which progresses to produce further lesions called the plaque leading to the thickening of the artery wall.

As inflammation and atherosclerotic insult continues, more white blood cells migrate to the lesion. The white blood cells become activated leading to increased production of cytokines, chemokines, growth factors and hydrolyti

Coronary heart disease (also called Atherosclerosis) is a disease of the arteries. It causes it to 'harden' affecting both medium and large arteries. It is the main cause of heart attacks and strokes responsible for over 50% of all bereavement in the western world and continues to be a major worry in developing countries.

The disease is one of the single most financial drain of the health service of several nations. The disease is mainly triggered as a response to chronic injury to the vascular endothelium. This can be due to a variety of insults such as blood pressure, stress and oxidative damage (such as smoking).

The endothelial damage from this injury leads to a response that causes the arteries to compensate the damage by altering the normal homeostatic properties. For example, the damage increases the adhesiveness of the endothelium to leukocytes (white blood cells) and platelets. Additionally this injury enhances the permeability of the artery. The injury also causes the endothelium (cells that line the blood flow of blood vessels) to produce agents such as cytokines and growth factors (signaling molecules) that then cause further progression of the inflammatory response. This then causes the migration and the proliferation of smooth muscle cells (contractile cells present in hollow organs) to form an intermediate lesion, which progresses to produce further lesions called the plaque leading to the thickening of the artery wall.

As inflammation and atherosclerotic insult continues, more white blood cells migrate to the lesion. The white blood cells become activated leading to increased production of cytokines, chemokines, growth factors and hydrolytic

e is one of the single most financial drain of the health service of several nations. The disease is mainly triggered as a response to chronic injury to the vascular endothelium. This can be due to a variety of insults such as blood pressure, stress and oxidative damage (such as smoking).

The endothelial damage from this injury leads to a response that causes the arteries to compensate the damage by altering the normal homeostatic properties. For example, the damage increases the adhesiveness of the endothelium to leukocytes (white blood cells) and platelets. Additionally this injury enhances the permeability of the artery. The injury also causes the endothelium (cells that line the blood flow of blood vessels) to produce agents such as cytokines and growth factors (signaling molecules) that then cause further progression of the inflammatory response. This then causes the migration and the proliferation of smooth muscle cells (contractile cells present in hollow organs) to form an intermediate lesion, which progresses to produce further lesions called the plaque leading to the thickening of the artery wall.

As inflammation and atherosclerotic insult continues, more white blood cells migrate to the lesion. The white blood cells become activated leading to increased production of cytokines, chemokines, growth factors and hydrolyti

to a response that causes the arteries to compensate the damage by altering the normal homeostatic properties. For example, the damage increases the adhesiveness of the endothelium to leukocytes (white blood cells) and platelets. Additionally this injury enhances the permeability of the artery. The injury also causes the endothelium (cells that line the blood flow of blood vessels) to produce agents such as cytokines and growth factors (signaling molecules) that then cause further progression of the inflammatory response. This then causes the migration and the proliferation of smooth muscle cells (contractile cells present in hollow organs) to form an intermediate lesion, which progresses to produce further lesions called the plaque leading to the thickening of the artery wall.

As inflammation and atherosclerotic insult continues, more white blood cells migrate to the lesion. The white blood cells become activated leading to increased production of cytokines, chemokines, growth factors and hydrolyti

ls that line the blood flow of blood vessels) to produce agents such as cytokines and growth factors (signaling molecules) that then cause further progression of the inflammatory response. This then causes the migration and the proliferation of smooth muscle cells (contractile cells present in hollow organs) to form an intermediate lesion, which progresses to produce further lesions called the plaque leading to the thickening of the artery wall.

As inflammation and atherosclerotic insult continues, more white blood cells migrate to the lesion. The white blood cells become activated leading to increased production of cytokines, chemokines, growth factors and hydrolyti

which progresses to produce further lesions called the plaque leading to the thickening of the artery wall.

As inflammation and atherosclerotic insult continues, more white blood cells migrate to the lesion. The white blood cells become activated leading to increased production of cytokines, chemokines, growth factors and hydrolytic enzymes that then cause further damage. This ultimately leads to the formation of advanced lesions and blockade of the arteries causing clinical complications such as stoke and heart attack.