Friday, December 5, 2008

Breakthrough in Heart Research


September 25, 2006, 6:01 PM CT

Breakthrough In Heart Research

For the first time ever, scientists at the University of Bristol have been able to directly measure energy levels inside living heart cells, in real time, using the chemical that causes fireflies to light up. This is hailed as a major breakthrough in research and could lead to improved recovery of the heart when it is re-started after a heart attack or cardiac surgery.

Dr Elinor Griffiths said: "Being able to see exactly what's going on in heart cells will be of great benefit to understanding heart disease.".

The research is published today (22nd September, 2006) in the Journal of Biological Chemistry.

The 'power stations' within heart cells that make energy are called mitochondria. They convert energy from food into chemical energy called adenosine triphosphate, or ATP.

Under normal conditions, mitochondria are able to make ATP extremely rapidly when the heart is stressed, such as during exercise or in 'fight-or-flight' mode.

However, if the cells are made to beat suddenly from rest, a situation that happens when the heart is re-started after cardiac surgery or a heart attack, the team found there is a lag phase where the supply of ATP drops before mitochondrial production starts again, potentially preventing the heart from beating properly.........


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Wednesday, November 26, 2008

Heart Muscle Cell



Cardiac muscle, unlike skeletal muscle, is composed of separate cellular elements. A cardiac muscle cell has a large nucleus (light blue) and numerous mitochondria (purple). The high concentration of mitochondria reflects the large energy demands of predominant the heart. Contractile proteins of actin and myosin myofilaments are in the cytoplasm. They form bands of varying density: A band - orange, I band - yellow, Z line - red. The Z lines are regions with dense arrangements of actin. The heart produces regular electrical impulses causing the muscle myofibrils to slide over one another and contract the cardiac muscle.
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Tuesday, November 25, 2008

Ejection Fraction


Tuesday, November 25, 2008

(When I learned a had an ejection fraction of 35 after a severe heart attack, I was severely depressed and anxious. That was three years ago. Apparently I am still alive, and the ejection fraction hasn't changed. I can walk for several hours; this "functional capacity" was of more interest to my doctors at the Mayo Clinic than the ejection fraction. -- sparker)
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Ejection Fraction & Its Importance
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Ejection Fraction is a key indicator of a healthy heart and is frequently used by physicians to determine how well your heart is functioning as a pump.
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Ejection Fraction is the percentage of blood that is pumped out of the heart during each beat. In a healthy heart, 50 to 75 percent of the blood is pumped out during each beat. Many people with heart disease or heart failure pump out less than 50% and many people with heart failure pump out less than 40%.'
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Ejection Fraction is one of the many ways doctors classify the type and severity of heart failure and damage to the heart muscle..Ejection Fraction Ranges
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An Ejection Fraction above 50 percent indicates that your heart is pumping normally and able to deliver an adequate supply of blood to your body and brain.
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An Ejection Fraction that falls below 50 percent could indicate that the heart is no longer pumping efficiently and not able to meet the body's needs. .
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An Ejection Fraction of 35 percent or less indicates a weakened heart muscle and that the heart is pumping poorly, which can significantly increase a person's risk for Sudden Cardiac Arrest (SCA).
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Measuring Your Ejection Fraction
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For heart patients, knowing your Ejection Fraction is just as important as knowing your cholesterol and blood pressure. Ejection Fraction is often measured using an echocardiogram, a simple and painless test often performed right in the doctor's office, but it can also be measured with other tests including:
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MUGA scan (Multiple Gated Acquisition Scan)CAT scan (Computed Axial Tomography Scan)Cardiac catheterizationStress test or nuclear stress testT-Wave Assessment
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A Low Ejection Fraction is a Serious Health Risk
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Recent medical research shows that people with an Ejection Fraction of 35% or lower may be at increased risk of Sudden Cardiac Arrest (SCA). If you have a low Ejection Fraction, your doctor may prescribe medications, recommend lifestyle adjustments or suggest other therapies.

Sunday, November 23, 2008

Cholesterol





Whenever we hear the word 'cholesterol' we think hamburgers, thickshakes, people who need a double seat in an aircraft, clogged arteries and an early death.
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In fact cholesterol is essential to life. It's a compound – a steroid – that occurs naturally in the body. It's manufactured by the liver, and is essential for many of the body's metabolic processes. It helps make hormones like oestrogen, testosterone and adrenaline (the name originates from the Greek 'chole' meaning bile and stereos meaning solid). It's used in the production of vitamin D, and also in the production of bile acids, which help the body digest fat and absorb fat-soluble vitamins in the small intestine.
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The trouble starts when we get too much cholesterol – when the intake of fats in our diet causes the levels of cholesterol in our blood to rise to more than we need.
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If it rises above normal levels – that is, 5.5 millimoles per litre – it can build up into fatty deposits on the surface of our arteries, which can form calcium plaques. These narrow the arteries and block blood from flowing, leading to heart disease, stroke and other conditions. This is a condition known as atherosclerosis. High cholesterol is one of the risk factors for atherosclerosis, along with smoking, being overweight, and having high blood pressure.
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Good fats, bad fats
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Most cholesterol is manufactured in the liver from fats in our diet. The liver makes cholesterol and attaches it to carrier molecules made of fat and protein called lipoproteins.
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There are two major types of these 'carrier' lipoproteins – low-density lipoprotein (LDL) and high-density lipoprotein (HDL). LDL is the major carrier of cholesterol from the liver to the rest of the body. When cholesterol levels are excessive, LDL deposits cholesterol onto the arteries causing the damage.
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HDL, on the other hand, mops up cholesterol from the bloodstream and takes it back to the liver. So it reduces cholesterol, and lessens the chance of it being deposited in the arteries.
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HDL cholesterol is sometimes called 'good cholesterol' and LDL cholesterol 'bad cholesterol'. The more HDL you and have and the less LDL – that is, the higher the ratio of HDL to LDL – the lower your risk of artery disease.
How much LDL and HDL we have in our blood is influenced by the types of fats we eat. Biochemists divide fats in our diets into different types, according to their chemical composition. They talk about saturated, monounsaturated and polyunsaturated fats. These terms refer to the differences in the numbers of hydrogen atoms in the fat molecules.
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Eating a lot of saturated fat tends to elevate the levels of LDL in the blood, so these kinds of fats are often called 'bad fats'. Foods high in saturated fats include full fat dairy products, processed meats like salami and sausages, snack foods like chips, takeaway foods (especially deep fried foods), cakes, biscuits and pastries, coconut oil and palm oil. If you want to avoid artery disease, stay away from these foods.
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Eating monounsaturated or polyunsaturated fats, on the other hand, tends to increase the levels of HDL. And HDL reduces cholesterol in the blood, so these fats are called 'good fats'. Eating these will reduce your risk of artery disease. Foods high in monounsaturated fats include olive oil, canola oil, avocados and most nuts. Foods high in polyunsaturated fats include oils of seeds and grains, such as sunflower, safflower, corn, soybeans and walnuts.
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Familial hypercholesterolaemia
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In some people, cholesterol levels are high because they have a familial (inherited) condition in which cholesterol isn't properly cleared by the liver and builds up in the blood. These people have a high risk of arterial disease, heart attack and stroke - and at an early age. It's a dominant genetic disorder; a person inherits it from one parent, and has a one in two chance of passing it on. It affects about one person in 500.
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Cholesterol test
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How do you know if you have abnormally high cholesterol? You don't – it doesn't produce any symptoms and many people first learn they have high cholesterol only when they have a heart attack or a stroke.
The National Heart Foundation recommends that all adults over 45 years old have a regular blood cholesterol test every few years. People younger than 45 who are at higher risk of coronary heart disease – for example, those who have a family history of hypercholesterolaemia, heart disease, high blood pressure and/or diabetes, should also have a regular cholesterol test.
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The test is a simple blood test taken after a period of fasting (not eating) for 12 hours. The test measures the total cholesterol level (LDL plus HDL and other fats called triglycerides). Normal is below 5.5 millimoles/litre. Most people are between 4 and 5.5. In someone young and healthy with no other risk factors, a little over 5.5 is acceptable. Individual LDL, HDL and triglyceride levels are sometimes also tested. Normal levels are:
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Total cholesterol: less than 5.5 mmol/l
LDL: less than 3.5 mmol/l
HDL: greater than 1.0 mmol/l
LDL to HDL ratio: less than 4
Triglycerides: less than 2.0 mmol/l.
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How to lower cholesterol
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It's worth taking steps to lower cholesterol because lowering cholesterol by 10 per cent reduces the risk of heart attack by 20 per cent. So if your doctor finds you have elevated cholesterol, he or she will recommend the following:
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Diet
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A diet low in saturated fats and high in monounsaturated and polyunsaturated fats. This means:
low-fat or reduced-fat milk, yoghurt and other dairy products
lean meat (meat trimmed of fat or labelled as 'heart smart')
limited fatty meats, including sausages and salami, with leaner sandwich meats like turkey breast or cooked lean chicken instead
fish (fresh or canned) at least twice a week
butter and dairy blends replaced with polyunsaturated margarines
plenty of fresh fruit, vegetables and wholegrain foods, nuts, legumes and seeds
plant sterols are a type of alcohol structurally similar to cholesterol and found in some margarines and fortified foods, in corn, rice, vegetable oils and nuts. They can also lower cholesterol.
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Exercise
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regular exercise (for example, at least 30 minutes of brisk walking daily). Exercise increases HDL levels and reduces LDL levels in the body.
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Medications
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After three months of diet and exercise, a doctor will usually do another cholesterol test. If it's still high (over 6.5, or if it's over 5.50 and the person has risk factors for artery disease), the next step may be to add medication to diet and exercise. People will familial hypercholesterolaemia will usually also need medications. There are several different types, which can be taken alone or in combination.
Statins. Also known as HMG CoA reductase inhibitors, these drugs block an enzyme (HMG CoA reductase) used in the production of cholesterol. They also accelerate turnover of cholesterol by the liver. Common statins are atorvastatin (brand name Lipitor), fluvastatin (Lescol or Vastin), pravastatin (Pravachol), and simvastatin (Lipex or Zocor). They can drop blood LDL levels by anywhere between 20 and 50 per cent, and increase HDL by 5 to 15 per cent. They're expensive, but they're on the Pharmaceutical Benefits Scheme. Side effects include stomach upset and headache.
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Cholestyramine and colestipol. These are older medications, also known as bile-acid-binding resins. They bind to bile acids in the intestine, preventing them from being absorbed into the body. The liver needs bile acids to make cholesterol – so less bile acids means less cholesterol. Examples include cholestyramine (brand name Questran Lite) and colestipol (Colestid granules). They both come in sachets of powder which need to be mixed with water, juice or other fluid and can be taken with or without food. Constipation is a common side effect.
Gemfibrozil and fenofibrate. These drugs are used when the others don't work, or when levels of triglycerides (another common type of fats) are high – though they also increase the amount of HDL in the blood. Fenofibrate also lowers total cholesterol.
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Nicotinic acid can lower LDL (bad) cholesterol and triglycerides, and increase HDL cholesterol. It can cause flushing of the face and neck.
Ezetimibe (brand name Ezetrol) is a new drug in a class called the cholesterol absorption inhibitors. It works by reducing the absorption of cholesterol from the intestine into the bloodstream. It reduces total cholesterol and LDL, and increases HDL cholesterol.
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Saturday, November 22, 2008

Morphing Bone Marrow Stem Cells into Cardiac Cells


Stem cells placed in the heart have morphed into cardiac muscle cells.
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Study finds stem cells morph in the heart
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In April 2001, Dr. Donald Orlic of the National Institutes of Health and Dr. Piero Anversa of New York Medical College announced that bone marrow injected into the damaged hearts of mice had morphed into cardiac muscle cells to replace those damaged after a heart attack.
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This promising news led clinicians worldwide to attempt similar treatments using humans. Ten human trials have been completed with all but one having positive results; however, the degree of improvement in patients' heart function has been minimal and variable.
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In Brazil, where only the sickest patients were enrolled in testing, Perin found significant evidence that the treatment worked. His patients went from being bedridden to being able to either jog on the beach, climb eight flights of stairs, or reopen a business.
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Despite the fact that some individual cases seem to be favorable, overall statistics have only shown a five to 10 percent improvement in heart function with approximately 200 patients having already been treated.
In addition to the human testing that is taking place, many researchers are trying to recreate the original research on mice that was completed in 2001 but have had no success. At least two separate laboratories, one at Stanford University and another at University of Washington in Seattle, reported that they were unable to replicate the findings of the Orlic-Anversa experiment; they found that bone marrow stem cells did not turn into heart tissue as was originally reported.
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Meanwhile, Anversa is standing by his original work and recently reported that he repeated his experiment and found the same results. In an article in the journal Circulation Research, he suggested that his critics did not follow the procedure properly and are suffering from "emotional disbelief" that bone marrow cells are capable of accomplishing this feat.
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One explanation as to why there has been a mild degree of improvement in heart function among some patients is the action of injecting the heart. This can cause local inflammation, leading to improved circulation in the inflamed area.
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Despite this possible explanation, some clinicians are convinced that something in the bone marrow mix is causing the improvement in heart function.
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Dr. Helmut Drexler in Hannover, Germany believes that the bone marrow stem cells were secreting hormones that are causing a beneficial response from the heart's cells.
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A lot of time and energy has also been put into figuring out which of the several different kinds of stem cells in the bone marrow is producing this beneficial response.
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Dr. Douglas Losordo at St. Elizabeth's Medical Center and Dr. Young-sup Yoon reported that they had isolated a specific type of bone marrow stem cell that can morph into the three kinds of cells that build the heart. They believe that this could be a better and more specific type of vehicle to inject into patients.
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While clinicians are continuing their work on testing humans, researchers are arguing that clinical trials are unlikely to give any definitive answers since the science behind this work is still unknown.
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Researchers are working on finding out the role of stem cells in maintaining the heart. Some claim that the stem cell system itself may age, thereby making it ineffective in older people. As a result, using stem cells to treat heart attacks would be pointless for elderly patients.
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In addition to their differences on where to take stem cell research in cardiac health, clinicians and researchers differ on the time scale of bone marrow stem cells being used as a therapy for suffering patients.
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Clinicians believe that this research will be in use within three to five years. Researchers, on the other hand, believe that the most important thing to do is find the right cell that is causing these beneficial effects; they believe that this alone will take years.


Thursday, November 20, 2008

Heart Lung Bypass Machine


Traditional Open-Heart Surgery

For this type of surgery, you're given medicine to make you fall asleep. A doctor checks your heartbeat, blood pressure, oxygen levels, and breathing during the surgery. A breathing tube is placed in your lungs through your throat and connected to a ventilator (breathing machine).
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A surgeon makes a 6- to 8-inch incision (cut) down the center of your chest wall. Your chest bone is cut and your rib cage is opened so that the surgeon can get to your heart.
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You're given medicine to thin your blood and keep it from clotting. A heart-lung bypass machine is connected to your heart. This machine takes over for your heart by replacing the heart's pumping action. A specialist oversees the machine. The bypass machine allows the surgeon to operate on a heart that isn't moving and full of blood.
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Heart-Lung Bypass Machine
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The illustration shows a heart-lung bypass machine attached to a heart during surgery.
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You're given medicines to stop your heartbeat once you're connected to the heart-lung bypass machine. A pipe is placed in your heart to drain blood to the machine. The machine removes carbon dioxide (a waste product) from your blood, adds oxygen, and then pumps the blood back into your body. Tubes are inserted into your chest to drain fluid.
Once the bypass machine begins to work, the surgeon performs the surgery to repair your heart problem.
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At the end of the surgery, your heart is restarted using mild electric shocks. The pipes and tubes are removed from your heart, and the heart-lung bypass machine is stopped. You're given medicine to allow your blood to clot again.
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Your chest bone is closed with wires. Stitches or staples are used to close the incision. The breathing tube is removed.
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An advantage of traditional open-heart surgery is that it's easier for the surgeon to operate. This is very important for long and complex surgeries.

Wednesday, November 19, 2008

Screening men over 65 for abdominal aortic aneurysms


Between 5% and 10% of men aged 65 to 79 have abdominal aortic aneurysms, but don't know it. If their weakened arteries burst they stand a very high risk of dying. Ultrasound screening of men in this age group can significantly reduce the numbers of men who die from this condition. The overall benefits of screening are complex, however, because a number of men may be subjected to unnecessary anxiety and/or to the complications of surgery.An aneurysm is a localised widening of an artery. It occurs because the artery wall is weakened and without therapy it could easily burst. If the aneurysm is in the aorta, the main artery that carries blood through the abdomen, the result often can be fatal. Doctors think that any abdominal aortic aneurysm that is greater than 5cm is at a high risk of bursting.To see whether a program of ultrasound screening could detect these aneurysms before they burst, and save lives as a result, Cochrane Scientists performed a systematic review of screening trials. They identified four controlled trials that were conducted in the UK, Denmark and Australia, and involved a total of 127,891 men and 9,342 women.The results showed that men aged 65-79 could benefit from screening, but there were insufficient data on women (whose risk of death from ruptured aortic aneurysm is much lower than the risk in men) to ascertain effectiveness in women....

Nanotechnology and Artheroschlerosis


These before (left) and after images show the effects of fumagillin-laden nanoparticles, which inhibit the growth of plaque-feeding microvessels, in a rabbit aorta.
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Nanotechnology And Atherosclerosis
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These before (left) and after images show the effects of fumagillin-laden nanoparticles, which inhibit the growth of plaque-feeding microvessels, in a rabbit aorta. In laboratory tests, one very low dose of a drug was enough to show an effect on notoriously tenacious artery-clogging plaques. What kind of drug is that potent?.It's not so much the drug itself as how it was delivered. Fumagillin - a drug that can inhibit the growth of new blood vessels that feed atherosclerotic plaques - was sent directly to the base of plaques by microscopically small spheres called nanoparticles developed by scientists at Washington University School of Medicine in St. Louis."Previously we reported that we can visualize plaques using our nanoparticle technology, but this is the first time we've demonstrated that the nanoparticles can also deliver a drug to a disease site in a living organism," says Patrick Winter, Ph.D., research assistant professor of medicine. "After a single dose in laboratory rabbits, fumagillin nanoparticles markedly reduced the growth of new blood vessels that feed plaques."The scientists report their findings in the recent issue of the journal Arteriosclerosis, Thrombosis, and Vascular Biology, and the article is now available on line.An atherosclerosis plaque results when a buildup of cholesterol, inflammatory cells and fibrous tissue forms inside an artery. If a plaque ruptures, it can block blood flow to the heart or brain, causing heart attack or stroke.........

Tuesday, November 18, 2008

Coronary CT angiograhy as good as angiogram


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Newer Cardiac Imaging Machines Effective In Detecting Coronary Artery Stenosis

ScienceDaily (Aug. 27, 2008) — The first multicenter study of the accuracy of some of the latest cardiac imaging technology found it was 99 percent as effective in ruling out obstructive coronary artery stenosis - or narrowing of these arteries – as the more expensive and invasive coronary angiography traditionally used by physicians, according to new research.
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Matthew J. Budoff, M.D., a principal investigator at the Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed), is the lead author of the study conducted at 16 different sites with 230 research volunteers with chest pain but no known coronary artery disease.
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"The research found this noninvasive method of cardiac imaging will effectively detect stenosis – a constriction or narrowing – of the coronary arteries which can lead to heart attacks and may require surgery to repair," Dr. Budoff said. "This is good news for patients who, in the past, might have been forced to undergo a more expensive and invasive procedure to determine if they suffered from blockages in the arteries leading to their hearts."
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In the study, each of the research volunteers was examined using some of the newer cardiac CT technology - electrocardiographically gated 64-multidetector row coronary computed tomographic angiography (CCTA). Each volunteer also underwent the more expensive and invasive coronary angiography, which is often called the "gold standard" for evaluating coronary artery stenosis.
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The researchers found CCTA provided high diagnostic accuracy for detection of obstructive coronary stenosis at the thresholds of a 50 percent narrowing and at 70 percent stenosis. It also found CCTA was accurate 99 percent of the time in ruling out coronary artery stenosis.
The study was paid for by GE Healthcare, which manufactures the cardiac CT imaging devices used in the study. Dr. Budoff and Dr. James K. Min, who also participated in the study, are on the Speakers' Bureau for General Electric.
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Source of Image:

View of Coronary Arteries



Technology Gives 3-D View Of Human Coronary Arteries

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OFDI fly-through view of same patient's right coronary artery, white arrowheads indicate area of white dotted line in image at right. (Credit: Massachusetts General Hospital)
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ScienceDaily (Nov. 18, 2008) — For the first time researchers are getting a detailed look at the interior of human coronary arteries, using an optical imaging technique developed at the Wellman Center for Photomedicine at Massachusetts General Hospital (MGH). In their report in the journal JACC: Cardiovascular Imaging, the research team describes how optical frequency-domain imaging (OFDI) gives three-dimensional, microscopic views of significant segments of patients' coronary arteries, visualizing areas of inflammation and plaque deposits.
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"This is the first human demonstration of a technique that has the potential to change how cardiologists look at coronary arteries," says Gary Tearney, MD, PhD, of the MGH Pathology Department and the Wellman Center for Photomedicine at MGH, the study's lead author. "The wealth of information that we can now obtain will undoubtedly improve our ability to understand coronary artery disease and may allow cardiologists to diagnose and treat plaque before it leads to serious problems."
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OFDI is an advance over optical coherence tomography (OCT), another imaging technology developed by the MGH investigators. While OCT examines tissues one point at a time, OFDI can look at over 1,000 points simultaneously using a device developed at MGH-Wellman. Inside a fiberoptic probe, a constantly rotating laser tip emits a light beam with an ever-changing wavelength. As the probe moves through the structure to be imaged, measuring how each wavelength is reflected back allows rapid acquisition of the data required to create the detailed microscopic images. Besides providing three-dimensional images of an artery's microstructure in seconds, the increased speed also reduces signal interference from blood, which had plagued the first-generation technology. In 2006 members of the MGH-Wellman team reported the successful use of OFDI to image the esophagus and coronary arteries of pigs.
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The current study enrolled three patients scheduled to have stents placed in their coronary arteries at the Lahey Clinic in Burlington, Mass. After the completion of stent placement, OFDI was used to image 3- to 7-centimeter-long segments of the patients' coronary arteries including the stented areas. OFDI provided detailed images along the length of the arteries – visualizing lipid or calcium deposits, immune cells that could indicate inflammation, and the stents – and dramatic "fly-through" views looking down the artery's interior. More detailed, cross-sectional images of narrowed vascular segments revealed features associated with the type of atherosclerotic plaques that are likely to rupture and cause a heart attack.
Tearney and his colleagues note that these findings need to be duplicated in a larger group of patients, and the time required to process the "fly-through" images – currently several hours – needs to be reduced to provide the real-time information most useful for clinical applications. Combining OFDI with intravascular ultrasound might help with another of the technique's limitations, the inability to penetrate deep into tissues.
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"While more work remains, the technology is advancing at a rapid pace. We expect to see commercial devices available in a one- to two-year time frame," says Brett Bouma, PhD, of the Wellman Center, senior author of the report. "Our goal now is to help put the pieces in place to ensure that this technique will be widely available to interventional cardiologists." Bouma is an associate professor of Dermatology, and Tearney an associate professor of Pathology at Harvard Medical School.
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Additional co-authors of the JACC: Cardiovascular Imaging report are Milen Shishkov, PhD, Ben Vakoc, PhD, Melissa Suter, PhD, Adrien Desjardins, PhD, Wang-Yul Oh, PhD, Lisa Bartlett and Mireille Rosenberg, PhD, MGH-Wellman; and Sergio Waxman, MD, and Mark Freilich, MBBS, Lahey Clinic. The MGH has licensed cardiovascular applications of OFDI to Terumo Corporation, which has supported nonclinical OFDI studies by Tearney and Bouma. The current study was supported by a grant from the National Institutes of Health.


Monday, November 17, 2008

Placement of EKG leads


Bipolar recordings utilize standard limb lead configurations depicted at the right. By convention, lead I has the positive electrode on the left arm, and the negative electrode on the right arm, and therefore measures the potential difference between the two arms. In this and the other two limb leads, an electrode on the right leg serves as a reference electrode for recording purposes. In the lead II configuration, the positive electrode is on the left leg and the negative electrode is on the right arm. Lead III has the positive electrode on the left leg and the negative electrode on the left arm. These three bipolar limb leads roughly form an equilateral triangle (with the heart at the center) that is called Einthoven's triangle in honor of Willem Einthoven who developed the electrocardiogram in 1901. Whether the limb leads are attached to the end of the limb (wrists and ankles) or at the origin of the limb (shoulder or upper thigh) makes no difference in the recording because the limb can simply be viewed as a long wire conductor originating from a point on the trunk of the body.

Based upon universally accepted ECG rules, a wave a depolarization heading toward the left arm gives a positive deflection in lead I because the positive electrode is on the left arm. Maximal positive ECG deflection occurs in lead I when a wave of depolarization travels parallel to the axis between the right and left arms. If a wave of depolarization heads away from the left arm, the deflection is negative. Also by these rules, a wave of repolarization moving away from the left arm is recorded as a positive deflection. Similar statements can be made for leads II and III in which the positive electrode is located on the left leg. For example, a wave of depolarization traveling toward the left leg produces a positive deflection in both leads II and III because the positive electrode for both leads is on the left leg. A maximal positive deflection is recorded in lead II when the depolarization wave travels parallel to the axis between the right arm and left leg. Similarly, a maximal positive deflection is obtained in lead III when the depolarization wave travels parallel to the axis between the left arm and left leg.

If the three limbs of Einthoven's triangle (assumed to be equilateral) are broken apart, collapsed, and superimposed over the heart, then the positive electrode for lead I is said to be at zero degrees relative to the heart (along the horizontal axis) (see figure at right). Similarly, the positive electrode for lead II will be +60º relative to the heart, and the positive electrode for lead III will be +120º relative to the heart as shown to the right. This new construction of the electrical axis is called the axial reference system. With this system, a wave of depolarization traveling at +60º produces the greatest positive deflection in lead II. A wave of depolarization oriented +90º relative to the heart produces equally positive deflections in both lead II and III. In this latter example, lead I shows no net deflection because the wave of depolarization is heading perpendicular to the 0º, or lead I, axis (see ECG rules).

EKG


Almost everyone knows what a basic EKG tracing looks like. But what does it mean?

The first little upward notch of the EKG tracing is called the "P wave." The P wave indicates that the atria (the 2 upper chambers of the heart) are contracting to pump out blood.

The next part of the tracing is a short downward section connected to a tall upward section. This next part is called the "QRS complex." This part indicates that the ventricles (the 2 lower chambers of the heart) are contracting to pump out blood.
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The next short upward segment is called the "ST segment." The ST segment indicates the amount of time from the end of the contraction of the ventricles to the beginning of the rest period before the ventricles begin to contract for the next beat.
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The next upward curve is called the "T wave." The T wave indicates the resting period of the ventricles.
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When your physician studies your EKG, he/she looks at the size and length of each part of the EKG. Variations in size and length of the different parts of the tracing may be significant. The tracing for each lead of a 12-lead EKG will look different, but will have the same basic components as described above. Each lead of the 12-lead is "looking" at a specific part of the heart, so variations in a lead may indicate a problem with the part of the heart associated with the lead.
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Why is an EKG done?
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Many conditions can cause changes to the EKG. Because the EKG is a fast, simple, painless and relatively inexpensive test, it may be used as a part of an initial examination to help the physician narrow the scope of the diagnostic process. EKG's are also done with routine physical examinations so that comparisons can be made with previous EKG's to determine if a hidden or undetected condition might be causing changes in the EKG. Some conditions which may cause changes in the EKG pattern may include, but are not limited to, the following:
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ischemia - decreased flow of oxygenated blood to an organ due to obstruction in an artery.
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heart attack - also called myocardial infarction; damage to the heart muscle due to insufficient blood supply.
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conduction disorders - a dysfunction in the heart's electrical conduction system, which can make the heartbeat too fast, too slow, or at an uneven rate.
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electrolyte disturbances - an imbalance in the level of electrolytes, or chemicals, in the blood, such as potassium, magnesium, or calcium.
pericarditis - an inflammation of the sac (thin covering) that surrounds the heart.
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valvular heart disease - one or more of the heart's four valves becomes defective, or may be congenitally malformed.
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enlarged heart - a condition of the heart in which it is abnormally larger than normal; can be caused by various factors, such as valve disorders, high blood pressure, congestive heart failure, conduction disturbances, etc.
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chest trauma - blunt trauma to the chest, such as a motorist hitting the steering wheel in an automobile accident.
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NOTE: This list is presented as an example. It is not intended to be a comprehensive list of all conditions which may cause changes in the EKG pattern.
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An EKG may also be done for the following reasons:
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to obtain a baseline tracing of the heart's function (during a physical examination). This baseline tracing may be used later as a comparison with future EKG's, to see if any changes have occurred.
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as part of a work-up prior to a procedure such as surgery to make sure a heart condition does not exist that might cause complications during or after the procedure
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to check the function of an implanted pacemaker
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to check the effectiveness of certain heart medications
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to check the heart's status after an MI, or after a heart-related procedure such as a cardiac catheterization, heart surgery, electrophysiological studies, etc.
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How is an EKG done?
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An EKG is one of the simplest and fastest procedures used to evaluate the heart. An EKG technician, nurse, or physician will place 12 separate electrodes (small plastic patches) at specific locations on your chest, arms, and legs. Eight of the electrodes will be placed on your chest, and one electrode will be placed on each arm and leg. The electrodes may be self-sticking, or a gel may be applied to make the electrodes adhere to the skin. You will be lying down on a stretcher or bed, and the leads (wires) will be connected to the electrodes on your skin. You will need to lie very still and not talk during the EKG procedure, as movement or talking may interfere with the tracing. The technician, nurse, or physician will start the tracing, which will take just a few minutes. You will not feel anything during the tracing. Once a clear tracing has been obtained, the leads and electrodes will be removed, and you will be free to continue on with your usual activities, unless directed otherwise by your physician. An EKG can indicate the presence of arrhythmias (an abnormal rhythm of the heart), damage to the heart caused by ischemia (lack of oxygen to the heart muscle) or myocardial infarction (MI, or heart attack), a problem with one or more of the heart valves, or other types of heart conditions.
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The Electrical System of the Heart

The heart's electrical system

The heart is, in the simplest terms, a pump made up of muscle tissue. Like all pumps, the heart requires a source of energy in order to function. The heart's pumping energy comes from an intrinsic electrical conduction system.
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How does the heart beat?
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An electrical stimulus is generated by the sinus node (also called the sinoatrial node, or SA node), which is a small mass of specialized tissue located in the right atrium (right upper chamber) of the heart. The sinus node generates an electrical stimulus periodically (60-100 times per minute under normal conditions). This electrical stimulus travels down through the conduction pathways (similar to the way electricity flows through power lines from the power plant to your house) and causes the heart's chambers to contract and pump out blood.
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The right and left atria (the 2 upper chambers of the heart) are stimulated first and contract a short period of time before the right and left ventricles (the 2 lower chambers of the heart). The electrical impulse travels from the sinus node to the atrioventricular (AV) node, where it stops for a very short period, then continues down the conduction pathways via the bundle of His into the ventricles. The bundle of His divides into right and left pathways to provide electrical stimulation to both ventricles.
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Normally, as the electrical impulse moves through the heart, the heart contracts about 60 to 100 times a minute. Each contraction represents one heartbeat. The atria contract a fraction of a second before the ventricles so their blood empties into the ventricles before the ventricles contract.
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Under some conditions, almost all heart tissue is capable of starting a heartbeat, or becoming the pacemaker. An arrhythmia occurs when:
the heart's natural pacemaker develops an abnormal rate or rhythm
the normal conduction pathway is interrupted another part of the heart takes over as pacemaker

Sunday, November 16, 2008

Mitral Valve, Aortic Valve, Pulmonary Valve

Thee mitral valve (also known as the bicuspid valve or left atrioventricular valve) is a dual-flap (bi from the Latin, meaning double, and mitral from the Latin, meaning shaped like a miter) valve in the heart that lies between the left atrium (LA) and the left ventricle (LV). The mitral valve and the tricuspid valve are known collectively as the atrioventricular valves because they lie between the atria and the ventricles of the heart and control the flow of blood.
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Overview
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A normally-functioning mitral valve opens to pressure from the superior surface of the valve, allowing blood to flow into the left ventricle during left atria systole (contraction), and closes at the end of atrial contraction to prevent blood from backflowing into the atria during left ventricle systole. In a normal cardiac cycle, the atria contracts first, filling the ventricle. At the end of ventricular diastole, the bicuspid valve shuts, and prevents backflow as the ventricle begins its systolic phase. Backflow may occur if the patient suffers from mitral valve prolapse, causing an audible heart murmur during auscultation.
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Anatomy
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The mitral valve has two cusps, or leaflets, (the anteromedial leaflet and the posterolateral leaflet) that guard the opening. The opening is surrounded by a fibrous ring known as the mitral valve annulus. (The orientation of the two leaflets resemble a bishop's miter, whence the valve receives its name.[1]) The anterior cusp protects approximately two-thirds of the valve (imagine a crescent moon within the circle, where the crescent represents the posterior cusp). These valve leaflets are prevented from prolapsing into the left atrium by the action of tendons attached to the posterior surface of the valve, chordae tendineae.
The inelastic chordae tendineae are attached at one end to the papillary muscles and the other to the valve cusps. Papillary muscles are fingerlike projections from the wall of the left ventricle. Chordae tendineae from each muscle are attached to both leaflets of the mitral valve. Thus, when the left ventricle contracts, the intraventricular pressure forces the valve to close, while the tendons keep the leaflets coapting together and prevent the valve from opening in the wrong direction (thus preventing blood to flow back to the left atrium). Each chord has a different thickness. The thinnest ones are attached to the free leaflet margin, whereas thickest ones (strut chords) are attached quite away from the free margin. This disposition has important effects on systolic stress distribution physiology [2].
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Normal physiology
During left ventricular diastole, after the pressure drops in the left ventricle due to relaxation of the ventricular myocardium, the mitral valve opens, and blood travels from the left atrium to the left ventricle. About 70-80% of the blood that travels across the mitral valve occurs during the early filling phase of the left ventricle. This early filling phase is due to active relaxation of the ventricular myocardium, causing a pressure gradient that allows a rapid flow of blood from the left atrium, across the mitral valve. This early filling across the mitral valve is seen on doppler echocardiography of the mitral valve as the E wave.
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After the E wave, there is a period of slow filling of the ventricle.
Left atrial contraction (left atrial systole) (during left ventricular diastole) causes added blood to flow across the mitral valve immediately before left ventricular systole. This late flow across the open mitral valve is seen on doppler echocardiography of the mitral valve as the A wave. The late filling of the LV contributes about 20% to the volume in the left ventricle prior to ventricular systole, and is known as the atrial kick.
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 Surface anatomy
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The opening and closing of the mitral valve is difficult to hear directly, but the flow of blood to the left ventricle is most audible at the apex of the heart, and so auscultation is usually performed at the intersection of the fifth intercostal space and the midclavicular line.
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Source of image:

Friday, November 14, 2008

Echocardiogram



Echocardiography can provide the following information:
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Cardiac structures: The various components of the heart (muscle, valves, etc.) could be seen. Therefore a hole in a heart septal wall or deformity of a cardiac valve, etc could be identified.
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The motion of the ventricular muscular walls can be seen (as ventricles pump blood out of them). Reduction in the capability of the ventricles to pump can therefore be evaluated.
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The flow of blood within the heart and blood vessels could also be seen in a feature termed color Doppler. This will represent the blood in usually two different colors: blue and red. The blue represents the blood which is heading away from the transducer and the red represents the blood which is flowing towards the transducer. This enables the visualization of abnormalities of blood flow such as leakage of blood through valves (regurgitation or insufficiency) since blood would be seen to leak back after the valve closes.
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In addition the pressure difference between one part of the heart and the other could be determined since the ultrasound waves bouncing off blood would change its sound wave length depending upon the speed with which the blood flows (blood velocity).
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This is known as the Doppler phenomenon. Blood travels at higher velocities when there is a greater pressure difference between two parts of the heart. For example, if there is a narrowing of the pulmonary valve (pulmonary stenosis) the right ventricle will squeeze harder to push the blood through the smaller than normal pulmonary valve opening resulting in propelling the blood at a higher speed. This higher speed (velocity) of blood can then be measured by the Doppler equipment of the echocardiogram and an estimation of pressure gradient across the pulmonary valve can be calculated.
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Limitations of echocardiography:
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Ultrasound waves can not travel through air as well as it can through body tissue, therefore blood vessels within the lungs can not be seen such as parts of the pulmonary arteries and veins far away from the heart.
Doppler can measure the pressure difference between one part of the heart and the other, however, it is not capable of measuring the blood pressure at any given point within the heart as it is possible in the cardiac catheterization laboratory.
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Thursday, November 13, 2008

Atrioventricular Block ECG tracing

Atrioventricular block
From Wikipedia, the free encyclopedia

An atrioventricular block (or AV block) is a type of heart block involving impairment of the conduction between the atria and ventricles of the heart. It usually involves the atrioventricular node, but it can involve other structures.
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There are three types:
First degree AV block
Second degree AV block
Third degree AV block

Source of Image

Wednesday, November 12, 2008

Heart Valve Surgery


Every few days, I see a picture or image on the Internet that REALLY captures my attention. Many times, those pictures are diagrams and illustrations that relate to heart valve surgery.
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As I remember it, before my aortic valve replacement and pulmonary valve replacement surgery, I had a difficult time grasping what actually occurs during the operation.
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That said, I have included many pictures, drawings and images in this blog (and in my book) to help you better contemplate what occurs during the pre- and post-operative heart valve replacement or heart valve repair experience.
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Your responses have so far been very positive. So, I am going to continue posting many more pictures - including human heart diagram, animated anatomy of heart functioning, mitral valve replacement diagram and more.
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Above, you will see a very interesting diagram of the patient’s chest following the incision and median sternotomy - the sternum is already broken. As you can see, the surgeon now has full access to operate on the heart once the patient is placed on the heart-lung machine (bypass) if required. Then, the heart can be stopped, cooled and then fixed!
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Transmyocardial laser revascularization (TMLR) involves the use of a laser to create tiny channels in the lower left chamber of the heart (the left ventricle), which may increase blood flow within the heart. Surgeons make an incision in the left side of the chest. While the heart is still beating, the surgeons use the laser to make between 20 and 40 tiny (one-millimeter-wide) channels through the oxygen-deprived heart muscle and into the left ventricle. These channels give a new route for blood to flow into the heart muscle, which may reduce the pain of angina. TMLR is generally considered less invasive than open heart procedures. It involves only a small incision, and patients usually do not need a blood transfusion. And because the procedure is done on a beating heart, surgeons do not need to use a heart-lung machine. Although the procedure has been approved by the Food and Drug Administration, TMLR is only being used on patients who have not responded to other treatments such as medicines, angioplasty, or coronary artery bypass surgery.

http://www.texasheart.org/HIC/Topics/Cond/CoronaryArteryDisease.cfm

Vulnerable Plaque: The real cause of heart attacks


Vulnerable Plaque
(kinda looks like a watermelon)

Swelling (inflammation) is your body's natural reaction to an injury. Inflammation can happen anywhere—on the skin, within the body, and even inside the arteries. In fact, scientists are now learning that inflammation may play a part in many of the diseases that come with aging, including coronary artery disease.
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What is vulnerable plaque?
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For many years, doctors have thought that the main cause of a heart attack or stroke was the buildup of fatty plaque within an artery leading to the heart or brain. With time, the plaque buildup would narrow the artery so much that the artery would either close off or become clogged by a blood clot (much like a clogged drain). The lack of oxygen-rich blood to the heart would then lead to a heart attack. But these types of blockages cause only about 3 out of 10 heart attacks.
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Researchers are now finding that many people who have heart attacks do not have arteries severely narrowed by plaque. In fact, vulnerable plaque may be buried inside the artery wall and may not always bulge out and block the blood flow through the artery. This is why researchers began to look at how inflammation affects the arteries, and if inflammation could lead to a heart attack. What they found was that inflammation leads to the development of "soft" or vulnerable plaque. They also found that vulnerable plaque was more than just debris that clogs an artery, but that it was filled with different cell types that help with blood clotting.
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What causes vulnerable plaque?
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Researchers now think that vulnerable plaque is formed in the following way.
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Fat droplets are absorbed by the artery, which causes the release of proteins (called cytokines) that lead to inflammation.
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The cytokines make the artery wall sticky, which attracts immune-system cells (called monocytes).
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The monocytes squeeze into the artery wall. Once inside, they turn into cells called macrophages and begin to soak up fat droplets.
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The fat-filled cells form a plaque with a thin covering.
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When this inflammation is combined with other stresses, such as high blood pressure, it can cause the thin covering over the plaque to crack and bleed, spilling the contents of the vulnerable plaque into the bloodstream.
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The sticky cytokines on the artery wall capture blood cells (mainly platelets) that rush to the site of injury. When these cells clump together, they can form a clot large enough to block the artery.
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How is vulnerable plaque detected?
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Patients with this kind of plaque may not feel symptoms. In the early stages of the process, the change in blood flow may not be detected with standard testing, but researchers are looking at special scanning techniques that may highlight the presence of vulnerable plaque.
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Cardiologists have found that by measuring the level of a substance called C-reactive protein in the bloodstream, they can predict a person's risk of heart attack or stroke. C-reactive protein is a marker that doctors use to measure inflammation activity in the body. Two large studies showed that the higher the C-reactive protein levels in the blood, the greater the risk of a heart attack.
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Not all vulnerable plaque ruptures, and researchers at the Texas Heart Institute are looking at ways to determine which vulnerable plaques are most likely to rupture. Some of our researchers are measuring the temperature of vulnerable plaque. They found that the warmer the plaque, the more likely it will crack or rupture. We are testing catheters that use infrared radiation and metal heat-sensing systems to measure the temperature of vulnerable plaque. Also, scientists at THI have discovered that vulnerable plaque has a low pH (is more acidic) and that such acidic plaques are more likely to rupture. Our researchers are testing a device for the tip of a fiberoptic catheter that will allow them to measure the pH of plaque.
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Can vulnerable plaque be prevented?
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Patients can lower their C-reactive protein levels in the same ways that they can cut their heart attack risk: take aspirin, eat a proper diet, quit smoking, and begin an exercise program. Researchers also think that obesity and diabetes may be tied to high levels of C-reactive protein. Your doctor can check your C-reactive protein levels with a blood test, and many doctors across the country are adding the test to their patients' cholesterol screening.
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Medicines like ACE inhibitors (for treating high blood pressure) and aspirin appear to reduce inflammation in the body, which may prevent heart attacks in people who already have high C-reactive protein levels.
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Cholesterol-lowering medicines called statins have been found to lower C-reactive protein levels, and doctors are now looking at how these medicines may be used to prevent heart attacks in people with normal cholesterol levels. Doctors are still studying the use of cholesterol-lowering medicines for this purpose.
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Recent studies have shown that smoking is very dangerous for people who have vulnerable plaque in their arteries. The nicotine in cigarettes directly affects the inflammatory response, causing the release of more cytokines. Researchers are also studying how your family history and your genes factor into the inflammation process. But most doctors agree that heart-healthy habits still play the most important role in reducing your risk of heart attack.
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