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Tuesday, April 6, 2010
Friday, December 5, 2008
Mini Heart Attacks Lessen Damage From Major Ones
Mini Heart Attacks Lessen Damage From Major Ones
ScienceDaily (Dec. 3, 2008) — Researchers have discovered one potential mechanism by which briefly cutting off, then restoring, blood flow to arteries prior to a heart attack lessens the damage caused, according to a study published today in the journal Cardiovascular Research. The new mechanism points to how future drugs could provide protection ahead of heart attacks and strokes for those at highest risk.
In the nearer term, the work may help to prevent damage caused as U.S. heart surgeons temporarily cut off blood flow 450,000 times each year to perform coronary artery bypass graft surgeries. Lastly, the discoveries hold clues to the value of the Mediterranean diet beyond red wine.
In severely diseased coronary arteries, fatty deposits in blood vessel walls become more likely to rupture, which releases proteins into the blood that cause blood clots and cut off blood flow. When a vessel becomes completely blocked (ischemia) the downstream tissue begins to die for lack of oxygen and nutrients. Worse yet, when blood flow is restored (reperfusion), the returning blood throws off cellular chemistry, creating as a side-product a burst of highly reactive "free radicals" that tear apart cell components and cause cells to self-destruct. Later in the process, the immune system attacks the cardiac tissue damaged by ischemia and reperfusion, causing inflammation which can lead to heart failure.
In 1986 then medical student Chuck Murry at Duke University first described a technique called ischemic preconditioning (IPC), which quickly cuts off then restores blood flow to the heart. He found that IPC somehow protected heart tissue against the damage caused by subsequent, prolonged blood vessel blockages. An emerging theory holds that this natural early warning system of IPC has evolved to protect against heart attack. Labs worldwide are seeking to re-create or strengthen this natural protection against ischemia/reperfusion (IR) injury. In the current study, researchers for the first time determined that IPC caused more of a key molecule, nitro-linoleic acid (LNO2), to be made in ischemic cells.
"LNO2 appears to be important in the mechanism by which IPC triggers the body's natural defense mechanisms against heart attack before the major attack comes," said Paul S. Brookes, Ph.D., associate professor of Anesthesiology and of Pharmacology and Physiology at the University of Rochester Medical Center. "Obviously, this natural response, when it follows a major heart attack, is often too little too late. Our hope is that boosting the effect in patients at high risk, perhaps by administering LNO2 beforehand, will reduce heart attack damage in the future. Even sooner, we may be able dramatically reduce reperfusion injury suffered in surgical settings."
Study Details
Going into the study, the mechanisms underlying IPC protection were controversial, but a consensus had emerged recently that mitochondria were involved. The cell's powerhouse, mitochondria use oxygen to convert nutrients into cellular energy supply.
As they do so, they create a gradient of protons across their membranes. When the gradient becomes too large, it triggers the mitochondria to use oxygen to generate free radicals. The problem gets much worse when blood returns to a vessel after a blockage, bringing with it a surge of oxygen and nutrients.
It has long been thought that a group of proteins in the mitochondrial membrane act as a "safety valve" by dissipating too large proton gradients when necessary, which slows free radical generation. The current study identified a novel mechanism involving LNO2, by which IPC turns on this safety valve.
Given their results, the authors propose the following protective mechanism: temporary ischemia causes the generation of nitrated lipids inside the mitochondria via currently unknown mechanisms involving metabolites of the gas nitric oxide (NO). These lipids, including LNO2, then become attached to two proteins – adenine nucleotide translocase and uncoupling protein 2 – changing their shape such that they allow a proton leak across the mitochondrial membrane. The leak lowers the proton gradient just enough to lessen free radical production.
While the current study only looked at the immediate effects of LNO2 treatment, the literature suggests that LNO2 also limits the misplaced immune response seen after reperfusion, suggesting a dual treatment effect. Past studies found that LNO2 inhibits Nfkappa B, a protein known to switch on genes that drive inflammation. LNO2 also activates peroxisome proliferator activated receptor gamma and heme oxygenase 1, both of which block inflammation.
The major finding of the study is that LNO2 is formed naturally in mitochondria during IPC in an isolated rat heart, and that adding extra LNO2 protects heart muscle cells from IR injury. The team measured the ability of isolated rat heart cells to survive ischemia using a dye that the live cells keep out, but that dead cells take in. That enabled researchers to count how many cells survived with and without LNO2 added.
In normal cells following ischemia 70 percent died, but for those receiving extra LNO2 (0.5 micromolar), only 30 percent died. The amount of the LNO2 added was not much more than naturally occurs, suggesting its effect is "extremely potent," researchers said. The LNO2-related proton leak also occurs at the protein level within seconds, a vital quality of any future therapy, considering that IR injury greatly increases with each second it is allowed to proceed.
Brookes is part of the Mitochondrial Research & Innovation Group (MRIG) at the Medical Center, which last year reported in the Journal of Molecular and Cellular Cardiology on the design and testing of a series of patented nitric oxide donors that break down and release NO only within the mitochondria, and protect the heart from ischemia. The team believes these NO donors may work in part by increasing LNO2 supply. In the acute setting, such drugs may offer an advantage over standard nitric oxide donors like nitroglycerin, which increase blood flow in diseased arteries by causing them to dilate throughout the body. Standard NO donors also depress cardiac function by decreasing the pressure of blood returning from the body back into the heart. Early tests in a mouse model have confirmed that the new MRIG NO donor drugs are cardioprotective in-vivo, and do not cause system-wide vessel dilation side effects.
Bruce Freeman, Ph.D., chair of the Department of Pharmacology & Chemical Biology at the University of Pittsburgh School of Medicine, also led the study. Other contributors included postdoctoral fellow Sergiy Nadtochiy, Ph.D. in Rochester, and Paul Baker, Ph.D. research assistant professor in Pittsburgh.
"Our interest in this area stems from the fact that many different stimuli appear to funnel down into the mitochondria where they may trigger LNO2 production, any of which may suggest a new way to prevent damage," Freeman said. "Along with IPC, olive oil has been shown to produce LNO2 in the stomach, offering an explanation for the value of the Mediterranean diet."
http://www.sciencedaily.com/releases/2008/12/081202080819.htm
Tuesday, December 2, 2008
Music and the Heart
Joyful Music in Tune With Heart Health
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By Amanda Gardner
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By Amanda Gardner
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HealthDay Reporter
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TUESDAY, Nov. 11 (HealthDay News) -- Throw on a little Bach, Beatles or Beyonce, and then sit back and relax in the knowledge that your blood vessels are expanding wide open, letting the blood flow freely.
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TUESDAY, Nov. 11 (HealthDay News) -- Throw on a little Bach, Beatles or Beyonce, and then sit back and relax in the knowledge that your blood vessels are expanding wide open, letting the blood flow freely.
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Nothing could be healthier for your heart, a new study suggests.
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Nothing could be healthier for your heart, a new study suggests.
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"Listening to music that makes you feel good may also be a good preventive measure for heart health," said study author Dr. Michael Miller, director of the Center for Preventive Cardiology at the University of Maryland Medical Center, in Baltimore. "There's no downside. It's simple, economic and it may pay off dividends in regard to a healthy heart."
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Added Dr. Carl Lavie, medical director of cardiac rehabilitation and prevention director of the Stress Testing Laboratory at the Ochsner Heart and Vascular Institute in New Orleans: "Although this was just an acute [short-term] study, it suggests that laughter and listening to relaxing music may provide cardioprotection or be heart-healthy. I suspect that the authors are correct in this theory. But the important thing to know is whether regular performance of this or similar activity would have long-term benefits on the cardiovascular system, similar to, superior, or additive to such things as regular aerobic exercise that has been extensively studied and proven to have substantial long-term benefits."
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Miller, who presented the findings Tuesday at the American Heart Association's annual scientific sessions, in New Orleans, said many people look at heart health in terms of negative risk factors that need to be overcome. "There are not a lot of positive risk factors," he noted.
Previous studies had found that music could affect heart rate and blood pressure. Prayer has also been shown to improve cardiac performance. And Miller's group previously found that laughter improved vascular health.
For the new study, 10 healthy, nonsmoking volunteers (70% of them men with a mean age of 36) selected music that made them feel good and other music that made them feel anxious. Selections differed according to the person. Participants also were asked to look at humorous video clips and relaxation audio tapes.
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Previous studies had found that music could affect heart rate and blood pressure. Prayer has also been shown to improve cardiac performance. And Miller's group previously found that laughter improved vascular health.
For the new study, 10 healthy, nonsmoking volunteers (70% of them men with a mean age of 36) selected music that made them feel good and other music that made them feel anxious. Selections differed according to the person. Participants also were asked to look at humorous video clips and relaxation audio tapes.
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The researchers measured brachial artery flow, in the forearm, using a blood pressure cuff, before and after each "stimulus."
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"In the minute after you release [the rubber bulb], you see how the inner lining of the blood vessel reacts, the endothelial response," Miller said. "People with risk factors for heart disease like smoking and hypertension don't dilate normally. We believe that means that their vasculature is not healthy."
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Among the study participants, brachial artery flow increased 26% during the joyful music phase and decreased 6% after listening to anxiety-producing music.
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Blood flow also increased 19% during the laughter (video clip) phase and 11% during relaxation.
Blood flow also increased 19% during the laughter (video clip) phase and 11% during relaxation.
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The increase in dilation seen after listening to joyful music was "about the same level we see after someone does aerobic activity. It's also similar to what we see after taking statin medication," Miller said. "The effect lasts for about an hour."
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The increase in dilation seen after listening to joyful music was "about the same level we see after someone does aerobic activity. It's also similar to what we see after taking statin medication," Miller said. "The effect lasts for about an hour."
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The positive effect may come from the release of endorphins, Miller speculated, referring to the body chemicals that block pain and ease anxiety and depression.
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"Clearly, the role of psychological risk factors, and particularly psychological stress, has been neglected in preventive cardiology," Lavie said. "Clearly, extreme emotional stress -- the classic example is public speaking, especially for novice speakers -- has the exact opposite effects as what Miller showed with laughter and relaxing music. Acute and chronic job stress also has deleterious effects which could be countered by laughter or relaxing music."
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"Clearly, the role of psychological risk factors, and particularly psychological stress, has been neglected in preventive cardiology," Lavie said. "Clearly, extreme emotional stress -- the classic example is public speaking, especially for novice speakers -- has the exact opposite effects as what Miller showed with laughter and relaxing music. Acute and chronic job stress also has deleterious effects which could be countered by laughter or relaxing music."
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SOURCES: Michael Miller, M.D., director, Center for Preventive Cardiology, University of Maryland Medical Center, Baltimore; Carl J. Lavie, M.D., medical director, cardiac rehabilitation, and prevention director, Stress Testing Laboratory, Ochsner Heart and Vascular Institute, New Orleans; Nov. 11, 2008, presentation, American Heart Association's annual scientific sessions, New Orleans
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Monday, December 1, 2008
Flu Shots Can Help Prevent Cardiac Death
The three-dimensional structure of influenza virus from electron tomography. The viruses are about 120 nanometers -- about one ten thousandth of a millimeter -- in diameter.
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Patients with heart disease ought to get flu shots, say the American Heart Association and the American College of Cardiology. A number of studies over the past few years suggest that patients with underlying heart disease (or even an increased risk of heart disease) who get flu vaccine substantially reduce their risk of cardiac death.
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In 2007, the American Heart Association (AHA) and the American College of Cardiology (ACC) joined forces to advise doctors to give flu shots to all their patients with cardiovascular disease. The message is especially aimed at cardiologists -- the doctors who are most likely to see these high-risk patients.
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This advisory is in compliance with guidelines for treating patients with cardiovascular disease, issued by the AHA and ACC in May, where influenza vaccination was recommended as routine preventative therapy for heart patients for the first time. This recommendation follows the results of several studies showing the benefits of flu vaccine in cardiac patients, studies that began appearing several years ago. In some reports, the risk of cardiovascular mortality was reduced as much as 50% in cardiac patients receiving flu shots, leading the AHA/ACC advisory to recommend vaccination "with the same enthusiasm as cholesterol and blood-pressure control." The reduction in deaths is due not only to preventing the increased death rate that the flu itself has in those with cardiovascular disease, but also in preventing flu-triggered heart attacks. .
This advisory is in compliance with guidelines for treating patients with cardiovascular disease, issued by the AHA and ACC in May, where influenza vaccination was recommended as routine preventative therapy for heart patients for the first time. This recommendation follows the results of several studies showing the benefits of flu vaccine in cardiac patients, studies that began appearing several years ago. In some reports, the risk of cardiovascular mortality was reduced as much as 50% in cardiac patients receiving flu shots, leading the AHA/ACC advisory to recommend vaccination "with the same enthusiasm as cholesterol and blood-pressure control." The reduction in deaths is due not only to preventing the increased death rate that the flu itself has in those with cardiovascular disease, but also in preventing flu-triggered heart attacks. .
DrRich Comments:
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The AHA/ACC advisory on influenza vaccine is commendable. Keep in mind, however, that it often takes 5 to 10 years for formal guidelines such as these to penetrate down to the average doctor. Don't wait: If you've got heart disease take the initiative yourself, and get a flu shot.
The AHA/ACC advisory on influenza vaccine is commendable. Keep in mind, however, that it often takes 5 to 10 years for formal guidelines such as these to penetrate down to the average doctor. Don't wait: If you've got heart disease take the initiative yourself, and get a flu shot.
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Heart Disease Reversed in Mice
November 30, 2008
Heart disease 'reversed in mice'
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Tiny fragments of genetic material can play a role in heart disease.
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Scientists have halted the advance of heart disease in mice - and even reversed some of its effects.
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The study provides hard evidence that tiny pieces of genetic material called microRNA can play a key role in the development of heart disease. .
The therapy, featured in the journal Nature, targets and blocks microRNA in heart cells.
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A US specialist said that, with trials under way in other animals, human tests may be only a few years away.
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This is one of the hottest topics in biology at the moment .
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Professor Eric OlsonUniversity of Texas Southwestern Medical Center
The importance of microRNAs to heart disease - and a host of other diseases - has already been suggested by other scientists.
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Their job is to regulate the activity of our genes, but with many different types present in the cell, scientists are trying to establish which plays the biggest role.
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The US and German scientists are focusing on one type labelled microRNA-21, and their role in a type of heart cell called the cardiac fibroblast, which helps provide the structure of the organ, and plays a critical role in the progressive scarring which stops it working properly in heart disease.
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Until recently, that process was thought to be an irreversible one.
The researchers found that cells in a failing heart had higher levels of this microRNA, and linked it to a chemical signalling pathway which leads to the tissue damage found in the condition.
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Animal studies
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In mice, they used a chemical which blocked microRNA-21, and found that not only that this pathway was interrupted, but that cardiac function in the animals improved.
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This, they wrote, proved its potential as a new target for drugs in heart diseased humans.
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Professor Eric Olson, from the University of Texas Southwestern Medical Center, whose own research focuses on microRNAs and heart disease, said that the results were "exciting".
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"This is one of the hottest topics in biology at the moment," he said.
"Micro-RNAs are being very seriously considered as a therapeutic target - there is a lot of promise and potential in this area.
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"This research suggests you can reverse or prevent aspects of heart disease."
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He said: "There are already studies in large animals using micro-RNA inhibitors in heart disease - I can envisage that in a few years we will see this in human trials."
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The study provides hard evidence that tiny pieces of genetic material called microRNA can play a key role in the development of heart disease. .
The therapy, featured in the journal Nature, targets and blocks microRNA in heart cells.
.
A US specialist said that, with trials under way in other animals, human tests may be only a few years away.
.
This is one of the hottest topics in biology at the moment .
.
Professor Eric OlsonUniversity of Texas Southwestern Medical Center
The importance of microRNAs to heart disease - and a host of other diseases - has already been suggested by other scientists.
.
Their job is to regulate the activity of our genes, but with many different types present in the cell, scientists are trying to establish which plays the biggest role.
.
The US and German scientists are focusing on one type labelled microRNA-21, and their role in a type of heart cell called the cardiac fibroblast, which helps provide the structure of the organ, and plays a critical role in the progressive scarring which stops it working properly in heart disease.
.
Until recently, that process was thought to be an irreversible one.
The researchers found that cells in a failing heart had higher levels of this microRNA, and linked it to a chemical signalling pathway which leads to the tissue damage found in the condition.
.
Animal studies
.
In mice, they used a chemical which blocked microRNA-21, and found that not only that this pathway was interrupted, but that cardiac function in the animals improved.
.
This, they wrote, proved its potential as a new target for drugs in heart diseased humans.
.
Professor Eric Olson, from the University of Texas Southwestern Medical Center, whose own research focuses on microRNAs and heart disease, said that the results were "exciting".
.
"This is one of the hottest topics in biology at the moment," he said.
"Micro-RNAs are being very seriously considered as a therapeutic target - there is a lot of promise and potential in this area.
.
"This research suggests you can reverse or prevent aspects of heart disease."
.
He said: "There are already studies in large animals using micro-RNA inhibitors in heart disease - I can envisage that in a few years we will see this in human trials."
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MicroRNA Drugs Startup Miragen Nears Close of Series A, Begins Defining Pipeline
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May 15, 2008
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By Doug Macron
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Miragen Therapeutics, a Boulder, Colo.-based startup developing microRNA-targeting drugs for cardiovascular disease and related muscle disorders, is close to closing a Series A round of financing, RNAi News has learned.
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“A big part” of what Miragen will work on over the next six months will be “defining the key microRNAs and … [specific] clinical indication we want to go after,” he added.
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Given the fact that delivery continues to be the biggest hurdle for nucleic acid-based drugs, Marshall said that Miragen will initially focus on developing a therapeutic that can be directly delivered to the heart.
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By Doug Macron
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Miragen Therapeutics, a Boulder, Colo.-based startup developing microRNA-targeting drugs for cardiovascular disease and related muscle disorders, is close to closing a Series A round of financing, RNAi News has learned.
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“A big part” of what Miragen will work on over the next six months will be “defining the key microRNAs and … [specific] clinical indication we want to go after,” he added.
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Given the fact that delivery continues to be the biggest hurdle for nucleic acid-based drugs, Marshall said that Miragen will initially focus on developing a therapeutic that can be directly delivered to the heart.
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Saturday, November 29, 2008
Purkinje Fibers
Heart muscle with purkinje fibers on the surface of heart muscle fibers. Purkinje fibers are modified cardiac muscle fibers that originate from the atrioventricular node and spread into the two ventricles. They transmit the electrical impulse from the atrioventricular node to the ventricles enabling almost simultaneous contraction. The spread of excitation through the ventricles from the atrioventricular node is extremely rapid, moving at one to four meters per second.
Friday, November 28, 2008
Pericarditis
Pericarditis is a swelling and irritation of the pericardium, the thin sac-like membrane that surrounds your heart. Pericarditis often causes chest pain and sometimes other symptoms. Pericarditis may be acute or chronic. The sharp chest pain associated with acute pericarditis occurs when the pericardium rubs against the heart's outer layer.
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Mild cases may improve on their own. Treatment for more-severe cases may include medications and, rarely, surgery. Early diagnosis and treatment may help to reduce the risk of long-term complications.
.Mild cases may improve on their own. Treatment for more-severe cases may include medications and, rarely, surgery. Early diagnosis and treatment may help to reduce the risk of long-term complications.
Symptoms
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If you have acute pericarditis, the most common symptom is sharp, stabbing chest pain behind the breastbone or in the left side of your chest. However, some people with acute pericarditis describe their chest pain as dull, achy or pressure-like instead, and of varying intensity. The sharp pain may travel into your left shoulder and neck. It often intensifies when you lie down or inhale deeply. Sitting up and leaning forward can often ease the pain. At times, it may be difficult to distinguish pericardial pain from the pain that occurs with a heart attack.
If you have acute pericarditis, the most common symptom is sharp, stabbing chest pain behind the breastbone or in the left side of your chest. However, some people with acute pericarditis describe their chest pain as dull, achy or pressure-like instead, and of varying intensity. The sharp pain may travel into your left shoulder and neck. It often intensifies when you lie down or inhale deeply. Sitting up and leaning forward can often ease the pain. At times, it may be difficult to distinguish pericardial pain from the pain that occurs with a heart attack.
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Other signs and symptoms often associated with pericarditis include:
Shortness of breath when reclining
Other signs and symptoms often associated with pericarditis include:
Shortness of breath when reclining
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Low-grade fever
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An overall sense of weakness, fatigue or feeling sick
Dry cough
An overall sense of weakness, fatigue or feeling sick
Dry cough
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Abdominal or leg swelling
Abdominal or leg swelling
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Causes
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Under normal circumstances, the two-layered pericardial sac that surrounds your heart contains a small amount of lubricating fluid. In pericarditis the sac becomes inflamed and the resulting friction from the inflamed sac rubbing against the outer layer of your heart leads to chest pain.
Under normal circumstances, the two-layered pericardial sac that surrounds your heart contains a small amount of lubricating fluid. In pericarditis the sac becomes inflamed and the resulting friction from the inflamed sac rubbing against the outer layer of your heart leads to chest pain.
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In some cases the amount of fluid contained in the pericardial sac may increase, causing what is called pericardial effusion.
In some cases the amount of fluid contained in the pericardial sac may increase, causing what is called pericardial effusion.
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The cause of pericarditis is often hard to determine. In most cases doctors are either unable to determine a cause (idiopathic) or suspect a viral infection.
The cause of pericarditis is often hard to determine. In most cases doctors are either unable to determine a cause (idiopathic) or suspect a viral infection.
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Pericarditis can also develop shortly after a major heart attack due to the irritation of the underlying damaged heart muscle. In addition, a delayed form of pericarditis may occur weeks after a heart attack or heart surgery because of antibody formation. This delayed pericarditis is known as Dressler's syndrome. Many experts believe Dressler's syndrome is due to an autoimmune response, a mistaken inflammatory response by the body to its own tissues — in this case, the heart and pericardium.
Other causes of pericarditis include:
Pericarditis can also develop shortly after a major heart attack due to the irritation of the underlying damaged heart muscle. In addition, a delayed form of pericarditis may occur weeks after a heart attack or heart surgery because of antibody formation. This delayed pericarditis is known as Dressler's syndrome. Many experts believe Dressler's syndrome is due to an autoimmune response, a mistaken inflammatory response by the body to its own tissues — in this case, the heart and pericardium.
Other causes of pericarditis include:
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Systemic inflammatory disorders. These may include lupus and rheumatoid arthritis.
Systemic inflammatory disorders. These may include lupus and rheumatoid arthritis.
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Trauma. Injury to your heart or chest may occur as a result of a motor vehicle or other accident.
Trauma. Injury to your heart or chest may occur as a result of a motor vehicle or other accident.
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Other health disorders. These may include kidney failure, AIDS, tuberculosis and cancer.
Other health disorders. These may include kidney failure, AIDS, tuberculosis and cancer.
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Certain medications. Some medications can cause pericarditis, although this is unusual.
Certain medications. Some medications can cause pericarditis, although this is unusual.
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When to seek medical advice
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Seek immediate medical care if you develop chest pain.
Seek immediate medical care if you develop chest pain.
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