for a heart transplant. It looks like a casual family stroll.

But Matthew Green is a walking miracle. His heart has been removed. Green is kept alive by a device called a Total Artificial Heart powered by a magnetic charger kept in his shoulder bag. The 40-year-old was suffering from end-stage biventricular heart failure. Neither side of his heart worked as it should.

Doctors at Cambridge’s Papworth Hospital feared he’d die while waiting for a donor heart to become available for transplant, and decided an artificial heart was his best option. Surgeons led by Dr Steven Tsui operated on him in June. [Dr. Steven Tsui, Consultant Cardiothoracic Surgeon and Director]: “We removed the patient’s diseased native heart, including both of the failed ventricles, as well as all the heart valves. And then we put in the new machine and the insertion is stitching the machine in, in a way very similar to a heart transplant.

The operation itself went very smoothly. It took us about six hours to do the operation.” Mechanical hearts have been transplanted before, but have usually only replaced parts of the organ. The device works by replacing both failing ventricles and the heart …

by Wootang01

Cure your High Blood Pressure forever with Ayurveda

Approximately, 8 to 12 months continuous treatment with our medicine will maintain blood pressure within normal limits.

However, it is advisable to check blood pressure regularly.

It increases the efficiency of the heart by lowering the high blood pressure and by keeping it within normal limits.
It reduces the risk of hemorrhage from a vessel by increasing the elasticity of blood vessels.
It reduces risk of stroke by ensuring proper blood circulation.
It cures Insomnia.
It also eliminates possibilities ofHeart attack & Kidney failure by maintaining the blood pressure within normal limits.

Allopathic medicines should not be stopped completely at the time of starting this medicine.

After 15-21 days of the simultaneous treatment with our medicine, dose of allopathic medicine should be reduced gradually and should be stopped completely within next 60 to 90 days.

One Capsule per day.

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High blood pressure (HBP) is a serious condition that can lead to coronary heart disease, heart failure, stroke, kidney failure, and other health problems.

“Blood pressure” is the force of blood pushing against the walls of the arteries as the heart pumps out blood. If this pressure rises and stays high over time, it can damage the body in many ways.

About 1 in 3 adults in the United States has HBP. HBP itself usually has no symptoms. You can have it for years without knowing it. During this time, though, it can damage the heart, blood vessels, kidneys, and other parts of your body.

This is why knowing your blood pressure numbers is important, even when you’re feeling fine. If your blood pressure is normal, you can work with your health care team to keep it that way. If your blood pressure is too high, you need treatment to prevent damage to your body’s organs.

Blood pressure numbers include systolic (sis-TOL-ik) and diastolic (di-a-STOL-ik) pressures. Systolic blood pressure is the pressure when the heart beats while pumping blood. Diastolic blood pressure is the pressure when the heart is at rest between beats.

You will most often see blood pressure numbers written with the systolic number above or before the diastolic, such as 120/80 mmHg. (The mmHg is millimeters of mercury—the units used to measure blood pressure.)

The table below shows normal numbers for adults. It also shows which numbers put you at greater risk for health problems. Blood pressure tends to go up and down, even in people who have normal blood pressure. If your numbers stay above normal most of the time, you’re at risk.

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Normal                         Less than 120                 And Less than 80

Prehypertension            120–139                        Or 80–89

High blood pressure

Stage 1                          140–159                       Or 90–99

Stage 2                       160 or higher                   Or 100 or higher

The ranges in the table apply to most adults (aged 18 and older) who don’t have short-term serious illnesses.

All levels above 120/80 mmHg raise your risk, and the risk grows as blood pressure levels rise. “Prehypertension” means you’re likely to end up with HBP, unless you take steps to prevent it.

by Christiana Care

What are the symptoms of congestive heart failure CHF ?

The term congestive is used because lung congestion causes some of the main symptoms of heart failure. Congestive heart failure or CHF is a condition in which the heart’s function as a pump to deliver oxygen rich blood to the body is inadequate to meet the body’s needs. Generally classified as systolic or diastolic heart failure and becomes progressively more common with increasing age.

Symptoms of heart failure include fatigue, abdomen, leg and ankle swelling, shortness of breath, sleeplessness, increased urination, nausea, abdominal pain, and decreased appetite, which occurs with exertion as the disease progresses. Other symptoms include a wheezing or hacking cough and shortness of breath during sleep, called orthopnea. Congestive heart failure information including; causes, types, symptoms, and treatment.

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The heart can contract normally but is stiff, or less compliant, when it is relaxing and filling with blood. Doctors can usually make a diagnosis of congestive heart failure based upon a physical exam and the symptoms alone.

However, you may not have any symptoms of heart failure, or the symptoms may be mild to severe. In the early stages of congestive heart failure, a person may have no symptoms. Symptoms are often gradual in their development, as the body has great capacity to compensate for early changes in many diseases. Some patients with heart failure have no symptoms.

When symptoms do develop, they may include shortness of breath on exertion and fatigue. And over time, the symptoms worsen and quality of life suffers.

Medications can improve the signs and symptoms of heart failure and lead to improved survival. Increasing shortness of breath can be tempered by the medications.  Always carry a list of medications with you wherever you go.

Read More detailed information about the symptoms, causes, and treatments of Congestive Heart Failure.

Heart disease affects more than 20 million Americans. Let’s explore the various forms that heart disease can take.Watch More Health Videos at Health Guru: www.healthguru.com

by Tuftronic10000

Heart Attack – 3 Signs

Coronary heart disease, in its various forms, is the number one killer in the United States. One way that it kills is heart attack. Most of us have seen a movie or television show in which someone has a dramatic heart attack. The actor clasps the chest, and falls to the floor in pain. The message is clear: he or she had a heart attack. Such a theatrical show of heart attack is not always present in real life, however. According to the American Heart Association, most heart attacks start slowly. If you know the signs, you can get help before they reach the dramatic point.

What Are 3 Signs of a Heart Attack That You Should Know?

Not everyone who has a heart attack will experience the same symptoms. It has been learned that men and women can have very different signs. There is enough similarity, however, that anyone, male or female, who has one of the basic three signs of a heart attack, should seek medical help immediately.

What are the three signs of a heart attack that should make you call for help?

1. Chest Discomfort: In most cases, a heart attack involves pain or some form of discomfort in the center of your chest. The feeling of distress usually lasts more than 2 or 3 minutes. It may stop temporarily, and then return as before. Heart attack discomfort can be experienced in various ways. It may be pressure that makes you uncomfortable. You may feel as though someone is squeezing your chest inside. Some patients say that it feels like the chest is too full, while others simply say it is pain.

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2. Other Discomfort: In some heart attacks, the chest discomfort is accompanied by similar feelings in one or both arms. There may be pain in the back or stomach. Pain may also extend to the neck or jaw. The discomfort of heart attack is usually limited to the upper body.

3. Breathing Trouble: A heart attack victim is likely to have trouble breathing. This sign may be present whether or not there is chest discomfort.

Any of those three signs of heart attack should send you to a doctor. It may not be heart attack, but you should have it checked immediately.

Additional signs of heart attack might include lightheadedness, nausea, or a cold sweat.

First 5 Minutes of a Heart Attack

Time is of the essence in a heart attack! It is important to take action quickly if you are to save the person’s life. If that person is you, seek medical help immediately.

Some people decide unwisely to wait until they are sure they are having a heart attack. Often, they wait too long before getting help.

Call 911, or your country’s emergency number, within the first 5 minutes of heart attack symptoms! Do not wait longer than 5 minutes! If you cannot get emergency services within 5 minutes, have someone drive you to the hospital’s emergency room as quickly as possible.

It is important to get medical help quickly. Normally, 911 is the best way to get rapid life-saving care. Ambulance staff can take action the moment they arrive. They can take action to keep your heart beating – and can often revive you if your heart has stopped. Finally, those who arrive at the hospital by ambulance usually receive faster treatment for heart attack than those who arrive by car – as much as an hour faster!

No Embarrassment

What are 3 signs of a heart attack? Those given above.

What is 1 sign that you may be acting unwisely? Waiting.

Doctors stress that there is no embarrassment in seeking medical help for a heart attack and learning that it was not that at all. Doctors and nurses would much rather you acted quickly on a false alarm than that you waited when the heart attack was real.

Learn the three signs of a heart attack – especially if you have any heart disease or risks for such. If you experience any of them, seek help.

Disclaimer: The author is not a physician, and shares this research for educational purposes only. Please ask your physician for more information on heart attack.

This two minute film lets you experience what it’s like to have a heart attack first hand. Take the time to watch it then you’ll be prepared if and when it happens for real. This is two minutes which could save your life. Or the life of someone you love. Find out more at: www.bhf.org.uk
Video Rating: 4 / 5

Find More Heart Attack Articles

by Wootang01

Blood Pressure Readings…Safe and Natural Control

Your blood pressure is one of the principal vital signs. For those of you being monitored, diastolic blood pressure, represented by the bottom number in a blood pressure reading, is when your heart is resting. Most doctors agree that in adults the normal blood pressure range should be 120 over 80 (120/80 mmHg). The higher reading 120 or systolic pressure, is the force of the blood against the artery walls as your heart beats. Depending on your physical condition and life choices, you may suffer from either high or low blood pressure. As defined in Wikipedia, blood pressure (BP) is the pressure (force per unit area) exerted by circulating blood on the walls of blood vessels. The pressure of the circulating blood decreases as it moves away from the heart through arteries and capillaries, and toward the heart through veins. The name given to high and low blood pressure is Hypertension and Hypotension, respectively.

Hypertension, perhaps the most well known of the two, comes in three stages according to WebMD.

“Prehypertension” is systolic pressure of 120-139 or diastolic pressure of 80-89 mmHg

Stage 1 Hypertension is blood pressure greater than systolic pressure of 140-159 or diastolic pressure of 90-99 mmHg or greater.

Stage 2 Hypertension is systolic pressure of 160 or greater or diastolic pressure of 100 or greater.

If you are looking at this or any other literature  for help, concerning whether or not you have high blood pressure, you are terribly misguided. Only a health care professional can diagnose hypertension. Although high blood pressure in and of itself, doesn’t show symptoms that can be felt, if extremely high it can lead to migraine headaches, chest pain, and even heart failure. If you have close relatives or you fall into a risk factor, you should always make sure you are checked out on a regular basis.

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Cause, what cause? While a variety of conditions arise because of high blood pressure, for the most part, the cause of hypertension remains unclear. What we do know is that there are risk factor groups associated  with these conditions such as, overweight, poor diet, insomnia, older age, and of course getting little or no exercise.

There are many serious and potentially serious health problems that are associated with high blood pressure. The most common are:

Atherosclerosis: a disease of the arteries caused by a buildup of plaque, or fatty material, on the inside walls of the blood vessels. Hypertension contributes to this buildup by putting added stress and force on the artery walls.

Heart Disease: heart failure (the heart can’t adequately pump blood), ischemic heart disease (the heart tissue doesn’t get enough blood), and hypertensive hypertrophic cardiomyopathy (enlarged heart) are all associated with high blood pressure.

Kidney Disease: Hypertension can damage the blood vessels and filters in the kidneys, so that the kidneys cannot excrete waste properly.

Stroke: Hypertension can lead to stroke, by either contributing to the process of atherosclerosis (which can lead to blockages and/or clots), or by weakening the blood vessel wall and causing it to rupture.

Eye Disease: Hypertension can damage the very small blood vessels in the retina.

You can beat high blood pressure and reclaim your life with a totally relaxing and enjoyable process that takes just 15 minutes a day. My research brought me to an online solution that professes to safely lower your blood pressure, without the use of drugs. If you believe as I do that the pharmaceutical companies have gone too far, than this just might be what you’re looking for.

Don’t take my word for it because it was featured in the American Journal of Hypertension, June 2003.
Doctors Prove 82% Of Even Resistant Hypertensives Can Achieve
Lower Blood Pressure Through A Surprising New Discovery  Hypertensives are people who were previously resistant to other forms of treatment. Does that sound familiar? Than you should look into this amazing treatment. If you can breathe, you can perform this exercise. You can control your blood pressure. Obviously, I can’t get into it in great detail, but I can say that this method was developed by medical doctors and has even won FDA approval. Please see for yourself at:
My RecomMANNdations

You can find other Natural Cures like; ending insomnia, help with constipation, and hemorrhoids, and much more.

by james_gordon_los_angeles

Primary Cause of Demise in US

Potassium diet plan is crucial such as fruits, greens and essential fatty acids mainly because they can wipe out the ingestion of sucrose.

In diets for substantial blood stress, the crucial to a balanced ingesting method is to try to eat foods that are reduced in sodium. A large sodium intake along with reduced amounts of potassium in the human body results in higher fluid volume and speedy dysfunction of the mechanisms of BP regulation. Primarily, a superior-potassium minimal sodium diet program is pretty efficient. For example, during the onset of psychological anguish or stress, diet program minimizes the results of constriction of blood vessels of adrenaline.

The American Heart Association suggests restricting sodium consumption to a lot less than two.four grams per day. Next the diets for higher blood strain is quite significant, it can conserve a lot of people today from dying.

Heart ailment is the major bring about of dying in the United States, killing an individual particular person every single 34 seconds. The phrase heart disorder encompasses additional than just one situation. It encompasses eight different circumstances affecting the heart, all of which can be fatal.

People 8 problems are coronary heart disorder, cardiomyopathy, cardiovascular disease, ischaemic heart illness, heart failure, hypertensive heart disease, inflammatory heart sickness and valvular heart disorder.

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Coronary heart disorder (CHD) is the failure of the coronary circulation to deliver adequate blood and oxygen to the cardiac muscle. This is the primary induce of dying for the two adult males and ladies in the United States. It is brought about by the shrinking of the compact blood vessels that provide blood and oxygen to the heart. This normally requires place when plague and fats construct up on the artery walls, in the end narrowing them. Sure aspects that arrive into play for a person to experience from CHD are age, diabetes, large blood pressure, lousy cholesterol, being overweight, smoking, absence of physical exercise and even menopause. Solutions for clients with CHD include things like a coronary artery bypass surgery, exercising and dieting, quitting smoking cigarettes and/or minimally invasive heart surgery.

Cardiomyopathy literally usually means heart muscle sickness. Patients that endure from cardiomyopathy are at danger for arrhythmia or sudden cardiac dying mainly because cardiomyopathy is the deterioration of the true heart and its capabilities. Cure for this problem incorporates a pacemaker, ventricular support devices, defibrillators and medication.

Cardiovascular disorder includes the heart or blood vessels and is taken care of by cardiologists, neurologists and thoracic surgeons. This sickness was the foremost trigger of dying in the United States and Europe till 2005. This ailment has to be prevented setting up in childhood with proper ingesting behavior and exercise. Avoiding using tobacco also allows to avert cardiovascular disorder.

Ischaemic heart disease is the decreased movement of blood supply to the organs due to coronary artery disease. It is normally diagnosed in persons that smoke, are older in age, or are diabetic.

Heart failure is the end result of the heart not remaining ready to pump enough blood into itself or during the rest of the physique. Most sufferers who endure from heart failure will have shortness of breath when basically strolling from position to stage. This is due to the failure of the left ventricle which brings about obstruction of the pulmonary capillaries.

Hypertensive heart disease incorporates a quantity of hypertensive problems that affects the heart.

On February 13, 2009 Pearl was diagnosed with Dilated Cardiomyopathy. She was suffering from congestive heart failure and doctors began to work to shrink her enlarged heart and improve her heart function. Medication helped Pearl’s heart tremendously, However… On October 26, 2009 Pearl had an ultrasound to examine a hard spot found on her right side. The ultrasound showed several cysts inside her kidneys, and the radiologist diagnosed her with Polycystic Kidney Disease. Over the next week, Pearl became very restless, started running a fever, and her abdomen began to swell. On November 5, 2009 her abdomen had swollen into her chest and back area. She had an ultrasound that determined she was actually suffering from bi-lateral kidney cancer, and not Polycystic Kidney Disease. We were again brought to St. Louis Children’s Hospital by ambulance. Pearl began her fight against kidney cancer with weekly chemotherapy. On February 1st, 2010 surgeons removed her right kidney, 1/3 of her left kidney, and a portion of her liver. Pearl is now in end stage renal disease and requires dialysis at home 12 hours a day. She will have to have her other kidney removed soon so that the cancer doesn’t return. She will then be on dialysis until she receives a kidney transplant which she is not eligible for until Spring of 2012. Pearl doesn’t see herself as sick and often tells her parents how sad she is that the kids in the hospital are sick. She loves Dora, playing on the computer and feeding …
Video Rating: 5 / 5

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by anetz

Hypertension a disease that kills

Hypertension is a disease of diverse causes. And which is manifested by the sustained increase in blood pressure, or in systole and diastole in both.

The increase in blood pressure (hypertension) is a major cause, but more susceptible to treatment, disease, and is divided into primary and secondary schools. In the general population, blood pressure is a continuous variable and its increase is associated with an increased risk of disease. Hypertension can be arbitrarily defined as a sustained diastolic pressure greater than 90 mmHg. However, there is no risk of a disease in which blood pressure is a pathogenic factor.

Primary hypertension (essential) is the elevation of blood pressure with age, but without apparent cause. Represents over 90% of cases and usually appears after age 40 The phenotype of high blood pressure in hypertension is due to an interaction between genetic predisposition, obesity, alcohol consumption, physical activity and other factors not yet identified .

Secondary hypertension, which represents about 10% of cases, is due to an identifiable cause, the most frequent renovascular disease, which raises blood pressure by activating the renin-angiotensin-aldosterone. Depending on their clinical course, both the primary and secondary hypertension can be classified into two types. In benign hypertension, there is a stable elevation of blood pressure for many years, whereas hypertension accelerated the elevation of blood pressure is intense and worsens in a short time.

Blood pressure can be raised by increasing the volume of cardiac or peripheral vascular resistance. The first rises with increasing blood volume or contractility and heart rate, the second can be enhanced by humoral factors, neural and self.

According to the degree of damage produced organic, hypertension can be found in different stages:

: No functional changes.

The patient shows one of the following signs, even when you are asymptomatic.

a) left ventricular hypertrophy (palpation, chest radiograph, ECG, echocardiogram).
b) Angiotonía in retinal arteries.
c) Proteinuria and / or slight elevation of creatinine (up to 2 mg / d).
d) arterial atheroma plaque (radiography, ultrasonography) in carotid arteries, aorta, iliac and femoral.

symptomatic manifestations of organic injury:

a) Angina pectoris, myocardial infarction or heart failure.
b) transient cerebral ischemia, cerebral thrombosis and hypertensive encephalopathy.
c) Exudates and retinal hemorrhages, papilledema.
d) Chronic renal insufficiency.
e) aortic aneurysm or atherosclerosis obliterans of lower limbs.

Hypertension in benign vascular changes occur gradually in response to stable and sustained hypertension. These degenerative changes of the walls of small vessels such as arterioles reduces the effective light with. consequent tissue ischemia, and increased vascular fragility in the brain, with bleeding risk.

In malignant hypertension there is a destruction of the walls of small vessels

When blood pressure rises so much sudden acute destructive changes occur in the walls of small blood vessels, along with remedial proliferative responses in
walls of small arteries. These alterations produced by lack of blood flow to small vessels, with formation of multiple foci of necrosis, eg in renal glomeruli.

High blood pressure affects mainly the heart, brain, kidneys and aorta

The pathological consequences of hypertension are observed mainly in four tissues:
• Heart. With increasing pressure, left ventricular myocardial hypertrophy. Since hypertension is often associated with a greater intensity of atherosclerosis, the coronary flow may be insufficient, and produced a
ischemic heart disease. The left ventricular failure is a normal consequence of hypertensive heart disease.
• Brain. Hypertensive patients are especially prone to intracerebral hemorrhage from ruptured intracerebral blood vessels. The lesion of small vessels of the cerebral hemispheres microinfartos occurs as small areas of brain destruction filled with fluid ( “gaps hypertensive).
• Kidney. The progressive arteriolosclerosis produces ischemia of the nephron, which ends up destroying the glomeruli, and atrophy of the tubular system. The disease progresses slowly, as the injured nephron at a time. When the number of functional nephron by ischemia is not high enough, the patient developed a chronic renal failure slowly

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progressive. If hypertension has produced significant ischemia of the nephron, the kidney is said to have suffered a mild hypertensive nefrosclerosis. This is a major cause of kidney failure
Chronic middle and advanced age.
• Aorta. Hypertension predisposes to the development of large abdominal aortic aneurysms and dissections of the mean.

Secondary hypertension is less than 10% of cases

In a minority of cases it is considered that there is any structural alteration responsible for the development of systemic hypertension. For example, stenosis
of the renal artery (usually at its root) may cause atherosclerosis by hypertension, with possible surgical treatment. Hypertension is associated with elevated levels of renin and angiotensin II in the circulation from the ischemic kidney, and can be cured in early stages through
removal of the kidney affection. Hypertension is also a symptom of diffuse nephropathies such as glomerulonephritis and pyelonephritis. Hypertension is transient in the initial acute phase of glomerular diseases (p, ej.,
acute nephritic syndrome), but standing diffuse chronic nephropathies.
Pheochromocytoma, an adrenaline-secreting tumor that arises normally noradrenaline in the adrenal medulla, produces a hypertension that
initially paroxysmal.

The aortic coarctation is a congenital malformation increased peripheral resistance due to a structural stenosis of the aorta. In these cases, systemic hypertension is not really because it only affects the arterial system ahead of the coarctation, usually to the arms, head and neck.

Hypertension is a symptom of diseases of the adrenal cortex that are associated with excessive production of glucocorticoids and mineralocorticoids (Cushing’s syndrome and Conn síndromede).

It is also a symptom of preeclampsia, and may be associated with endocrinopathies such as thyrotoxicosis, acromegaly, and sometimes hypothyroidism, or due to a neurogenic causes such as intracranial hypertension.

a) In patients with hypertension grade I or II, we recommend starting treatment with a single drug. If the patient has hypertension hyperkinetic syndrome, the best option is a beta blocker, it is inconvenient and the use of vasodilators such as alpha blockers or calcium antagonists as exacerbate circulatory hyperkinesia. In patients who are suspected of expanding the extracellular space (especially women) the best option is the diuretic as mono therapy, are less effective than beta blockers and vasodilators are contraindicated deteriorating fluid retention and expansion of the intravascular space. Can be equally effective inhibitors of ACE. In elderly with systolic hypertension is preferable to use calcium antagonists as drugs of first choice.

b) Patients with essential hypertension grade III, requires the use of multiple drugs to achieve an efficient control of hypertension. This form is preferred to initiate treatment with beta blockers and diuretics (thiazides and potassium-sparing). Failure to reach an effective control of blood pressure can add an ACE inhibitor. Where not achieved normalization of blood pressure can be used vasodilators (hydralazine, minoxidil, prazosin) which reduce vascular resistance. The calcium antagonists can be used in such patients are not able to control hypertension with drugs and or because there are two states that suspend their administration by undesirable side effects such as: attack of gout (thiazides), asthma or heart failure ( betablockers) or persistent cough (ACE inhibitors). The anta gonistas calcium can also produce undesirable side effects (edema, facial flushing) that can bind to the suspension or change to another drug of a different family.
As a general conclusion one can say that treatment of hypertensive patient should be individualized taking into account age, clinical conditions and hemodynamic effects of drugs.

c) The patient with grade IV hypertension is a hypertensive emergency or urgency, so that their treatment requires immediate hospitalization and therapy.

Hypertensive crisis

a) The patient was asymptomatic but with figures of diastolic blood pressure of 140 mmHg or greater should be hospitalized for observation and absolute rest, being administered by sublingual nifedipine at 10 mg.

b) The patient with hypertensive crisis, with increased blood pressure of 180/140 and acute pulmonary edema must be treated with Fowler position, sitting on the bed edge, rotating tourniquets, by IV furosemide at a rate between 20 and 60 mg by sodium nitroprusside and IV diluted in dextrose solution at a rate of 0.3 to 8 mg / kg / min, and in some cases these measures achieves jugular table, but others should also scan the patient in a timely manner (or C lanata Ouabain). When the patient is already in clinical conditions will be acceptable to initiate antihypertensive oral.

c) The patient with hypertensive crisis which is associated with hypertensive encephalopathy is presented to the doctor with a very ostentatious manifesting headache, nausea, projectile vomiting, blurred vision and a progressive state of mental obnubilación all this coincides with elevations exaggerated the figures for blood pressure (> 180/140). The appropriate procedure will also be treated with sodium nitropusiato given as mentioned in the previous paragraph, although such cases can also be used diazoxide at a starting dose of 300 mg IV which can be repeated w / 4 or 6 hours, depending on the response. It should be remembered that the prolonged administration of this drug produces sodium and water retention, so when their use is extended for more than 24 hours should join the administration of diuretics. As soon as possible to initiate oral therapy.

d) The hypertensive crisis which is complicated with an aortic dissection is presented as an acute where the patient can present intense chest pain or back accompanied by feelings of death, pallor, diaphoresis, and elevated mind exaggerated figures (> 180/140 mmHg). This table should be treated with sodium nitroprusside, another alternative is alfametildopa drug at a rate of 250 to 500 mg IV c / 4 to 6 hours and has been checked in to start oral antihypertensive therapy.

e) If a hypertensive crisis due to a pheochromocytoma patient relate headache, palpitations and was found with pallor and diaphoresis, sinus tachycardia and excessively high numbers (> 180 / 140 mmHg), in which case the ideal treatment should be done with phentolamine, injected an initial bolus of 5 to 15 mg IV and then on a continuous drip to maintain blood pressure numbers at acceptable levels. If heart rate is exageradeamente high (> 150 per minute) or appear as tachyarrythmia paroxysmal atrial fibrillation by propranolol should be administered by IV at a rate of 1 mg / min up to 3 to 5 mg total dose.

Patients with essential hypertension grade III, requires several drugs to achieve the desired control. In summary, the treatment should be individualized according to age, clinical conditions and hemodynamic sensitivity to drugs.

* Quitting smoking reduces mortality to half of those who continue to smoke.
* Controlling hypertension.
* Reduction of body weight.
* Increase physical activity.
* Controlling Diabetes
* Changes in eating habits.

The onset may be abrupt, such as acute myocardial infarction or may be a chronic disorder, with increasing loss of functions of the heart. In turn this may be offset a disease where the activity remains normal or decompensated, in which the patient suffers dyspnea and precordial pain in this case should rest and receive medication and diuretics.
From a nutritional point of view it is the implementation of a diet hiposódica (containing less than 5grs. Salt daily).

In coronary disease should avoid foods rich and abundant as they impose an excessive burden on the heart and circulation.

When making a food choice for these patients should be sought to replace the salt and no abdominal distension, constipation and flatulence.

Bibliography:
• Patologia Roobins 2007
• Patologia Rubin
• Web Journal Cardiology hypertensive crisis
• Institute of Cardiology http://www.drscope.com/cardiologia/pac/arterial.htm
• Goodman and Gilman, Farmacologia.
• National Institute of Cardiology – Ignacio Chávez, Hypertension Articles
• National Association of Cardiologists of Mexico
• Society of Interventional Cardiology of Mexico
• National Society of Echocardiography in Mexico
Nutrition zonadiet.com 2004 • Hypertension
• Vascular Health. is
• Book Fisiologia Guyton
• Stevens Patologia

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by Wootang01

Emotional Sensitivity:An approach to Decision making

 There are numerous organisations operating in same environment, producing same product, catering to the same market and facing the same challenges yet some are highly successful while others fight for their survival. What makes them successful or failure is the decisions they take. A single right decision can make an organization at the same time, a single wrong decision can break the organisation. Decision making, in short, is a major activity in organisational life as its outcomes are crucial for the survival of an organisation. Success and failure of any organisation depends on not only the decisions they make but to a large extent how they make the decisions.

Decisions do not exist by themselves they are made by people who are not only ‘thinking’ but also ‘feeling beings. Despite this, over the years the emphasis has been on rationality and cognition and on ways of diminishing the influence of subjectivity and emotions while making decisions. It was assumed that emotions could seize decision making process, thus leading to poor decisions. As a consequence, emotions were considered as a disruptive force in rational thought and adaptive action(Bernstone et.al.1993).However, unlike the past where emotions were typically considered outside the purview of a rational analysis, emotions are increasingly recognized for the role they play in decision making.

 This shift perhaps, was due to the finding of a researcher named Antonio Damasio. Damasio (1994), drew this finding from patients with specific lesion. Some patients who have suffered damage in their frontal lobes became emotionally flat and lost their ability to make, while retaining other cognitive functions. From the analysis of these patients, Damasio (1994) concluded that they were unable decision making due to lack of emotions. Antonio Damasio (1994) has described vivid examples of this lack of rationality in his book “Descartes Error”. He argued that emotions actually promote rational behaviour in situation of indeterminacy. He showed that emotions allow us to avoid potentially problematic choices because we have a feeling or a hunch that something about the choice is not worthwhile. Without this feeling, we might not notice anything wrong or we might get lost trying to reason out unimportant differences between options. Thus he claimed that not only that person (who suppresses emotions while making decisions) would make irrational decision, he also claimed that in many situations this person would make no decision at all or might delay it for very long.Thus in order to behave rationally we need emotions.

 Contrary to the popular notion that decision makers are very rational and logical in their approach while taking decision, they do not always follow logically optimal path or conform to organisationally defined rationality. Since they have to be contended with the information at hand and as there are too many possible alternatives for them to evaluate, therefore rationality is subjective and bounded. Relevant informations, therefore can be missed and hunches, preferences and gut feelings might play an important role in decision making process (Fineman, 1993).

In decision making process both cognitions and emotions play an important role. If cognitions help us in generating ideas, emotions allow us to decide, what is worth thinking about what is not. Emotions also help us in deciding what is appropriate and inappropriate. Emotions block ideas which are irrational when both time period and our ability to test all possible alternatives is limited .They allow us to act in a manner which is compatible with long term interest. When stakes are high and rational headed person is asked to make decision, he frequently becomes lost as to what decision he /she should take. When making decision at initial stage the decision maker has many rational thoughts with only a small amount of emotions. But when it comes to make a decision finally we find that ratio of rational to emotional thoughts is reversed. This intelligent and rational person changes into different person. He may not show his emotion, but his action or tone of voice however may provide a clue.By saying “I’ve got to think over it” or “It’s not a bright idea”. The decision maker shows that  she/he is not only thinking but also a feeling being. When executives are asked to make decision that involves significant considerations, risk and more importantly their honour and when their reputation and image is at stake then they are bound to use emotion in deciding.

 Reason and emotion, therefore, act as two complimentary systems in human brain for making decision. When it is important to get the answer right and we have a lot of time at our disposal, we can use the slow and tried method of reasoning things through. When we have little time and information or it is not simple but a complex decision that needs to be made, we use emotions to decide.

 Research indicates that emotion in decision making has been viewed as alternating between two contrasting positions. At one pole, researchers assume (often implicitly) that emotions are primarily impediments to adaptive action. According to view, emotions disorganize or interrupt current thought and disrupt ongoing behaviour. Emotion related thought processes are seen as lacking the direction and principled orderliness of reason (Dewey, 1985; Hebb, 1946; Mandler, 1984).Emotional expressions from anger to proclamation of love are seen as reflecting the more uncontrollable side of human nature that threatens the social order.

 At the other pole, theorists assume that emotions function in an organized and useful ways. Emotions are reliable guides to action and help in sustaining the harmony and continuity of social interaction and relationships. Emotions, according to this view,prioritize and organize the ongoing the individual’s adjustment to the demands of the physical and social environment (Darwin,1872 & Ekman,1992).Emotions often act a tiebreaker in decision  involving high degree of indeterminacy by enabling us to focus on the salient features of the situation(Nutt,1984).Thus emotion can facilitate as well as hinder the decision making process and whether they would facilitate or hinder would depend on a large number of factors like nature of decision, environment and organisational constraints.

 In most of the studies emotions have been categorized into two types- the positive emotions and the negative emotions. Studies have concentrated on how positive and negative emotions influence decision making in terms of processes and outcomes. Frank and Hirshlefer(1993) ,suggest that negative emotions such as anger, serve to enhance credibility of threat, while positive emotions such as love and affection ensures credibility of cooperation in decision process. Similarly whereas negative emotions can result in a limited search for new alternatives and less vigilant use of information, positive emotions can increase or enhance active generation of ideas such as inference making, productive thinking and facilitate the assimilation of information in decision making process( Ansoff,1965;Andrews,1980;Porter,1998).

 Contrary  to the popular assumption that, positive emotions would always  facilitate decision making and negative would hinder it , the effect of  positive and negative emotions on decision making process have not always been parallel or symmetrical. Negative emotions lead to more thorough treatment of information. People who are sad or depressed seek and consider more information and process persuasive messages more thoroughly. In contrast, positive emotions lead to reduction of deliberative or systematic processing of information. People, who are in positive mood tend to prefer the use of heuristics and decisional shortcuts and base their judgment on stereotypes.

 Thus both positive and negative emotions have both positive and negative implication. In order to maximize the positive aspects and minimize the negative aspects, organisations employ a variety of mechanism to neutralize emotions at workplace. These mechanisms aim either at preventing emotions from arising in the first place or to safely control these emotions when they arise. Hence organisations adopt strategies like feeling rules and emotionalized zones.

 Feeling rules play an important role in determining the nature of the decision process. Decisions like, layoff, demotion and dismissal are governed by feeling rules prevalent in the organisations. These decisions can be emotionally taxing; decision maker may feel guilt for the loss of someone’s job or livelihood. If such feelings are allowed to persist, then, there would be no layoff or suspension in the organisation. Feeling rules probably keep in check the personal feelings of individuals. Decision makers are not expected to feel compassionate, guilty, ashamed or sad as they may act as an obstacle in taking decision. Managers become impersonal and justify their actions by giving explanations like “It was for organisation’s survival”, “I was just doing my job”. Feeling rules help decision maker to adjust his focus and prioritize his preferences. When there is emphasis on being loyal towards organisation, the decision maker, may not mind taking decision, which involves, lying, fraud and deceit. On the other hand rigid feeling rules may prevent employees from airing their true feelings about various policies and decisions. Even when s/he expresses his/her discontent s/he might do so in low voice or mellowed tone and once his/her idea is rejected s/he might not take it up again. As a consequence the employee is likely to accept the suggestions or decisions of the MD even though s/he does agree with him.

 Since organisations do not allow or encourage expression of emotions like fear, uncertainty and apprehension, it creates problem at not only during the process but also during the implementation stage and when the decision is being evaluated as being good or bad. When doubts, fears, anger and apprehensions are not encouraged or even entertained, it might prevent the decision maker from expressing his /her genuine views or prevent him/her from expressing anything at all. Suppression of apprehension and fear might force the decision maker either to take decision which he himself does not approve of or lead to half hearted commitment towards the decision taken. So when such decisions backfire the decision maker does not feel guilty or responsible for the decisional outcome as he feels that he had already expressed his fear in decisional phase but the organisation went ahead with the decision, ignoring or downplaying his fear or apprehensions.

 What is needed, therefore that organisations become sensitive towards the emotions of the employees. It should be able to acknowledge and appreciate the significance of the emotions expresses by its employees’s, understand why that emotion has surfaced and do something by which that emotions gets overcomed. For example if  employee expresses fear towards a decision , organisation should try to understand why he/ she is expressing that emotion and by clarifying or giving patient  hearing help employees to overcome his/ her fear.

 If organization is emotional sensitivity, it would bind people more deeply than shared beliefs and ideas. There would be enhanced commitment and loyalty towards the decision taken. Emotional sensitivity, therefore, becomes important as it might help in minimizing the conflicts, miscommunications during the decision making phase and protect organisations from making poor or wrong decisions.

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 Emotional sensitivity is related to the concept of emotional intelligence. Emotional intelligence focuses on not only emotional but also on social skills, like how relationships are handled, ability to take perspective of others etc. It emphasizes on, not only being aware of only one’s own emotion but also of others. For emotional sensitivity, emotional intelligence is a prerequisite because unless one is aware of one’s own as well as others emotions one cannot be sensitive towards others. Both terms are overlapping and interrelated as emotional intelligence as well as emotional sensitivity talk about being aware of emotion of one’s own as well as that of others, understanding others and using emotions to attain a positive end.

 Emotional sensitivity like emotional intelligence does not ignore or suppress the emotion but try to understand its occurrence and use it in a constructive way. However there is a subtle difference between the two. Emotional sensitivity is one step ahead of emotional intelligence. Although emotional intelligence is prerequisite of emotional sensitivity however emotional sensitivity goes beyond emotional intelligence, for it  not only acknowledges and understand the emotion but emphasizes the way one handles the emotions that are being expressed whether one remains indifferent or empathizes with the person expressing the emotion.

 One the most, important prerequisite of being emotionally sensitive is to acknowledge the emotions being expressed and understand the reasons of its expression. Emotional sensitivity places emphasis on not only being aware of one’s emotions but also that of others. Unless one is aware of ones emotion one cannot understand what others are feeling and why s/he is feeling that way? However emotional sensitivity goes beyond the realm of being aware and understanding emotions. It is more about the way one handles emotions that are being expressed by oneself as well as by others.

 Dalip Singh(2003) talks about emotional sensitivity as one of the component of emotional intelligence and it constitutes understanding the threshold of emotional arousal, managing the immediate environment, maintaining rapport, harmony and comfort with others, letting others feel comfortable in your company. It also involves being honest in interpersonal dealing, interpreting emotional cues truthfully, realizing communicability of emotions, moods and feelings and having and insight into how others evaluate and relate to you. Singh talks about understanding why the emotion is occurring, empathizing with person expressing the emotion thereby improving interpersonal relationship. However he has overlooked the issue of handing of emotions once they get expressed. Organisation may become indifferent or express helplessness towards emotions being expressed. If acknowledging emotions is important, then the way one responds to emotions is equally important. Emotional sensitivity places emphasis on how emotions are handled once they are expressed. Reaction to the emotions expressed (whether the organisation empathizes or remains indifferent) becomes important because it governs the interpersonal dynamic in the organisation and various organisational activities. If an organization, while being aware of the emotions being expressed remains indifferent towards them, then it might give rise to feeling of apathy among the employees towards the organisation. This in turn, might also result in emotional distancing, lack of commitment and loyalty towards the organisation on the part of the employees. Thus one cannot be emotionally sensitive if one remains indifferent to what the other is feeling or if s/he does’nt bring about a change in his/her behaviour.

 Here it is important to clarify that emotional sensitivity of organisation does not mean that the organisation cater to each and every emotion that is being expressed or that it functions according to the whims and fancies of the employees. Emotional sensitivity means that the organisation pays attention to the emotions, (especially to those emotions which affect organisation functioning) tries to understand why it is being expressed and to do something which would ensure those expressing the emotion that they are valued by the organisation, are heard, and are important. In short, unless there is an effort to change the attitude or behaviour (which leads to arousal of negative feelings in others) so that other person feels comfortable, sensitivity cannot be achieved.

 As already mentioned, the way emotions are handled (whether the organisation empathizes or remain indifferent) becomes important because it would not only govern the interpersonal dynamic in the organisation but also various organisational activities. Handling of emotions is very important because the way organisation reacts towards the emotion being expressed would determine the nature of various organisational processes both at micro as well as macro level. At micro level attitude, motivation, leadership, power, group behaviour etc. would be influenced. At macro level it would influence interpersonal relations, decision making and more importantly organisational culture. For example an organisation which remains indifferent to the emotions being expressed would have employees, who would remain detached, have low commitment, would not feel free to discuss things related to their jobs; a leader who would neither listen to nor take suggestions; a culture which would be hypothetically an autocratic and characterized by lack of openness and impersonal relationship; decision making characterized by single man decision making. An organisation which shows helplessness would hypothetically refer to written rules for almost everything would refrain from risky decisions; would have bureaucratic culture characterized by task orientation; less willingness to make decision and shifting responsibilities and blaming others, would predominate in decision making. Organisation which acknowledges and pay attention and empathize with the emotions being expressed would be flexible in approach and attitude; suggestions and idea would be easily sought and given; there would be high level of commitment and loyalty among employees; would be proactive in problem solving and organisation culture would be participative in nature.

 Another aspect of emotional sensitivity is that,sensitivity could be best judged when there is a problem or a crisis situation. How crisis is handled would indicate the sensitivity level of the organisation aspect. Organisation could react in two ways-reactively (like blaming others, loosing confidence and becoming dejected with failures) or proactively (remaining composed during crises, understanding the reason behind failure and being optimistic about future).An organisation  which indulges in reactive behaviours would give rise to a culture characterized by risk avoidance, shrinking from taking responsibility, lack of accountability and fear of failure. It would also set the tone for dealing with the crisis in future. Handling of crisis becomes all the more important as not every activity in the organisation is successful. Some end up in failure therefore the way failure or crisis is handled strongly determines the sensitivity of the organisation.

Emotional sensitivity refers to the ability of the organisation to acknowledge and understand the importance of the emotions being expressed by its employees, to link how their emotions influence their performance and thereby base their subsequent action on the basis of these emotional cues.

 There are four dimensions of emotional sensitivity:

a) : referred to the ability to recognize and have clarity of one’s own emotions and that of others and to understand the relationship between emotional states and performance.

b) : referred to the ability to deal and mange emotions expressed by others. It consists of the following kind of responses – empathy, indifference and helplessness.

c) : referred to effectively managing interpersonal relationship through openness, bonding, trust and equality.

d) : referred to  the strategies adopted bt the organisation to effectively deal with inadequate resources and threat to system’s survival.It can be through understanding failure, making fresh plan , blaming others and maintaining poise during turmoil.

 McGregor (1960) in the context of decision making, outlined the characteristic of an effective group as one where the members listen to one another, every idea is given a patient hearing, members feel free to express their feelings as well as their ideas not only on the decision to be made but also on group’s operation and where there are disagreements they are not overridden, criticism are frequent and frank, and there are little evidences of personal attack and effort to dominate the group.

 When decisions are taken in group, group members contribute to its success by participating actively in the execution of assigned roles. Each member is valuable resource. The contributions of each member are secured through active participation and commitment. Successful decision making involves a rich debate on the issues marked by trust (Simons & Peterson, 2000) where team members feel free to express doubts, change in minds (Lovelace et.al., 2001) and show ability to resist pressures to compromise quickly (Montoya – Weiss et.al., 2001) or to reach a premature consensus (Choi &Kim, 1999).

 The way the organization handles the emotions that are being expressed would set the tone of the process. If organization is indifferent towards the emotions being expressed then the people may also become indifferent, alienated or detached with the process. For example suppose during decision making, a confident and enthusiastic manager comes up with an idea but the top management instead of understanding his/her view point simply shoots down his/her idea because according to them the idea is not feasible .This may perhaps lower the morale of the manager ands/he may withdraw during the entire decision making process. S/he may also feel that s/he is unwanted. Here the organisation needs to be sensitive regarding what is being said, why s/he is saying so and to the emotions attached to that particular idea. Organisation should give a patient listening and if the ides is not feasible, make him/her understand this. This would make him/her feel that organisation has nothing personal against him/her or his/ her idea. It is just that the idea is not appropriate for organisation’s survival and growth. This would help in encouraging people to actively participate in the process by giving their contributions or analyzing. 

 Handling of emotions predominately affects two most crucial and important stages of decision making they are the idea generation and evaluation of the idea stages. When an idea is expressed, it reflects the values belief and preferences of person expressing it and therefore it becomes difficult to detach our ego with the idea. When the idea is given due consideration it gives satisfaction to the one who gave the idea and a feeling that one has contributed positively to the outcome is instilled which increases his/ her commitment to and satisfaction with the decision ( Cialdini & Goldstein,2004).On the other hand, when ideas are criticized , ignored or downplayed, negative emotions are generated(Ayers, 2003) and therefore the  person starts  disassociating  with the process and the decision. As a result it gives rise to what Argyis (1957) called ‘pseudo participation) i.e. participation which looks like real but is not real. The participants become withdrawn, quite, and inattentive and restrain themselves from expressing their opinion. Thus it is important that each idea is given respect, clarified and evaluated in unbiased way. Apart from this, it is the stage which sets the rules for the way the decision has to be taken. If this stage is handled sensitively then rest of the decision making process follows a smooth pattern.

 Handling of emotion, in turn would define the nature of interpersonal relationship. An organization which handles the emotion effectively or in other words is emotionally sensitive then there would be trust and mutual concern for each other. Having mutual concern increases group cohesiveness, tolerance of personal differences in views and taking less time at the task. Therefore, another thing which enhances, not only, the quality of the decision but also the process is the, climate of support, trust, cooperation and openness. Trust in each other facilitates unilateral acts of cooperation and coordination (Meyerson et.al, 1996; Weick & Roberts, 1993). For members to have trust in the group, they must feel that the group will not harm the individual or his or her interests. Trust in decision making also enhances giving other the benefits of the doubt when views are being challenged or criticized. Criticism is structured, focused and ‘task oriented’ rather than ‘person oriented’ as a result they get appreciated and enhance the quality of decision. Where there is a lack of trust, people feel hesitant to express their views and opinions sincerely and frankly.

Emotional sensitivity enables one to frame criticism as a helpful critique rather than as a confrontational situation. It recognizes that feedback negative or positive is vital for running decision process smoothly. It helps employees in creating atmosphere where diversity in opinion is valued rather than as a source of friction. Thus it would enable employees to trust the management intentions even if their ideas had been rejected.

In a climate of indifference, distrust and close mindedness criticisms are taken as an attack on the person rather than his/ her ideologies. As such, participants spend more time and energy in defending themselves and downplaying others instead of taking decision When there is lack of, ability to cooperate, trust and respect for the fellow participants are missing the quality and speed of decision making suffers ( Forgas, 1998b; Mullen, et. al, 1994). Due to lack of cohesiveness there is lack of consensus regarding what the problem is, what has to be discussed first and how the problem is to be resolved. As a result more time is devoted to confirming, clarifying and substantiating ideas and less time in finding the appropriate solution. Where there is lack of consensus and mutual understanding, negative emotions get generated, interpersonal problems get created and time is wasted. Studies indicate that conflict in relationship has negative impact on team performance (Jehn, 1994).

 Lastly, not every decision can be successful, some decisions would backfire. The way organisation handles these failure would sets a tone for future decision making. If organisation is emotionally insensitive it would, instead of, confronting the failure and rectifying it would indulge in blame game, become anxious and spends all its energy in covering up the failure. An organisation which is emotionally sensitive would see failure as a learning process. When there is failure, the organisation would divert it energy in rectifying the loss and minimizing the damages done by the decision. The organisation would also provide emotional and moral support to the decision maker and not letting him/ her to feel abandoned. Failures would not inhibit the decision maker from taking decisions in future. Thus instead of being reactive, the organisation would confront the failure and proactively deals with them. 

 Thus sensitivity towards emotions of the people would not only help in understanding why decisions are taken the way they are, but also make people (especially those affected by the decision) confident that the management had taken into consideration their opinion and feeling (fears, doubts and apprehensions) and had made those decisions impartially in the overall interest of the organisation. Besides, it would also enable employees to trust the management intention even if their ideas had been rejected.

 When the process is marked by insensitivity towards the feelings and thoughts of the participants, it leads to poor interpersonal dealing which in turn affects the outcome of the process. Being insensitive to the emotions of the employees would not only lead to emotional distancing of the employees from the organisation but might also lead to indifference towards the decision process as well as the outcome. People are neither satisfied nor committed to the decision. They do not feel morally responsible for decisional outcomes. Thus the quality and speed of decision making suffers.

 In short, it must be emotionally sensitive, because by being emotionally sensitive, it would not only enhance the quality of the decisions in terms of time taken, satisfaction and commitment towards the decision, and their effective implementation, but also the accountability of the decision maker for the decision.

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by Vaughan

What You Need to Know About Heart Failure

As per the American Heart Association (AHA), over 5 million people in the United States are living with heart failure. Each year, over 550,000 new cases of failure are diagnosed, many of whom suffer from fatal heart attacks in a few years after diagnosis.

Heart failure is an often misunderstood condition, and this article will hopefully help you get the answers to a few common questions.

First of all, a lot of people believe that heart failure means that your heart has stopped or is about to stop pumping blood (i.e., a heart attack). This is false, as it simply means that the heart is not as efficient at pumping blood as it should be.

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Because of the reduced efficiency of the heart, there is an inadequate supply of oxygen and nutrients to the blood. This is the reason why people suffering from failure of the heart often feel excessively tired or weak for no apparent causes. Also, it can cause excessive fluid to build up in your lungs, which can cause congestion in the lungs. This is the reason why it is sometimes also called ‘Congestive Heart Failure (CHF)’.

The symptoms of heart failure range from shortness of breath, excessive and frequent coughing, a permanently increased heart rate for no apparent causes, fatigue, tiredness, weakness, inexplicable weight gain accompanied by a loss of appetite, swelling in the legs and ankles due to fluid buildup.

If not treated immediately, it can cause a fatal stroke or lead to permanent heart failure in which case the heart completely stops pumping blood. Usually, a number of intravenous drugs (IV drugs) are used to treat failure. A few of these include diuretics, inotropes and IV vasodilators.

If you feel you suffer from any of the conditions outlined above, please consult your doctor and get treatment as soon as possible. Remember that accurate diagnosis is the first step to treatment.

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by Wootang01

Cardiac markers new and old

Cardiac markers or cardiac enzymes are proteins that leak out of injured myocardial cells through their damaged cell membranes into the bloodstream.

They are:

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1.     Cardiac troponin I and cardiac troponin T

2.     Creatine kinase-MB isoenzyme (CK-MB).

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Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury.

1.C-reactive protein

2.B-type natriuretic peptide

3.Copeptin

4.lactate dehydrogenase

5.Aspartatetransferase

6.myoglobin

7.ischemia modified albumin.

8.Glycogen phosphorylase isoenzyme BB.

9.Adiponectin.

10.Adrenomedullin.

The troponins are part of the actomyosin contractile apparatus of muscle cells. Structurally unique forms of troponin T and troponin I are found in cardiac tissue, enabling the development of immunoassays, which recognise only the cardiac forms of these two proteins. In most clinicalsituations both cardiac troponin I (cTnI) and cardiac troponin T (cTnT) seem to offer similarly useful clinical information.

When a cardiac myocyte dies, CK-MB passes rapidly from the cytoplasm into the circulation and is cleared. In contrast, most of the troponin within the myocyte is found in the structural elements of the cell, so when necrosis occurs there is a steady leaching of troponin into the circulation. Consequently, troponin remains in the circulation for several days after a cardiac event.

Despite extended searching, there is currently no evidence that the cardiac troponins may be produced by tissues other than myocardium. However, the presence of cardiac troponin, while indicating that cardiac injury has occurred, provides no information as to the mechanism of injury. Cardiac troponin concentrations may rise in conditions unrelated to ischaemic damage such as pericarditis, trauma and sepsis. Such rises provide no information about the likelihood of future ischaemic cardiac disease.

When associated with coronary artery ischaemia even low concentrations of cardiac troponin predict an adverse outcome. This is regardless of whether the other WHO criteria for the formal diagnosis of myocardial infarction are met. The pathophysiological mechanism for these acute coronary syndromes is the presence of an unstable coronary plaque, with release of micro-emboli causing focal myocardial necrosis with release of cardiac troponin. The increased mortality is a reflection of a large thrombus separating from the unstable plaque.This improved understanding of the mechanism of the acute coronary syndrome, has led to a proposal to redefine myocardial infarction, using the presence of a cardiac biochemical marker, with some evidence of coronary artery ischaemia, as the central diagnostic criterion.

A small proportion of patients with renal failure undergoing dialysis have detectable concentrations of cTnT. This finding was originally thought to be a false positive test, but careful analysis has shown that these patients do have a worse cardiac prognosis. When one considers that approximately 20% of patients on dialysis die each year and that cardiac disease is the commonest cause of mortality, this result is not unexpected. Although there is some increase in cTnI in dialysis patients, this appears to be one area where cTnT is more informative.

Cardiac troponin I is prone to modification in the circulation. It may be phosphorylated and oxidised and can exist as a complex with either cTnT or cardiac troponin C. This has some clinical relevance, because the different antibodies used in commercial assays may recognise these different molecular forms to varying extents. A major problem with cTnI assays is that the different assays are calibrated with different standards. The same blood sample may give quite different apparent concentrations in different assays. If it is accepted that the presence of any cardiac troponin in the presence of coronary artery ischaemia indicates a worse prognosis, then the absolute concentration is less important.

Creatine kinase (CK) and more particularly its isoenzyme CK-MB still have a formal place in defining myocardial infarction. However the current definition is not a particularly useful one because studies have shown that, as currently defined, patients with myocardial infarction and unstable angina have similar outcomes.

Interpretation of CK-MB is problematic, with both false positives and false negatives occurring. While CK-MB is relatively cardiac-specific, even healthy people may have low concentrations of this isoenzyme in their blood. People with chronic myopathies may have high concentrations of CK-MB because it is produced by regenerating skeletal muscle. A high concentration of CK-MB may therefore be unrelated to cardiac disease (false positive).

The half-life of CK-MB in the circulation is relatively short (approximately 12 hours). Samples collected many hours after an infarction may have both a low absolute concentration of CK-MB and a low ratio of CK-MB to total CK (due to the longer half-life of the major isoenzyme, CK-MM). This can give a false negative result.

Some specialists believe that it is no longer appropriate to use CK-MB in the diagnosis of myocardial infarction. It may be more helpful for investigating possible reinfarction, where its short half-life may be useful compared to the longer time that cardiac troponins spend in the circulation.

C-reactive protein (CRP) is an acute phase reactant produced by the liver in response to cytokine release during inflammation. It has long been used in clinical practice to follow systemic inflammation, especially bacterial infection. More recently, epidemiological evidence has shown that basal levels of CRP, in the absence of apparent inflammatory disease (so-called hs-CRP) may be informative in predicting future myocardial or cerebrovascular events.

The value of hs-CRP appears to relate to activity in the atherosclerotic plaque. Amongst the cellular elements of the atherosclerotic plaque are inflammatory cells, which, by releasing interleukin-6, cause secretion of CRP into the circulation. In the Physicians’ Health Study, when people in the highest quartile of CRP values were compared to people with the lowest quartile of CRP values, they had a relative risk of future myocardial infarction of 1.9. In the Women’s Health Study the relative risk was 4.4.

There are a number of problems in using CRP measurements to predict the likelihood of future cardiovascular events. These are both biological and analytical.

Biological variability in basal CRP concentration is considerable. Even mild, subclinical infections can cause significant increases in CRP concentration that are unrelated to cardiovascular disease. For this reason, no measurements should be made within two weeks of any infection. Even with this precaution, CRP concentrations may vary markedly. Several studies have investigated the variability of the CRP concentration in blood collected repeatedly from individuals over periods of weeks to months. The standard deviation for each individual varies from 30% to 63% of the mean value.Thus it might be highly misleading to contemplate using a single measurement to guide possible therapy. It has been proposed that two separate measurements should be made on each individual, while they are quite well, and at intervals of more than a week apart. The lowest value is then used to determine which quartile the person is in. Even this approach may be insufficient to correct for the variability.

There are outstanding laboratory problems with use of hs-CRP. Not all assays produce identical results. No laboratory has the resources to determine its own reference ranges, so transportability of results between assays is obviously of great importance in defining the concentrations that relate to the different quartiles of basal CRP concentration. At the present time it appears undesirable to attempt to use hs-CRP in individual risk stratification.

The cardiac natriuretic peptide family of neuro-endocrine hormones has a complex physiological role in modulating blood volume and pressure. This involves natriuresis and diuresis as well as antagonism to the angiotensin-renin system. These peptides are also antimitotic and may modulate cardiac hypertrophy. In the presence of left ventricular dysfunction, with worsening cardiac failure, the concentration of plasma B-type natriuretic peptide (BNP) increases in proportion to the New York Heart Association’s (NYHA) classification of severity. However, there are a number of other pathophysiological states in which BNP may be elevated, such as hypertension and cardiac hypertrophy, pulmonary hypertension and renal disease. The most appropriate use of this marker remains to be defined.

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As with cTnI, several different assays for BNP or its associated peptides (e.g. NT-proBNP) have been used in the published studies. As these assays are not yet standardised, numerical values from one assay cannot be compared quantitatively with those from another.

Many patients hospitalized with acute exacerbations of heartfailure are cared for by primary care physicians after discharge.Although some patients avoid rehospitalization within the next6 months, others are prone to multiple hospital admissions.Recently, BNP determinations have shown the potential to bea good prognostic marker for morbidity and mortality in patientswith heart failure, including predicting future cardiac eventin patients with acute exacerbations

One prospective study found that an initial BNP concentrationof 480 pg/mL had a sensitivity of 68%, specificity of 88%, andan accuracy of 85% of predicting a congestive heart failureendpoint (death, hospital admissions, and repeated emergencydepartment visits) after a 6-month follow-up period after hospitaldischarge. Patients with BNP levels greater than 480 pg/mLhad a 51%, 6-month cumulative probability of a heart failureevent (35% of these patients had death from heart failure astheir event), whereas BNP levels of less than 250 pg/mL hada much better prognosis, with only a 2.5% cumulative probabilityof a heart failure event. The authors reported that increasedBNP levels were associated with progressively worse prognosis.

Another well-designed study compared BNP levels with the patient’sheart failure survival score (HFSS), a recognized and acceptedtool in determining a patient’s prognosis. Patientswere classified into three different prognostic groups basedon the HFSS score: low risk, medium risk, or high risk. Therewere significant differences in each group. The mean BNP concentrationfor the low-risk group was 95.7 ± 11.2 pg/mL, for themedium-risk group was 244.4 ± 33.4 pg/mL, and for thehigh-risk group was 419.9 ± 55.5 pg/mL. More importantly,the authors were able to show that higher BNP levels were associatedwith a change in cardiovascular functional class with time.The initial BNP level in patients who improved during the ensuing12 months had a BNP concentration of 42.4 ± 8.6 pg/mL,those who remained stable had a BNP level of 102.2 ±16.1 pg/mL, and those who deteriorated during the ensuing 12months had a BNP level of 256.9 ± 28.5 pg/mL.

Primary care physicians have the task of managing patients withcongestive heart failure. An important aspect of patient managementis the ability to monitor the therapeutic efficacy of the patient’spharmacological regimen. BNP levels have been found to followventricular function in response to medical management.

One study evaluated left ventricular volume and mass, includingneurohormone levels, in patients with mild to moderate nonischemiccongestive heart failure before and after 4 months of treatmentwith spironolactone or placebo. Patients who received a fixed25-mg dose of spironolactone had a change in their mean BNPconcentration from 200 ± 66 pg/mL at baseline to 89.7± 27 pg/mL at 4 months (P< .01), whereas the controlgroup showed no significant change.

Another study managed to show that BNP-guided treatment of heartfailure reduced total cardiovascular events and delayed timeto first event compared with intensive clinically guided treatment.The BNP concentration decreased 79 pmol/L in the BNP-guidedgroup compared with 3 pmol/L in the clinically-guided group.More importantly, the primary combined clinical endpoint (cardiovasculardeath, hospital admission, and outpatient heart failure) wassignificantly reduced in the BNP-guided group (P< .02).This significance increased when covariates were accounted for(baseline left ventricular ejection fraction, baseline BNP,and medication dosages, New York Heart Association heart failureclass, and systolic blood pressure) in the regression model(P< .001). The authors suggested that BNP-guided treatmentrepresents a preventive strategy targeting more intensive pharmacotherapyand follow-up for patients with elevated circulating BNP levelswho are at high risk of cardiovascular events.

Although both studies describe an important use of BNP, thesmall study sizes should raise caution when applying these findingsto clinical practice

Approximately 15 million patients present to the Emergency Department (ED) with symptoms suggestive of Acute Myocardial Infarction (AMI) every year. The vast majority (70 to 80%) of them finally prove not to have AMI. However, due to a delayed increase of circulating levels of Troponin it takes up to six hours before it can be measured. Therefore serial blood sampling is recommended by the European Guidelines. Study results indicate that by testing for both markers, along with an Electrocardiogram (ECG) and the clinical findings, approximately two-thirds of the patients would not need to wait those six hours in the ED for the second Troponin test. This may obviate the need for prolonged monitoring and serial blood sampling in the majority of patients.

“In the very situation of a patient presenting to the Emergency Department (ED) with symptoms suggestive of Acute Myocardial Infarction (AMI) the clinician quickly needs to know whether the person is in real danger or not. Ruling out AMI in this setting is an urgent and unmet need. The use of Copeptin together with Troponin can accelerate the rule out of AMI and thus improves patient management in the ED immensely. Two thirds of these patients may be ruled out with the first blood draw and most of them probably could leave the ED very soon,” explained Dr. Tobias Reichlin from the Department of Internal Medicine at the University Hospital, Basel, Switzerland. While the concentration of Troponin rises four to six hours after the event of an AMI, concentrations of the new Copeptin biomarker are highest right after the onset of symptoms and then begin to drop. This difference makes the use of the combination of the two extremely promising.

The study was conducted in the University Hospital of Basel, Switzerland. In 487 consecutive patients presenting to the Emergency Department (ED) with symptoms suggestive of Acute Myocardial Infarction (AMI), the research team measured levels of copeptin at presentation, using a novel sandwich immunoluminetric assay in a blinded fashion. The final diagnosis was adjudicated by two independent cardiologists using all available data.

The adjudicated final diagnosis was Acute Myocardial Infarction (AMI) in 81 patients (17%). Copeptin levels were significantly higher in AMI patients compared with those in patients having other diagnoses (median 20,8pmol/l vs. 6,0 pmol/l, p<0,001). The combination of Troponin and Copeptin at initial presentation resulted in an area under the receiver-operating characteristic curve of 0,97 (95% confidence interval: 0,95 to 0,98), which was significantly higher than the 0,86 (95% confidence interval: 0,80 to 0,92) for Troponin alone (p<0,001). A Copeptin level < 14 pmol/l in combination with a Troponin ? 0,01 µg/l correctly ruled out AMI with a sensitivity of 98,8% and a negative predictive value of 99,7%.

Copeptin, the C-terminal part of the vasopressin prohormone, is a marker of acute endogenous stress. Arginine vasopressin (AVP) is a key hormone in the human body. Despite the clinical relevance of AVP in maintaining fluid balance and vascular tone, measurement of mature AVP is difficult and subject to preanalytical errors. Recently, Copeptin, a 39-amino acid glycopeptide that comprises the C-terminal part of the AVP precursor (CT-proAVP), was found to be a stable and sensitive surrogate marker for AVP release, analogous to C-peptide for insulin. Copeptin measurement has been shown to be useful in various clinical indications, including the diagnosis of diabetes insipidus and the monitoring of sepsis and cardiovascular diseases.

Copeptin is scheduled for fall introduction on the European market and joins a series of excellent BRAHMS biomarkers for cardiovascular diseases. The study results were already presented in a Late Breaking Clinical Trial Session at the ACC-Meeting in March. It marks the third time in just a few months that BRAHMS, with a new cardiac marker, succeeded in joining a Late Breaking Clinical Trial Session at a major cardiology congress.

The BRAHMS Aktiengesellschaft conducts researches, develops, produces and markets innovative diagnostic biomarkers. It is one of the three largest biotechnology companies in Germany. The company sells its products in more than 65 countries via its own subsidiary companies and sales organizations as well as laboratory systems from its own production and globally operating licensees. The headquarter of BRAHMS is at Hennigsdorf / Berlin, where about 220 out of 400 of the world wide employees of the company are posted.

lactate dehydrogenase

Peak in  72 hours

Lactate dehydrogenase catalyses the conversion of pyruvate to lactate. LDH-1 isozyme is normally found in the heart muscle and LDH-2 is found predominately in blood serum. A high LDH-1 level to LDH-2 suggest MI. LDH levels are also high in tissue breakdown or hemolysis. It can mean cancer, meningitis, encephalitis, or HIV. this usually back to normal 10–14 days.

5.

(AST) This was the first used.It is not specific for heart damage, and it is also one of the liver function tests.

6.

Rinsing in 2 hours.

Myoglobin is used less than the other markers. Myoglobin is the primary oxygen-carrying pigment of muscle tissue. It is high when muscle tissue is damaged but it lacks specificity. It has the advantage of responding very rapidly, rising and falling earlier than CK-MB or troponin. It also has been used in assessing reperfusion after thrombolysis.

7.

(IMA) low specificity IMA can be detected via the albumin cobalt binding (ACB) test, a limited available FDA approved assay. Myocardial ischemia alters the N-terminus of albumin reducing the ability of cobalt to bind to albumin. IMA measures ischemia in the blood vessels and thus returns results in minutes rather than traditional markers of necrosis that take hours. ACB test has low specificity therefore generating high number of false positives and must be used in conjunction with typical acute approaches such as ECG and physical exam. Additional studies are required.

8.

High sensitivity and specificity early after chest pain.Glycogenphosphorylaseisoenzyme BB (abbreviation: GPBB) is an isoenzyme of glycogen phosphorylase. Glycogen phosphorylase exists in 3 isoforms. One of these Isoforms is GP-BB. This isoform exists in heart and brain tissue. Because of the blood-brain barrier GP-BB can be seen as heart muscle specifc. During the process of ischemia, GP-BB is converted into a soluble form and is released into the blood. This isoform of the enzyme exists in cardiac (heart) and brain tissue. GP-BB is one of the “new cardiac markers” which are discussed to improve early diagnosis in acute coronary syndrome. A rapid rise in blood levels can be seen in myocardial infarction and unstable angina. GP-BB elevated 1-3 hours after process of ischemia.

ADIPONECTIN IS AN adipocyte-derived protein that has gainedconsiderable interest due to its positive effects on insulinsensitivity , atherosclerosis , and inflammation , hereby linking adipose tissue with the cornerstones of themetabolic syndrome.

There is substantial experimental and clinical evidence thatadiponectin protects the vascular endothelium against the processesleading to atherosclerosis. Experimentally, adiponectinknockout animals show an increased neointimal formation aftervascular injury as compared with wild-type littermates ,whereas adiponectin-deficient mice infected with an adenovirusoverexpressing mouse adiponectin showed a normal vascular responseto injury . Furthermore, in the ApoE-deficient mouse, a modelof accelerated atherosclerosis, breeding with adiponectin transgenicmice inhibited the progression of atherosclerosis despite anunaltered glucose and lipid metabolism, suggesting that adiponectinpossessed direct antiatherogenicactions .

In keeping with the experimental support for a vasoprotectiveeffect of adiponectin, several clinical investigations basedon cross-sectional study cohorts have reported on reduced circulatingadiponectin levels in patients with verified coronary heartdisease (CHD). However, some studies have not beenable to demonstrate an association between low levels of adiponectinand an increased risk for CHD , and others have shown thatthe relationship becomes insignificant after adjustment forhigh-density lipoprotein (HDL) cholesterol . On theother hand, nested case control studies have shown that healthysubjects with adiponectin levels within the upper 20% rangehave a 2-fold reduced risk for myocardial infarction  anda 7-fold reduced risk for progression of coronary artery calcification. We are not aware of studies describing the relationshipbetween adiponectin and the risk for CHD in population-basedcohorts.

Insulin resistance is a major risk factor for the developmentof atherosclerosis , and it also affects plasma levelsof adiponectin, which become gradually decreased with increasinginsulin resistance . Although adiponectin exerts potentinsulin-sensitizing actions in experimental in vivo models, it remains to be clarified whether the inverse associationbetween adiponectin and insulin sensitivity is a cause-effectrelationship. Thus, it could be speculated that the observedrelationship between adiponectin and the risk for CHD simplyreflects changes in insulin sensitivity. Based on these considerations,we found it of interest to study the risk for CHD and its relationshipwith plasma adiponectin and measures of insulin sensitivityin a population-based cohort of healthy 70-yr-old men followedfor more than 10 yr.

Adrenomedullinis a 52-amino acid peptide originally isolatedfrom pheochromocytoma cells. It has been detected in arange of tissues, including the heart, vasculature, kidney,adrenal medulla, lung, and brain. In experimental heartfailure, adrenomedullin expression is increased and peptidelevels rise, and administered peptide has powerful vasodilatoreffects, increases cardiac output and is natriuretic.Plasma concentrations are in the low picomolar range in healthyindividuals, but they increase in those with hypertension andcongestive heart failure (CHF) in proportion to the severityof the disease. In heart failure, plasma adrenomedullinis inversely related to left ventricular ejection fraction (LVEF)and is positively associated with left ventricular (LV) end-diastolicpressure. At least two reports have indicated that plasmaadrenomedullin levels act as an indicator of prognosis afteracute MI.

There are no published data relating plasma concentrations ofeither N-BNP or adrenomedullin to cardiovascular prognosis inpatients with established ischemic LV dysfunction. We hypothesizedthat plasma levels of either or both peptides would have independentprognostic utility in such patients and also assist in predictingany benefit from treatment with carvedilol. We report the resultsfrom 297 patients with ischemic LV impairment who were randomlyassigned to treatment with carvedilol or placebo for CHF

Kinetics of cardiac markers in myocardial infarction with or without reperfusion treatment.

References

1. The Joint European Society of Cardiology/American College of Cardiology Committee. Myocardial infarction redefined – a consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am CollCardiol 2000;36:959-69.

2. Schroeder JS, Lamb IH, Hu M. Do patients in whom myocardial infarction has been ruled out have a better prognosis after hospitalization than those surviving infarction? N Engl J Med 1980;303:1-5.

3. Hamm CW, Braunwald E. A classification of unstable angina revisited. Circulation 2000;102:118-22.

4. Pennell JP. Optimizing medical management of patients with pre-end-stage renal disease. Am J Med 2001;111:559-68.

5. Chen HH, Burnett JC Jr. The natriuretic peptides in heart failure: diagnostic and therapeutic potentials. ProcAssoc Am Physicians 1999;111:406-16.

6. Ridker PM. High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation 2001;103:1813-8.

7. Campbell B, Badrick T, Flatman R, Kanowski D. Limited clinical utility of high-sensitivity plasma C-reactive protein assays. Ann ClinBiochem 2002;39:85-8. BRAHMS Aktiengesellschaft

http://www.innovations-report.com/html/reports/life_sciences/cardiac_marker_copeptin_accelerates_diagnosis_acute_135172.html

9..for cardiac markers refrencereanges.

10.http://content.onlinejacc.org/cgi/content/full/37/7/1781.foradrenomedullin.