Mitral valve disease is usually a mixed pattern of stenosis and incompetence, one of which usually predominates. Both stenosis and incompetence lead to a poorly functioning valve and subsequent heart changes, which include: left ventricular hypertrophy (this is appreciably less marked in patients with mitral stenosis); increased pulmonary venous pressure; pulmonary edema; and enlargement (dilation) and hypertrophy of the left atrium.
Mitral valve stenosis can be congenital or acquired; in the latter, the most common cause is rheumatic fever. Stenosis usually occurs decades after an acute episode of rheumatic endocarditis.
Aortic valve disease, both aortic stenosis and aortic regurgitation (backflow), can produce marked heart failure. Aortic valve stenosis is the most common type of cardiac valve disease and results from atherosclerosis causing calcification of the valve leaflets. It can also be caused by postinflammatory or postrheumatic conditions. These may lead to aortic regurgitation such as infective endocarditis, degenerative valve disease, rheumatic fever, or trauma.
Valve disease in the right side of the heart (affecting the tricuspid or pulmonary valve) is most likely caused by infection. Intravenous drug use, alcoholism, indwelling catheters, and extensive burns predispose to infection of the valves, particularly the tricuspid valve. The resulting valve dysfunction produces abnormal pressure changes in the right atrium and right ventricle, and these can induce cardiac failure.
In the clinic
In practice, physicians use alternative names for the coronary vessels. The short left coronary artery is referred to as the left main stem vessel. One of its primary branches, the anterior interventricular artery, is termed the left anterior descending artery (LAD). Similarly, the terminal branch of the right coronary artery, the posterior interventricular artery, is termed the posterior descending artery (PDA).
In the clinic
A heart attack occurs when the perfusion to the myocardium is insufficient to meet the metabolic needs of the tissue, leading to irreversible tissue damage. The most common cause is a total occlusion of a major coronary artery.
Occlusion of a major coronary artery, usually due to atherosclerosis, leads to inadequate oxygenation of an area of myocardium and cell death (Fig. 3.80). The severity of the problem will be related to the size and location of the artery involved, whether or not the blockage is complete, and whether there are collateral vessels to provide perfusion to the territory from other vessels. Depending on the severity, patients can develop pain (angina) or a myocardial infarction (MI).
This is a technique in which a long fine tube (a catheter) is inserted into the femoral artery in the thigh and passed through the external and common iliac arteries and into the abdominal aorta. It continues to be moved upward through the thoracic aorta to the origins of the coronary arteries. The coronaries may also be approached via the radial or brachial arteries. A fine wire is then passed into the coronary artery and is used to cross the stenosis. A fine balloon is then passed over the wire and may be inflated at the level of the obstruction, thus widening it; this is termed angioplasty. More commonly, this is augmented by placement of a fine wire mesh (a stent) inside the obstruction to hold it open. Other percutaneous interventions are suction extraction of a coronary thrombus and rotary ablation of a plaque.
If coronary artery disease is too extensive to be treated by percutaneous intervention, surgical coronary artery bypass grafting may be necessary. The great saphenous vein, in the lower limb, is harvested and used as a graft.
It is divided into several pieces, each of which is used to bypass blocked sections of the coronary arteries. The internal thoracic and radial arteries can also be used.
In the clinic