New research shows how a bacterial community evolves to survive hostile host defenses in the body. (Credit: Image courtesy of University of Cincinnati Academic Health Center)

University of Cincinnati Academic Health Center, May 18, 2010   —   An international team led by a University of Cincinnati (UC) researcher has shown how a bacterial community evolves to survive hostile host defenses in the body.

The team, led by Malak Kotb, PhD, chair of UC’s of molecular genetics, biochemistry and microbiology department, analyzed the evolution over time of the community structure of Group A streptococcus (also known as GAS or Strep A), a bacterium often found in the throat or on the skin. It can cause many human diseases, ranging from strep throat to debilitating and often deadly diseases of the heart, skin, kidney and brain.

In the 1980s, hypervirulent strains of the Strep A bacteria emerged, including necrotizing fasciitis (commonly known as the flesh-eating disease), an invasive GAS that is an infection of the deeper layers of skin and subcutaneous tissue. About 9,000 to 11,500 cases of invasive GAS disease — in which bacteria get into parts of the body where bacteria usually are not found — occur each year in the United States, resulting in 1,000 to 1,800 deaths annually, according to the Centers for Disease Control and Prevention (CDC). In Greater Cincinnati, there have been several highly publicized cases associated with death or amputation.

The research team’s findings appear in PLoS ONE, an open-access online journal of peer-reviewed articles.

“This is the first organized attempt to capture the dynamics of bacterial evolution in live species and to discover molecular events that are associated with stark changes in the demographics of the bacterial community as they sacrifice the majority of their members and select the fittest ones to survive host defenses,” says Kotb, who is also director of the Midwest Center for Emerging Infectious Diseases (MI-CEID).

Researchers found that as dominant members of the population surrendered to host immune defenses, they were replaced by a hyperaggressive, mutant minority population that thrived and took over the abandoned community to become the new majority.

Using a mouse model, the team monitored evolutionary changes in the bacterial community as it faced different environmental factors and attempted to adapt to different host niches. The data confirmed that the bacterial community is mixed and that under certain conditions different populations can take over the community.

“What we perceive as a single bacterial colony is in fact a mixture of subpopulations whose members play different roles to achieve virulence,” says study author Ramy Aziz, PhD, of Cairo University’s department of microbiology and immunology. “The survivors, it turns out, have the final word.”

Authors call the study a first step toward exploring the sociomicrobiology of invasive Group A streptococci within a living organism. They plan to follow with single cell studies of bacteria associated with immune cells to further dissect the different roles played by members of the same bacterial community.

The study was supported by grants from the National Institutes of Health (NIH) National Institute of Allergy and Infectious Diseases (NIAID); the United States Army Medical Research Activity; the Research and Development Office, Medical Research Service, Department of Veterans Affairs; and the National Health and Merit Research Council of Australia.

Cincinnati researchers on the team, in addition to Kotb, included Bruce Aronow, PhD, co-director of the Computational Medicine Center, a collaboration between Cincinnati Children’s Hospital Medical Center and the University of Cincinnati; and Rita Kansal, PhD, and Sarah Rowe, members of Kotb’s lab at UC.

Source:  University of Cincinnati Academic Health Center

Journal Reference:

  1. 1.                     Ramy K. Aziz, Rita Kansal, Bruce J. Aronow, William L. Taylor, Sarah L. Rowe, Michael Kubal, Gursharan S. Chhatwal, Mark J. Walker, Malak Kotb, Niyaz Ahmed. Microevolution of Group A Streptococci In Vivo: Capturing Regulatory Networks Engaged in Sociomicrobiology, Niche Adaptation, and Hypervirulence. PLoS ONE, 2010; 5 (4): e9798 DOI: 10.1371/journal.pone.0009798

New research supports the idea of “a-ha” moments in the brain that are

associated with sudden insight. (Credit: iStockphoto/Kutay Tanir)

ScienceDaily.com, May 17, 2010  —  A recent study provides intriguing information about the neural dynamics underlying behavioral changes associated with the development of new problem solving strategies. The research, published by the Cell Press in the May 13 issue of the journal Neuron, supports the idea of “a-ha” moments in the brain that are associated with sudden insight.

Our daily lives are filled with changes that force us to abandon old behavioral strategies that are no longer advantageous and develop new, more appropriate responses. While it is clear that new rules are often deduced through trial-and-error learning, the neural dynamics that underlie the change from a familiar to a novel rule are not well understood.

“The ability of animals and humans to infer and apply new rules in order to maximize reward relies critically on the frontal lobes,” explains one of the researchers who led the study, Dr. Jeremy K. Seamans from the Brain Research Centre at the University of British Columbia (UBC) and Vancouver Coastal Health Research Institute. “In our study, we examined how groups of frontal cortex neurons in rat brains switch from encoding a familiar rule to a completely novel rule that could only be deduced through trial and error.”

Specifically, Dr. Seamans with colleagues from UBC and collaborator Dr. Daniel Durstewitz from the Central Institute of Mental Health in Germany were interested in determining whether networks of neurons change their activity in a slow gradual way as an old strategy is abandoned and a new one is learned or whether there is a more abrupt transition.

Using sophisticated statistical techniques to study ensembles of neurons in the medial frontal cortex on a trial-by-trial basis as rats deduced a novel rule in a specially designed task, they found that the same populations of neurons formed unique network states that corresponded to familiar and novel rules. Interestingly, although it took many trials for the animals to figure out the new rule, the recorded ensembles did not change gradually but instead exhibited a rather abrupt transition to a new pattern that corresponded directly to the shift in behavior, as if the network had experienced an “a-ha” moment.

Taken together, these findings provide concrete support for sudden transitions between neural states rather than slow, gradual changes. “In the present problem solving context where the animal had to infer a new rule by accumulating evidence through trial and error, such sudden neural and behavioral transitions may correspond to moments of ‘sudden insight,'” concludes Dr. Durstewitz.

The researchers include Daniel Durstewitz, University of Heidelberg, Mannheim, Germany; Nicole M. Vittoz, University of British Columbia, Vancouver, Canada; Stan B. Floresco, University of British Columbia, Vancouver, Canada; and Jeremy K. Seamans, University of British Columbia, Vancouver, Canada.


Story Source: 

Adapted from materials provided by Cell Press

Journal Reference:

  1. 1.                       Daniel Durstewitz, Nicole M. Vittoz, Stan B. Floresco, Jeremy K. Seamans. Abrupt Transitions between Prefrontal Neural Ensemble States Accompany Behavioral Transitions during Rule Learning. Neuron, 2010; 66 (3): 438-448 DOI: 10.1016/j.neuron.2010.03.029

This vintage engraving depicts the portrait of famed English naturalist Charles Darwin, whose theories of natural selection contributed to a greater understanding of biological evolution in the 19th century. This engraving was made by an unknown, uncredited artist after an 1869 photograph by J. Cameron. Published in a volume of Darwin‘s theories in 1874. (Credit: via iStockphoto)

Brandeis University, May 17, 2010  –  More than 150 years ago, Darwin proposed the theory of universal common ancestry (UCA), linking all forms of life by a shared genetic heritage from single-celled microorganisms to humans. Until now, the theory that makes ladybugs, oak trees, champagne yeast and humans distant relatives has remained beyond the scope of a formal test. Now, a Brandeis biochemist reports in Nature the results of the first large scale, quantitative test of the famous theory that underpins modern evolutionary biology.  The results of the study confirm that Darwin had it right all along. In his 1859 book, On the Origin of Species, the British naturalist proposed that, “all the organic beings which have ever lived on this earth have descended from some one primordial form.” Over the last century and a half, qualitative evidence for this theory has steadily grown, in the numerous, surprising transitional forms found in the fossil record, for example, and in the identification of sweeping fundamental biological similarities at the molecular level.  Still, rumblings among some evolutionary biologists have recently emerged questioning whether the evolutionary relationships among living organisms are best described by a single “family tree” or rather by multiple, interconnected trees — a “web of life.” Recent molecular evidence indicates that primordial life may have undergone rampant horizontal gene transfer, which occurs frequently today when single-celled organisms swap genes using mechanisms other than usual organismal reproduction. In that case, some scientists argue, early evolutionary relationships were web-like, making it possible that life sprang up independently from many ancestors.

According to biochemist Douglas Theobald, it doesn’t really matter. “Let’s say life originated independently multiple times, which UCA allows is possible,” said Theobald. “If so, the theory holds that a bottleneck occurred in evolution, with descendants of only one of the independent origins surviving until the present. Alternatively, separate populations could have merged, by exchanging enough genes over time to become a single species that eventually was ancestral to us all. Either way, all of life would still be genetically related.”  Harnessing powerful computational tools and applying Bayesian statistics, Theobald found that the evidence overwhelmingly supports UCA, regardless of horizontal gene transfer or multiple origins of life. Theobald said UCA is millions of times more probable than any theory of multiple independent ancestries.  “There have been major advances in biology over the last decade, with our ability to test Darwin’s theory in a way never before possible,” said Theobald. “The number of genetic sequences of individual organisms doubles every three years, and our computational power is much stronger now than it was even a few years ago.”  While other scientists have previously examined common ancestry more narrowly, for example, among only vertebrates, Theobald is the first to formally test Darwin’s theory across all three domains of life. The three domains include diverse life forms such as the Eukarya (organisms, including humans, yeast, and plants, whose cells have a DNA-containing nucleus) as well as Bacteria and Archaea (two distinct groups of unicellular microorganisms whose DNA floats around in the cell instead of in a nucleus).  Theobald studied a set of 23 universally conserved, essential proteins found in all known organisms. He chose to study four representative organisms from each of the three domains of life. For example, he researched the genetic links found among these proteins in archaeal microorganisms that produce marsh gas and methane in cows and the human gut; in fruit flies, humans, round worms, and baker’s yeast; and in bacteria like E. coli and the pathogen that causes tuberculosis.  Theobald’s study rests on several simple assumptions about how the diversity of modern proteins arose. First, he assumed that genetic copies of a protein can be multiplied during reproduction, such as when one parent gives a copy of one of their genes to several of their children. Second, he assumed that a process of replication and mutation over the eons may modify these proteins from their ancestral versions. These two factors, then, should have created the differences in the modern versions of these proteins we see throughout life today. Lastly, he assumed that genetic changes in one species don’t affect mutations in another species — for example, genetic mutations in kangaroos don’t affect those in humans.

What Theobald did not assume, however, was how far back these processes go in linking organisms genealogically. It is clear, say, that these processes are able to link the shared proteins found in all humans to each other genetically. But do the processes in these assumptions link humans to other animals? Do these processes link animals to other eukaryotes? Do these processes link eukaryotes to the other domains of life, bacteria and archaea? The answer to each of these questions turns out to be a resounding yes.

Just what did this universal common ancestor look like and where did it live? Theobald’s study doesn’t answer this question. Nevertheless, he speculated, “to us, it would most likely look like some sort of froth, perhaps living at the edge of the ocean, or deep in the ocean on a geothermal vent. At the molecular level, I’m sure it would have looked as complex and beautiful as modern life.”


Source:  Brandeis University

Journal Reference:  Douglas L. Theobald. A formal test of the theory of universal common ancestry. Nature, 2010; 465 (7295): 219 DOI: 10.1038/nature09014

FierceHealthcare.com, May 17, 2010  –  The number of children hospitalized for dangerous MRSA infections has exploded from two out of every 1,000 hospital admissions in 1999 to 21 out of 1,000 in 2008, according to a recent study published in this week’s Pediatrics.

Almost 30,000 children were hospitalized with MRSA infections at the 25 hospitals studied during the 10-year period. Although it isn’t clear whether MRSA caused their deaths or whether severity played a role, 374 of those infected died.

But in contrast to some other recent measures of MRSA rates, most of the children hospitalized had community acquired infections, pointing to more of an issue with antibiotic resistance than sub-par infection control. In particular, the study found a coinciding increase in use of clindamycin, an antibiotic that comes in easy-to-use pills and liquid, and smaller increases for two other antibiotics. Another drug effective against MRSA, vancomycin, is only available intravenously and its use decreased during the study.

The increasing use of clindamycin is concerning because in some regions MRSA is already becoming resistant to the drug, according to Dr. Jason Newland, the study’s lead author and an infectious disease physician at Children’s Mercy Hospitals and Clinics and the University of Missouri-Kansas City. Doctors need to use the antibiotic judiciously, he said.

ScienceDaily.com, May 17, 2010  —  Oxygen levels in the lab can permanently alter human embryonic stem (ES) cells, specifically inducing X chromosome inactivation in female cells, according to Whitehead Institute researchers. Human ES cells have been routinely created and maintained at atmospheric levels of oxygen, which is about 20%. Cells in the body are usually exposed to only 1-9% oxygen.

“When human ES cells are isolated at 20% oxygen, they are stressed and they inactivate one X chromosome in female cells,” says Founding Whitehead Member Rudolf Jaenisch. “This argues that the conventional way to make human ES cells is not optimal. We’re not saying our method is the only way or the best possible way, but it is better than the conventional method.”

These results are published in this week’s online issue of Cell.

Scientists are interested in human ES cells because they have the ability to mature into almost any cell type in the body, a trait known as pluripotency. Theoretically, this potential could be used to treat diseases or injuries.

“Also, human ES cells are the only tool we have to study the beginning of human development,” says Maisam Mitalipova, Director of the Whitehead Human Stem Cell Facility and designer of the study reported in Cell.

But human ES cells, even from the same cell lines, have been yielding different results in experiments. Inconsistent results may call into question an experiment’s methods or conclusions.

“The huge variation from lab to lab in culturing and isolating ES cells is one of the big problems in the field,” says Christopher Lengner, first author of the Cell paper and a postdoctoral researcher in the Jaenisch lab. “Just because of their growing conditions, the cells can be completely different from each other. So, we wanted to get back to the basics and really establish a ground state for how we isolate these cells and how we maintain them in the most pristine way possible.”

Human ES cells are usually derived from fertilized eggs that were designated for research by patients of in vitro fertilization (IVF) clinics. After an embryo grows to a ball of about 100 cells, researchers remove the ES cells. Traditionally, all of this work, from creating the fertilized eggs at the IVF clinic to the isolation and maintenance of the human ES cells in the lab, has been performed at atmospheric levels of oxygen. The resulting human ES cells display multiple differences in their genomes indicating they are at a slightly less flexible and pluripotent state than are mouse ES cells.

For example, after early random inactivation, female human ES cells always have the same X chromosome inactivated while mouse ES cells have two active X chromosomes until the cells begin differentiating, when one of the X chromosomes is randomly inactivated in each cell. X inactivation is vital for proper development in a female cell. If both X chromosomes are left active in an adult cell, the cell will have twice the expression of the X chromosome genes, which is fatal.

To test how oxygen levels during isolation and culture affect human ES cells, Mitalipova created six new human ES cell lines — two male and four female. Half of the cells isolated from each embryo were cultured in 20% oxygen, while the other half were created and maintained at 5% oxygen. The researchers then looked not only at the all of the genes expressed in these cells but also at their epigenetic state.

“When you expose the human ES cells to atmospheric oxygen for just a few days, the whole genome goes crazy — there are massive gene expression changes,” says Lengner.

But after a period of time the human ES cells adapt to the atmospheric oxygen and almost all of these changes normalized again, except for the X inactivation gene XIST, which remained strongly switched on. When Alexander Gimelbrant, who is Assistant Professor at Dana Farber Cancer Institute and co-first author of the article, checked, the female human ES cells exposed to 20% oxygen had one X chromosome permanently inactivated. However, the human ES cells derived at 5% oxygen did not exhibit the strong activation of the XIST gene, and both X chromosomes in the female cells remained active–an indication that these cells were in a more developmentally pristine state than their counterparts cultured in atmospheric oxygen.

Although this work focused on the effects of environmental oxygen levels, other factors may have similar negative effects on human ES cells.

“It seems that stress in general, like inefficiently freezing cells in the laboratory or embryos at the IVF clinic or manipulating the cells a lot, can make the cells inactivate an X chromosome and lose some pluripotency,” says Mitalipova.

Even if these stressors, including a high oxygen level, are eliminated, the human ES cells still are not as pluripotent as mouse ES cells.

However, in a paper published earlier this month in the Proceedings of the National Academy of Sciences (PNAS), Jacob Hanna in the Jaenisch lab describes two approaches to push existing and newly established human ES cells to the more pluripotent state seen in mouse ES cells. Hanna’s methods rely either on genes inserted into the ES cells’ DNA or on drugs added to the culture medium surrounding the cells, which appears to keep human ES cells in the more pluripotent state.

This research was supported by Hillel and Liliana Bachrach and Susan Whitehead.


Source:

Whitehead Institute for Biomedical Research. Original article written by Nicole Giese.


Journal References:

  1. Christopher J. Lengner, Alexander A. Gimelbrant, Jennifer A. Erwin, Albert Wu Cheng, Matthew G. Guenther, G. Grant Welstead, Raaji Alagappan, Garrett M. Frampton, Ping Xu, Julien Muffat, Sandro Santagata, Doug Powers, C. Brent Barrett, Richard A. Young, Jeannie T. Lee, Rudolf Jaenischsend, Maisam Mitalipova. Derivation of pre-X inactivation human embryonic stem cells under physiological oxygen concentrations. Cell, May 13, 2010 DOI: 10.1016/j.cell.2010.04.010
  2. Hanna et al. Human embryonic stem cells with biological and epigenetic characteristics similar to those of mouse ESCs. Proceedings of the National Academy of Sciences, 2010; DOI: 10.1073/pnas.1004584107

Heart failure affects nearly 5 million Americans. Roughly 550,000 people are diagnosed with heart failure each year. It is the leading cause of hospitalization in people older than 65.

What Is Heart Failure?

Heart failure does not mean the heart has stopped working. Rather, it means that the heart’s pumping power is weaker than normal. With heart failure, blood moves through the heart and body at a slower rate, and pressure in the heart increases. As a result, the heart cannot pump enough oxygen and nutrients to meet the body’s needs. The chambers of the heart respond by stretching to hold more blood to pump through the body or by becoming stiff and thickened. This helps to keep the blood moving for a short while but, in time, the heart muscle walls weaken and are unable to pump as strongly. As a result, the kidneys often respond by causing the body to retain fluid (water) and sodium. If fluid builds up in the arms, legs, ankles, feet, lungs, or other organs, the body becomes congested, and congestive heart failure is the term used to describe the condition.

What Causes Heart Failure?

Heart failure is caused by many conditions that damage the heart muscle, including:

  • Coronary artery disease. Coronary artery disease (CAD), a disease of the arteries that supply blood and oxygen to the heart, causes decreased blood flow to the heart muscle. If the arteries become blocked or severely narrowed, the heart becomes starved for oxygen and nutrients.
  • Heart attack. A heart attack occurs when a coronary artery becomes suddenly blocked, stopping the flow of blood to the heart muscle and damaging it. All or part of the heart muscle becomes cut off from its supply of oxygen. A heart attack damages the heart muscle, resulting in a scarred area that does not function properly.
  • Cardiomyopathy. Damage to the heart muscle from causes other than artery or blood flow problems, such as from infections or alcohol or drug abuse.
  • Conditions that overwork the heart. Conditions including high blood pressure, valve disease, thyroid disease, kidney disease, diabetes, or heart defects present at birth can all cause heart failure. In addition, heart failure can occur when several diseases or conditions are present at once.

What Are the Symptoms of Heart Failure?

You may not have any symptoms of heart failure, or the symptoms may be mild to severe. Symptoms can be constant or can come and go. The symptoms can include:

  • Congested lungs. Fluid back up in the lungs can cause shortness of breath with exercise or difficulty breathing at rest or when lying flat in bed. Lung congestion can also cause a dry, hacking cough or wheezing.
  • Fluid and water retention. Less blood to your kidneys causes fluid and water retention, resulting in swollen ankles, legs, abdomen (called edema), and weight gain. Symptoms may cause an increased need to urinate during the night. Bloating in your stomach may cause a loss of appetite or nausea.
  • Dizziness, fatigue, and weakness. Less blood to your major organs and muscles makes you feel tired and weak. Less blood to the brain can cause dizziness or confusion.
  • Rapid or irregular heartbeats. The heart beats faster to pump enough blood to the body. This can cause a fast or irregular heartbeat.

If you have heart failure, you may have one or all of these symptoms or you may have none of them. In addition, your symptoms may not be related to how weak your heart is; you may have many symptoms but your heart function may be only mildly weakened. Or you may have a more severely damaged heart but have no symptoms.

What Are the Types of Heart Failure?

Systolic dysfunction (or systolic heart failure) occurs when the heart muscle doesn’t contract with enough force, so there is less oxygen-rich blood that is pumped throughout the body.

Diastolic dysfunction (or diastolic heart failure) occurs when the heart contracts normally, but the ventricles do not relax properly or are stiff, and less blood enters the heart during normal filling.

A calculation done during an echocardiogram called the ejection fraction (EF) is used measure how well your heart pumps with each beat to help determine if systolic or diastolic dysfunction is present. Your doctor can discuss which condition you have.

How Is Heart Failure Diagnosed?

Your doctor will ask you many questions about your symptoms and medical history. You will be asked about any conditions you have that may cause heart failure (such as coronary artery disease, angina, diabetes, heart valve disease, and high blood pressure). You will be asked if you smoke, take drugs, drink alcohol (and how much you drink), and about what drugs you take.

You will also get a complete physical exam. Your doctor will listen to your heart and look for signs of heart failure as well as other illnesses that may have caused your heart muscle to weaken or stiffen.

Your doctor may also order other tests to determine the cause and severity of your heart failure. These include:

  • Blood tests. Blood tests are used to evaluate kidney and thyroid function as well as to check cholesterol levels and the presence of anemia. Anemia is a blood condition that occurs when there is not enough hemoglobin (the substance in red blood cells that enables the blood to transport oxygen through the body) in a person’s blood.
  • B-type Natriuretic Peptide (BNP) blood test. BNP is a substance secreted from the heart in response to changes in blood pressure that occur when heart failure develops or worsens. BNP blood levels increase when heart failure symptoms worsen, and decrease when the heart failure condition is stable. The BNP level in a person with heart failure — even someone whose condition is stable — is higher than in a person with normal heart function. BNP levels do not necessarily correlate with the severity of heart failure.
  • Chest X-ray. A chest X-ray shows the size of your heart and whether there is fluid build-up around the heart and lungs.
  • Echocardiogram. This test shows the heart’s movement.
  • Ejection fraction (EF). A test called the ejection fraction (EF) is used to measure how well your heart pumps with each beat to determine if systolic dysfunction or heart failure with preserved left ventricular function are present. Your doctor can discuss which condition is present in your heart.
  • Electrocardiogram (EKG or ECG) . An EKG records the electrical impulses traveling through the heart.
  • Cardiac catheterization.
  • Stress Test.

Other tests may be ordered, depending on your condition.

Electrocardiogram

Stress Test

Cardiac catheterization old standard” of heart disease tests.

  • Cardiac catheterization.

Echocardiogram

Is There a Treatment for Heart Failure?

Today there are more treatment options available for heart failure than ever before. Tight control over your medications and lifestyle coupled with careful monitoring are the first steps. As the condition progresses, doctors specializing in the treatment of heart failure can offer more advanced treatment options.

The goals of treating heart failure are primarily to decrease the likelihood of disease progression (thereby decreasing the risk of death and the need for hospitalization), to lessen symptoms, and to improve quality of life.

Together, you and your doctor can determine the best course of treatment for you.

Stages of Heart Failure

In 2001, the American Heart Association (AHA) and American College of Cardiology (ACC) developed the “Stages of Heart Failure.” These stages, which were updated in 2005, will help you understand that heart failure is often a progressive condition and can worsen over time. They will also help you understand why a new medication was added to your treatment plan and may help you understand why lifestyle changes and other treatments are needed.

The stages classified by the AHA and ACC are different than the New York Heart Association (NYHA) clinical classifications of heart failure that rank patients as class I-II-III-IV, according to the degree of symptoms or functional limits. Ask your doctor what stage of heart failure you are in.

Check the table below to see if your therapy matches what the AHA and ACC recommend. Note that you cannot go backward in stage, only forward.

The table below outlines a basic plan of care that may or may not apply to you, based on the cause of your heart failure and your special needs. Ask your doctor to explain therapies that are listed if you do not understand why you are or are not receiving them.

Stage Definition of Stage Usual Treatments
Stage A People at high risk of developing heart failure (pre-heart failure), including people with:

  • High blood pressure
  • Diabetes
  • Coronary artery disease
  • Metabolic syndrome
  • History of cardiotoxic drug therapy
  • History of alcohol abuse
  • History of rheumatic fever
  • Family history of cardiomyopathy
Exercise regularly.

  • Quit smoking
  • Treat high blood pressure
  • Treat lipid disorders
  • Discontinue alcohol or illegal drug use
  • An angiotensin converting enzyme inhibitor (ACE inhibitor) or an angiotensin II receptor blocker (ARB) is prescribed if you’ve had a coronary artery disease or if you have diabetes, high blood pressure, or other vascular or cardiac conditions
  • Beta blockers may be prescribed if you have high blood pressure or if you’ve had a previous heart attack
Stage B People diagnosed with systolic left ventricular dysfunction but who have never had symptoms of heart failure (pre-heart failure), including people with:

  • Prior heart attack
  • Valve disease
  • Cardiomyopathy

The diagnosis is usually made when an ejection fraction of less than 40% is found during an echocardiogram test.

  • Treatment methods above for Stage A apply
  • All patients should take an angiotensin converting enzyme inhibitor (ACE inhibitors) or angiotensin II receptor blocker (ARB)
  • Beta-blockers should be prescribed for patients after a heart attack
  • Surgery options for coronary artery repair and valve repair or replacement (as appropriate) should be discussed

If appropriate, surgery options should be discussed for patients who have had a heart attack.

Stage C Patients with known systolic heart failure and current or prior symptoms. Most common symptoms include:

  • Shortness of breath
  • Fatigue
  • Reduced ability to exercise
  • Treatment methods above for Stage A apply
  • All patients should take an angiotensin converting enzyme inhibitor (ACE inhibitors) and beta-blockers
  • African-American patients may be prescribed a hydralazine/nitrate combination if symptoms persist
  • Diuretics (water pills) and digoxin may be prescribed if symptoms persist
  • An aldosterone inhibitor may be prescribed when symptoms remain severe with other therapies
  • Restrict dietary sodium (salt)
  • Monitor weight
  • Restrict fluids (as appropriate)
  • Drugs that worsen the condition should be discontinued
  • As appropriate, cardiac resynchronization therapy (biventricular pacemaker) may be recommended
  • An implantable cardiac defibrillator (ICD) may be recommended
 
Stage D Patients with systolic heart failure and presence of advanced symptoms after receiving optimum medical care.
  • Treatment methods for Stages A, B & C apply
  • Patient should be evaluated to determine if the following treatments are available options: heart transplant, ventricular assist devices, surgery options, research therapies, continuous infusion of intravenous inotropic drugs and end-of-life (palliative or hospice) care
 

 

How Can I Prevent Heart Failure From Worsening?

  • Keep your blood pressure low. In heart failure, the release of hormones causes the blood vessels to constrict or tighten. The heart must work hard to pump blood through the constricted vessels. It is important to keep your blood pressure as low as possible, so that your heart can pump effectively without extra stress.
  • Monitor your own symptoms. Check for changes in your fluid status by weighing yourself daily and checking for swelling. Call your doctor if you have unexplained weight gain (3 pounds in one day or 5 pounds in one week) or if you have increased swelling.
  • Maintain fluid balance. Your doctor may ask you to keep a record of the amount of fluids you drink or eat and how often you go to the bathroom. Remember, the more fluid you carry in your blood vessels, the harder your heart must work to pump excess fluid through your body. Limiting your fluid intake to less than 2 liters per day will help decrease the workload of your heart and prevent symptoms from recurring.
  • Limit how much salt (sodium) you eat. Sodium is found naturally in many foods we eat. It is also added for flavoring or to make food last longer. If you follow a low-sodium diet, you should have less fluid retention, less swelling, and breathe easier.
  • Monitor your weight and lose weight if needed. Learn what your “dry” or “ideal” weight is. Dry weight is your weight without extra water (fluid). Your goal is to keep your weight within 4 pounds of your dry weight. Weigh yourself at the same time each day, preferably in the morning, in similar clothing, after urinating but before eating, and on the same scale. Record your weight in a diary or calendar. If you gain two pounds in one day or five pounds in one week, call your doctor. Your doctor may want to adjust your medications.
  • Monitor your symptoms. Call your doctor if new symptoms occur or if your symptoms worsen. Do not wait for your symptoms to become so severe that you need to seek emergency treatment.
  • Take your medications as prescribed. Medications are used to improve your heart’s ability to pump blood, decrease stress on your heart, decrease the progression of heart failure, and prevent fluid retention. Many heart failure drugs are used to decrease the release of harmful hormones. These drugs will cause your blood vessels to dilate or relax (thereby lowering your blood pressure).
  • Schedule regular doctor appointments. During follow-up visits, your doctors will make sure you are staying healthy and that your heart failure is not getting worse. Your doctor will ask to review your weight record and list of medications. If you have questions, write them down and bring them to your appointment. Call your doctor if you have urgent questions. Notify all your doctors about your heart failure, medications, and any restrictions. Also, check with your heart doctor about any new medications prescribed by another doctor. Keep good records and bring them with you to each doctor visit.

 

How Can I Prevent Further Heart Damage?

In an effort to prevent further heart damage:

What Medications Should I Avoid if I Have Heart Failure?

There are several different types of medications that are best avoided in those with heart failure including:

  • Nonsteroidal anti-inflammatory medications such as Motrin or Aleve. For relief of aches, pains, or fever take Tylenol instead.
  • Most antiarrhythmic agents
  • Most calcium channel blockers (if you have systolic heart failure)
  • Some nutritional supplements, such as salt substitutes, and growth hormone therapies
  • Antacids that contain sodium (salt)
  • Decongestants such as Sudafed

If you are taking any of these drugs, discuss them with your doctor.

It is important to know the names of your medications, what they are used for, and how often and at what times you take them. Keep a list of your medications and bring them with you to each of your doctor visits. Never stop taking your medications without discussing it with your doctor. Even if you have no symptoms, your medications decrease the work of your heart so that it can pump more effectively.

How Can I Improve My Quality of Life With Heart Failure?

There are several things you can do to improve your quality of life if you have heart failure. Among them:

  • Eat a healthy diet. Limit your consumption of sodium (salt) to less than 2,000 milligrams (2 grams) each day. Eat foods high in fiber. Limit foods high in fat, cholesterol, and sugar. Reduce total daily intake of calories to lose weight if necessary.
  • Exercise regularly. A regular cardiovascular exercise program, prescribed by your doctor, will help improve symptoms and strength and make you feel better. It may also decrease heart failure progression.
  • Don’t overdo it. Plan your activities and include rest periods during the day. Certain activities, such as pushing or pulling heavy objects and shoveling may worsen heart failure and its symptoms.
  • Prevent respiratory infections. Ask your doctor about flu and pneumonia vaccines.
  • Take your medications as prescribed. Do not stop taking them without first contacting your doctor.
  • Get emotional or psychological support if needed. Heart failure can be difficult for your whole family. If you have questions, ask your doctor or nurse. If you need emotional support, social workers, psychologists, clergy, and heart failure support groups are a phone call away. Ask your doctor or nurse to point you in the right direction.

Can Surgery Be Used to Treat Heart Failure?

In heart failure, surgery is aimed at stopping further damage to the heart and improving the heart’s function. Procedures used include:

  • Coronary artery bypass grafting surgery. The most common surgery for heart failure is bypass surgery. Your doctor will determine if your heart failure is caused by coronary artery disease and if you have blockages that can be bypassed. Although surgery is more risky for people with heart failure, new strategies before, during, and after surgery have reduced the risks and improved outcomes.
  • Heart valve surgery . Diseased heart valves can be treated both surgically (traditional heart valve surgery) and non-surgically (balloon valvuloplasty).
  • Implantable left ventricular assist device (LVAD). The LVAD is known as the “bridge to transplantation” for patients who haven’t responded to other treatments and are hospitalized with severe systolic heart failure. This device helps your heart pump blood throughout your body. It allows you to be mobile, sometimes returning home to await a heart transplant. It may also be used as destination therapy for long-term support in patients who are not eligible for transplant.
  • Heart transplant. A heart transplant is considered when heart failure is so severe that it does not respond to all other therapies, but the person’s health is otherwise good.

 

Heart Failure Treatment Is a Team Effort

Heart failure management is a team effort, and you are the key player on the team. Your heart doctor will prescribe your medications and manage other medical problems. Other team members — including nurses, dietitians, pharmacists, exercise specialists, and social workers — will help you achieve success. But it is up to YOU to take your medications, make dietary changes, live a healthy lifestyle, keep your follow-up appointments, and be an active member of the team.

What Is the Outlook for People With Heart Failure?

With the right care, heart failure will not stop you from doing the things you enjoy. Your prognosis or outlook for the future will depend on how well your heart muscle is functioning, your symptoms, and how well you respond to and follow your treatment plan.

Everyone with a long-term illness, such as heart failure, should discuss their desires for extended medical care with their doctor and family. An “advance directive” or “living will” is one way to let everyone know your wishes. A living will expresses your desires about the use of medical treatments to prolong your life. This document is prepared while you are fully competent in case you are unable to make these decisions at a later time.