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What You Should Know about the Healthy Heart

Updated on March 25, 2011

The efficiency of the heart depends on a whole series of properties. It needs blood with the appropriate amounts of oxygen and glucose to fuel the heart muscle. It needs a network of blood vessels, the coronary arteries, which are wide open, free of obstructions, and can expand to take a steep increase in blood flow when needed. It needs a healthy muscle mass, that contracts correctly to time and rhythmically, so that the flow of the circulation from the heart is smooth.

Obviously there are many ways in which we can upset this harmony between the blood, the blood vessels and the heart muscle itself. The act of smoking damages the heart muscle in two ways. First, nicotine is a nerve and muscle poison, so that the beat is faster and less efficient. Second, the carbon monoxide inhaled in cigarette smoke both starves the muscle of oxygen and is also a direct muscle poison. This means that the smoker's heart is not only much less efficient, but has much less capacity for recovery when a heart attack threatens.

Of healthy blood vessels

Crucial to the supply of oxygen and glucose to the heart muscle is the state of the coronary arteries that supply them. At birth, their inner lining, the surface in contact with the blood, is smooth, and their walls are muscular and elastic. The blood flows through them smoothly and without eddies or turbulence.


Sadly, as we grow older, this changes. Fatty deposits start to be laid down in the blood vessel walls - the more fat there is in the blood, the more deposits there are. The process starts early. American doctors examining the bodies of young soldiers killed in the Korean War were astonished by the extent of the fatty degeneration in their coronary arteries. It was this work that led to the first real American efforts to prevent heart disease.

In fact, everyone since involved in reducing the numbers of early deaths from heart disease has concentrated on this fatty degeneration in the coronary arteries. The disease has a medical name - atheroma - the ancient Greek word for porridge. Called this because the deposits had the looks and consistency of blobs of porridge, they are crucial to today's understanding about what happens in a heart attack.

Deposits or 'plaques' of atheroma are laid down in the walls of the arteries from childhood onwards. Their numbers and size depend almost entirely on one thing - the levels of cholesterol in the bloodstream. The higher the cholesterol level, the more extensive the atheroma: for people, like some Japanese who live on fish and vegetables, with very low cholesterol levels, there is very little atheroma, and almost no risk of heart attack.

Atheromatous plaques have been extensively analysed. They are made up of a mixture of cholesterol and a combination of fat and protein, known as low density lipoprotein, or LDL. It is enough here to know that there is a direct relationship between blood levels of LDL-choles-terol and heart attacks. The higher the LDL-cholesterol, the more atheroma appears in the arteries and the higher is the heart attack risk.

There is a simple, mechanical reason for the connection between the two. We now know that most heart attacks are triggered at the site of an atheromatous plaque, where the vessel wall is weakened. The surface of the plaque is roughened, and juts into the stream of blood. This narrowing of the tube within which the blood flows causes eddies and turbulence, with consequent strain on the wall of the blood vessel at precisely the spot where it is weakened.

If that strain becomes too great, the edge of the plaque can lift up with the force of the bloodstream. The blood rushes under the edge, lifting up the plaque to form a flap across the flow, which can be big enough to block it completely. With the flow of blood to the tissues beyond stopped, they will quickly die if they are not relieved - and the heart attack begins.


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