Health Coronary Heart Disease
Cause of Coronary Heart Disease
Big heart secrets 'aid athletes'
A study of top rowers has found how a naturally-produced hormone can actually make their hearts bigger and more powerful.
Italian scientists measured the hormone IGF-1 in 38 people, half of them rowers.
The journal Clinical Endocrinology reports rowers had higher hormone levels and larger hearts, both in terms of size and ability to pump blood.
A UK researcher said IGF-1 might be abused by future athletes.
Increases in the level of IGF-1, which stands for "insulin-like growth factor" can follow increases in the level of human growth hormone, a chemical which has figured in past doping scandals.
The hormone has been linked with the body's ability to trigger muscle strengthening, but this study looks specifically at how it might affect the heart.
The researchers from the Universities of Milan and Naples, used a battery of tests and measurements to look precisely at the structure and function of the rowers' hearts.
Compared with the "control" volunteers, they had larger chambers, and thicker muscle walls.
These measurements increased in line with increases in the amount of IGF-1 in their blood sample.
The rowers also had a far lower resting heart rate compared with the others.
Dr Giovanni Vitale, who led the study, said: "Our results show both the left and right sides of the rowers' hearts are larger, and function at an enhanced capacity compared with those of controls.
"The causes of this are not completely clear - it could be due to the production of growth factors, such as IGF-1, during training."
Professor Peter Sonksen, a professor in endocrinology from St Thomas' Hospital in London, has been asked by the World Anti-Doping Agency to investigate the possibility of a test for IGF-1 abuse in athletes.
He said that it would be difficult to detect artificially-heightened levels of the hormone.
He said: "People do have different levels of IGF-1 naturally, although elite athletes do tend to have higher levels.
"You can be born with higher levels, and then training can increase those further."
Blood pressure 'link to dementia'
Controlling blood pressure from middle-age onwards may dramatically reduce the chances of developing dementia, researchers have said.
Two studies support a link between high blood pressure and dementia risk - with one by an Imperial College London team suggesting treatment could cut this.
This study, by published in the Lancet Neurology journal, found blood pressure drugs reduce dementia by 13%.
The Alzheimer's Society said better control could save 15,000 lives a year.
As many as one in four people has high blood pressure, in many cases undiagnosed or untreated.
The precise reasons why high blood pressure might increase the risk of dementia are not fully understood although many scientists believe that it can starve the brain of bloodflow and the oxygen it carries.
Patients suffering this restricted bloodflow are often described as having "vascular dementia", and account for approximately a quarter of dementia patients.
Other types of dementia, such as Alzheimer's disease, have no obvious link to bloodflow, but some experts think that blood pressure may still be somehow contributory in some cases.
The Lancet Neurology study looked at a trial of elderly patients with high blood pressure to see if those who were receiving treatment were less likely to develop any form of dementia compared with those left untreated.
The trial was stopped early after the benefits of treatment in terms of reducing strokes and heart disease were so obvious it became unethical to deny them to everyone.
Although this meant that no benefits in terms of dementia could be found, when these results were combined with other similar studies in different age groups, the incidence of dementia was 13% lower in the treated groups.
Dr Ingmar Skoog, from the Institute of Neurosciences at Sweden's Goteburg University, said that the need to treat high blood pressure, reducing heart attacks and strokes, was clear, even without the additional results on dementia.
Rebecca Wood, from the Alzheimer's Research Trust, said the finding was an "exciting development", which, if repeated, could offer hope to the 700,000 people in the UK with dementia.
The Alzheimer's Society, however, stressed the need to try to prevent the disease.
Its own unpublished research suggested that vascular dementia was six times more likely to develop in people who had high blood pressure in their 40s and 50s.
If "best practice" in blood pressure treatment was applied to the UK population, it said, with every case detected and treated appropriately, this would save 15,000 lives a year.
Professor Clive Ballard, its director of research, said: "Only half of people over 65 receive effective treatment, yet we know treatment works."
The charity's chief executive, Neil Hunt, urged everyone, even those in middle age, to have regular blood pressure and cholesterol checks.
Cholesterol genes 'protect heart'
A third of the population have genes that could help them in the fight against heart disease, say scientists.
A study of 147,000 patients suggests that certain types of the CETP gene might increase the levels of so-called "good" cholesterol.
UK and Dutch research, published in the Journal of the American Heart Association, found a 5% cut in heart attacks for those with the key types.
A UK geneticist said it could point to drugs which help many more people.
Scientists already know that cutting the levels of "bad" cholesterol in the bloodstream protects your heart, and well-established drugs such as statins aim to do precisely this.
The relationship between the levels of "good", or HDL, cholesterol, and heart health are less clear, although there is some evidence that raising these levels is good for you.
The team from Cambridge and Newcastle universities, and the University of Groningen in the Netherlands, merged the results of almost 100 other studies, involving 147,000 people worldwide.
They looked for the effect of having one of six different variations of the CETP gene.
The most popular three all seemed to carry a modest positive effect, raising HDL cholesterol levels by between 3% and 5%, and people with them were less likely to have a heart attack.
Cause and effect
Professor John Danesh, who led the study, said that the findings added weight to the idea that heart disease could be prevented by raising HDL levels, perhaps by drugs that blocked CETP.
A trial into a drug which raised HDL cholesterol by influencing CETP was abandoned in 2006 due to an increase in heart disease and deaths, but some scientists believe it may still be possible to target the gene effectively and safely.
Professor Peter Weissberg, the British Heart Foundation, said: "Researchers are questioning whether approaches that raise HDL cholesterol could further prevent heart disease.
"This suggests that it may have benefits, but that more studies are needed to determine how much might be derived."
Dr Aroon Hingorani, a lecturer in genetics from University College London, said that the relatively small decrease in risk meant that the presence of a particular variant of the CETP gene could not help predict with any accuracy the risk of an individual falling prey to heart disease.
She said: "What it does provide are important insights into the 'cause and effect' relationship, and if you understand this better, you can develop drugs which target it."
Coronary Heart Disease, chronic illness in which the coronary arteries, the vessels that supply oxygen-carrying blood to the heart, become narrowed and unable to carry a normal amount of blood. Most often, the coronary arteries become narrowed because of atherosclerosis, a process in which fatty deposits called plaque build up on the inside wall of an artery (see Arteriosclerosis). Plaque is made of oily molecules known as cholesterol, fibrous proteins, calcium deposits, tiny blood cells known as platelets, and debris from dead cells. Plaque formation often begins in adolescence and progresses very slowly over the course of decades. Gradually, the growing plaque thickens the wall of the artery, reducing the space for blood to flow through.
Cardiac muscle, found only in the heart, drives blood through the circulatory system. Cardiac muscle cells connect to each other by specialized junctions called intercalated disks. Without a constant supply of oxygen, cardiac muscle will die, and heart attacks occur from the damage caused by insufficient blood supply to cardiac muscle.
The human heart is a hollow, pear-shaped organ about the size of a fist. The heart is made of muscle that rhythmically contracts, or beats, pumping blood throughout the body. Oxygen-poor blood from the body enters the heart from two large blood vessels, the inferior vena cava and the superior vena cava, and collects in the right atrium. When the atrium fills, it contracts, and blood passes through the tricuspid valve into the right ventricle. When the ventricle becomes full, it starts to contract, and the tricuspid valve closes to prevent blood from moving back into the atrium. As the right ventricle contracts, it forces blood into the pulmonary artery, which carries blood to the lungs to pick up fresh oxygen. When blood exits the right ventricle, the ventricle relaxes and the pulmonary valve shuts, preventing blood from passing back into the ventricle. Blood returning from the lungs to the heart collects in the left atrium. When this chamber contracts, blood flows through the mitral valve into the left ventricle. The left ventricle fills and begins to contract, and the mitral valve between the two chambers closes. In the final phase of blood flow through the heart, the left ventricle contracts and forces blood into the aorta. After the blood in the left ventricle has been forced out, the ventricle begins to relax, and the aortic valve at the opening of the aorta closes.
Atherosclerosis, or the narrowing of arteries due to the buildup of plaque along the inner lining, is the single most lethal condition in the United States. The plaques consist principally of fat and cholesterol deposits but also contain blood platelets, decomposing muscle cells, and other tissue. Since plaques usually reduce blood flow in major arteries, their presence represents a serious health risk, leading to heart disease, stroke, and the disruption of kidney and intestinal function. Poor circulation, also a result of plaque buildup, impairs movement of the limbs. Fragments of the plaques may break off and travel through the bloodstream to obstruct smaller vessels. The plaques unfortunately become larger and more numerous with age, especially in people with high levels of cholesterol in their diet and bloodstream.
When its blood supply is reduced, the heart does not receive sufficient oxygen. This oxygen deficit leads to two main consequences: chest pain known as angina pectoris, and heart attack, in which part of the heart dies because of oxygen deprivation. Coronary heart disease is the leading cause of death in the United States, responsible for about 515,000 deaths each year.