The heart is like any other muscle, requiring blood to supply oxygen and nutrients for it to function. It beats about 100,000 times a day, pumping blood through your circulatory system. The cycle of pumping blood throughout your body carries fresh oxygen to your lungs and nutrients to your body’s tissues. Blood also takes waste, such as carbon dioxide, away from your tissues,. Without this process, we could not live.  The heart pumps and circulates 5 or 6 gallons of blood each minute through the entire body.

Graphic: MedicineNet.com

 

By Crystal Phend, Senior Staff Writer, MedPage Today
Published: October 18, 2011
Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner

 

Video Source: JAMA

MedPageToday.com, October 19, 2011  —  Heart failure hospitalizations dropped 29.5% nationally over the past decade, largely because fewer patients were admitted rather than fewer admissions per patient, researchers found.

The risk-adjusted rate of heart failure hospitalization fell from 2,845 to 2,007 per 100,000 person-years from 1998 to 2008 (P<0.001) in a fee-for-service Medicare claims analysis by Jersey Chen, MD, MPH, of Yale University, and colleagues.

That decline — the first ever documented in the U.S. — likely saved $4.1 billion in Medicare costs since 1998, they reported in the Oct. 19 issue of the Journal of the American Medical Association.

Lower incidence of heart failure risk factors; modest improvements in blood pressure control; better use of evidence-based therapies; and a shift toward outpatient management of heart failure may have been contributing factors, the group suggested.

The main reason for the drop in hospitalizations was fewer unique patients hospitalized for heart failure, down from 2,014 per 100,000 in 1998 to 1,462 per 100,000 in 2008.

One-year mortality after heart failure hospitalization also dropped modestly by a relative 6.6% over the same period, from a risk-adjusted rate of 31.7% to 29.6% (P<0.001).

An accompanying editorial pointed to the results as a sign of hope, though with plenty of room for improvement.

The “persistently” and “unacceptably” high one-year mortality rates suggested a need for immediate attention to heart failure postdischarge practices, wrote Mihai Gheorghiade, MD, of Northwestern University in Chicago, and Eugene Braunwald, MD, Brigham and Women’s Hospital and Harvard in Boston.

They suggested the following strategies:

  • Using more aggressive treatment for subclinical congestion
  • Taking a mechanistic approach to underlying cardiac abnormalities
  • Boosting use of digoxin and mineralocorticoid antagonists
  • Scheduling an early postdischarge visit

“There is more work to be done,” agreed Ralph Brindis, MD, immediate past-president of the American College of Cardiology, in a statement. While overall trends are on the right track, not all groups benefited equally, he noted.

When Chen’s group analyzed all heart failure hospitalizations nationally in a complete sample of Medicare fee-for-service claims from 1998 to 2008, they found that all sex and race groups showed reductions in heart failure hospitalizations.

But black men had the lowest rate of decline, with heart failure hospitalizations falling from 4,142 to 3,201 per 100,000 person-years over the study period. This improvement was a significant 19% less than other groups after adjusting for age.

The rates didn’t fall evenly across states either.

Heart failure hospitalization changes happened significantly slower than the national mean in three states: Connecticut, Rhode Island, and Wyoming. One-year mortality rates actually increased in five states: South Dakota, Arizona, Alaska, Louisiana, and Kentucky.

“We must continue to work to understand the causes of these disparities in outcomes and continue to apply what we learn through research to improve care and prevention across the board,” Brindis said in the statement.

The researchers cautioned that the study could not determine causality for any of the findings.

Other limitations were sole inclusion of a Medicare population, which may differ in heart failure hospitalization and mortality trends from a younger population with different insurance, and use of administrative codes not confirmed clinically.

The study was supported by awards from the Agency for Healthcare Research and Quality and the National Heart, Lung, Blood Institute Cardiovascular Outcomes Center.

Chen and several co-authors reported that they develop and maintain performance measures under contract with the Centers for Medicare & Medicaid Services.

One co-author reported receiving consulting fees from Yale University. Another reported chairing a cardiac scientific advisory board for United Healthcare and receiving a research grant from Medtronic through Yale University.

Gheorghiade reported receiving consulting fees from Bayer, Novartis, Sigma Tau, Johnson & Johnson, Takeda, Otsuka, and Medtronic.

Braunwald reported having no conflicts of interest to disclose.

From the American Heart Association:

 


Primary source: Journal of the American Medical Association
Source reference:
Chen J, et al “National and regional trends in heart failure hospitalization and mortality rates for Medicare beneficiaries, 1998-2008” JAMA 2011; 306: 1669-1678.

Additional source: Journal of the American Medical Association
Source reference:
Gheorghiade M, Braunwald E “Hospitalizations for heart failure in the United States — A sign of hope” JAMA 2011; 306: 1705-1706.


 

 

 

What is Heart Failure?

 

Heart failure is the condition resulting from the heart’s inability to pump an adequate amount of blood through the body. Heart failure may be sudden, but may also develop slowly and gradually over many years. But in either case, the condition cases the heart to lose its ability to work and pump blood efficiently.

The result is that the body doesn’t get as much oxygen and nutrients as it needs, leading to problems like fatigue, loss of appetite, and kidney failure. Blood backs up behind the heart, leading to increased pressure or fluid in the lungs. This causes shortness of breath. The body also often holds on to fluid. Heart failure is usually a chronic, long-term condition that is managed with medications and lifestyle changes.

Types of Heart Failure

The two main categories of heart failure are systolic heart failure and diastolic heart failure.

Systolic heart failure is when heart failure is caused by the heart not contracting well. The heart can’t pump with enough force to push enough blood into the circulation. As a result, blood coming into the heart from the lungs can back up, causing fluid to leak into the lungs.

This is the most common type of heart failure, and the one doctors can treat and understand the best.

Diastolic heart failure is a different disease — it’s the heart not relaxing well. Very often, it’s associated with high blood pressure and a thick heart. This form may lead to fluid accumulation, especially in the feet, ankles, and legs. Some patients may have lung congestion. Although doctors can treat blood pressure and fluid volume, there are not as many treatment options for this type of heart failure.

 

 

 

Heart Diagnostic Test: Echocardiogram

 

 

Doctors may want to use echocardiography to detect heart disease. Echocardiography uses sound waves to generate images of the heart. The test serves as a tool to see how well the heart muscle is functioning. A normal heart pushes at least 50%-60% of the blood in the ventricle out to the body when it beats. Echocardiography can show if the heart muscle is weaker than this, which could indicate heart disease.

 

 

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Residual Damage After Heart Attack No Longer Inevitable

Residual damage after heart attack no longer inevitable – MedUni Vienna unveils revolutionary approach to treatment (Credit: Image courtesy of Medical University of Vienna)

 

 

 

ScienceDaily.com, (October, 2011) — A new treatment could revolutionize the treatment of patients after a heart attack. Hendrik Jan Ankersmit from the Medical University of Vienna has developed a protein solution which can be used to reduce the scarring of tissue caused by inflammation after a heart attack.

In 2009, 16,000 people were admitted to Austrian hospitals with an acute myocardial infarction, with 3,000 of them dying (source: Statistik Austria). Comparable figures from the European Union reveal 2.2 million deaths caused by ischaemic heart disease (source: WHO). Following the usually critical first phase of a heart attack, intensive rehabilitation is carried out and there is a risk of heart failure.

The results of the research carried out by Hendrik Jan Ankersmit, head of the CD Laboratory for Heart and Thorax Diagnosis and Regeneration at the MedUni Vienna, show that this need no longer be the case. Ankersmit has used white blood cells to create a protein solution (APOSEC™) that can be used as a drug during the acute therapy phase following a heart attack. In laboratory tests, the solution was administered as an intravenous infusion 40 minutes after an experimental infarction. As a result, there was virtually no scarring of the heart muscle.

APOSEC™ works by inhibiting the cardiac tissue’s inflammatory response following a heart attack. Tests on human cardiac muscle cells — with highly promising results — have already been carried out in vitro. Researchers at the MedUni Vienna are hoping to start a series of clinical studies on humans in the near future.

Like blood in a blood bank — available at all times APOSEC™ contains soluble proteins that are excreted by white blood cells. Harvesting white blood cells for use as ‘bio-reactors’ is as simple as taking blood. “With protein concentrates, there is little or no defense reaction from the body’s immune system. APOSEC™ can therefore be obtained even from unrelated donors,” says Ankersmit.

An even greater potential advantage over the conventional stem-cell-based treatment of myocardial infarctions is that the APOSEC™ protein solution can be produced in advance and stored for ready access, just like blood in a blood bank. In the event of an acute infarction, the patient can be treated immediately.

 

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Scientist Discovers Genetic Factor Implicated in Heartbeat Defect

 

In this view of a mouse heart, electrical impulses — which control the synchronization of the animal’s heartbeat — travel along a dedicated network of cardiac cells (dyed in blue), in order to pump blood efficiently to the rest of the body. When heartbeats fall out of sync–in mice or humans–potentially fatal heart arrhythmias can develop. (Credit: Image courtesy of Gladstone Institutes)

 

 

 

The Gladstone Institute, Summer/Fall 2011 (SAN FRANCISCO)  —  A team of scientists, including researchers at the Gladstone Institutes has discovered how gene regulation can make hearts beat out of sync, offering new hope for the millions who suffer from a potentially fatal heart condition.

In a paper being published this week in the online Early Edition of the Proceedings of the National Academy of Sciences, the scientists announce the identity of the molecular regulator that uses electrical impulses to synchronize each heartbeat.

Abnormalities in heartbeat synchronization, called heart arrhythmias, are a cause of death for the 5.7 million Americans who suffer from heart failure, a condition in which the heart can’t pump enough blood to meet the body’s needs. At least 300,000 people die of heart failure each year in the United States alone.

“This is important progress for a better understanding of heart arrhythmias, which when combined with heart failure can be fatal,” said Deepak Srivastava, MD, who directs all cardiovascular research at Gladstone. “This is the first published research about a genetic regulator that coordinates the timing of the electrical impulses that make the heart beat properly.”

In many animals, including humans, electrical impulses must spread rapidly and in a coordinated fashion along a dedicated network of cardiac cells in order for the heart to pump blood efficiently to the rest of the body.

A genetic regulator, called Irx3, coordinates these impulses. When the research team switched off the Irx3 gene in mice, the heart’s pumping fell out of sync. The electrical impulses — which normally follow a rapid path throughout the heart — diffused slowly and had trouble reaching their intended destinations. The mice developed arrhythmias as the heart’s chambers lost the capacity to beat in time.

Gladstone Investigator Benoit G. Bruneau, PhD, who is also a professor of pediatrics at the University of California San Francisco (UCSF), conducted the research in collaboration with scientists at Canadian labs, including those from the Hospital for Sick Children in Toronto and the University of Toronto. Gladstone, which is affiliated with UCSF, is a leading and independent biomedical-research organization that focuses on cardiovascular disease, neurodegenerative disease and viral infections.

“These findings have potential implications for the prevention and treatment of human heart disease, once we better understand Irx3’s role in the human heart,” said Dr. Bruneau. “An important avenue to explore could be whether humans with arrhythmias have mutations in the Irx3 gene.

“Now that we know the importance of Irx3,” Dr. Bruneau added, “We need to dig deeper to see if it’s possible to use drug therapy to target any of the electrical-impulse pathways that Irx3 regulates with drug therapy.”

Other scientists who participated in the research at Gladstone include Shan-Shan Zhang, Paul Delgado-Olguín, Nathalie Gaborit, Tatyana Sukonnik and John N. Wylie. Funding came from a wide variety of organizations including the American Heart Association, the National Institutes of Health, William H. Younger, Jr. Family Foundation and the American Recovery and Reinvestment Act of 2009.

Dr. Bruneau is a senior investigator at the Gladstone Institute of Cardiovascular Disease and a UCSF professor of pediatrics. He also holds the William H. Younger, Jr., endowed chair in cardiovascular disease, and is the recipient of the Lawrence J. and Florence A. DeGeorge Charitable Trust/American Heart Association Established Investigator Award. His research focuses on the regulation of genes that are important for fetal heart development, and the abnormal genetic functions that lead to congenital heart disease.

Journal Reference:

  1. 1.                Shan-Shan Zhang, Kyoung-Han Kim, Anna Rosen, James W. Smyth, Rui Sakuma, Paul Delgado-Olguín, Mark Davis, Neil C. Chi, Vijitha Puviindran, Nathalie Gaborit, Tatyana Sukonnik, John N. Wylie, Koroboshka Brand-Arzamendi, Gerrie P. Farman, Jieun Kim, Robert A. Rose, Phillip A. Marsden, Yonghong Zhu, Yu-Qing Zhou, Lucile Miquerol, R. Mark Henkelman, Didier Y. R. Stainier, Robin M. Shaw, Chi-Chung Hui, Benoit G. Bruneau, and Peter H. Backx. Iroquois homeobox gene 3 establishes fast conduction in the cardiac His–Purkinje network. Proceedings of the National Academy of Sciences, 2011; DOI: 10.1073/pnas.1106911108

 

The J. David Gladstone Institutes (the Gladstone Institutes) is a nonprofit, independent research and educational institution in San Francisco, consisting of the Gladstone Institute of Cardiovascular Disease, the Gladstone Institute of Virology and Immunology, and the Gladstone Institute of Neurological Disease, which conducts basic scientific research.[1] Independent in its governance, finances and research programs, Gladstone shares a close affiliation with the University of California, San Francisco (UCSF) through its faculty, who hold joint UCSF appointments.

 

 

To learn more about the Gladstone Institute of Cardiovascular Disease, click on the link, below

 

http://www.gladstone.ucsf.edu/gladstone/site/gicd/