Coronary artery disease

Coronary heart disease (CHD), also called coronary artery disease and atherosclerotic heart disease, results from the growth of atheromatous plaques (associated with progressive accumulation of macrophages) within the blood vessel wall. After decades of progression, some of these atheromatous plaques often rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle. Current views are that an inflammatory process of the lining of the arteries, though poorly understood in specifics, promotes the disease progression.

Pathophysiology

Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the myocardial cells. When myocardial cells die from lack of oxygen, this is called a myocardial infarction (commonly called a heart attack). It leads to heart muscle damage, heart muscle death and later scarring without heart muscle regrowth.

Myocardial infarction usually results from the sudden occlusion of a coronary artery when a plaque ruptures, activating the clotting system and atheroma-clot interaction fills the lumen of the artery to the point of sudden closure. The typical narrowing of the lumen of the heart artery before sudden closure is typically 20%, according to clinical research completed in the late 1990s and using IVUS examinations within 6 months prior to a heart attack. High grade stenoses exceeding 75% blockage, such as detected by stress testing, were found to be responsible for only 14% of acute heart attacks. The events leading up to plaque rupture are only partially understood. Myocardial infarction is also caused, far less commonly, by spasm of the artery wall occluding the lumen, a condition also associated with atheromatous plaque and CHD.

CHD is associated with smoking, obesity and hypertension. A family history of CHD is one of the strongest predictors of CHD. Screening for CHD includes evaluating homocysteine levels, high-density and low-density lipoprotein (cholesterol) levels and triglyceride levels.

Angina

The pain associated with very advanced CHD is known as angina, and usually presents as a sensation of pressure in the chest, arm pain, jaw pain, and other forms of discomfort. The word discomfort is preferred over the word pain for describing the sensation of angina, because it varies considerably among individuals in character and intensity and most people do not perceive angina as painful, unless it is severe. There is evidence that angina and CHD present differently in women and men.

Angina that occurs regularly with activity, upon awakening, or at other predictable times is termed stable angina and is associated with high grade narrowings of the heart arteries. The symptoms of angina are often treated with nitrate preparations such as nitroglycerin, which come in short-acting and long-acting forms, and may be administered transdermally, sublingually or orally. Many other more effective treatments, especially of the underlying atheromatous disease, have been developed.

Angina that changes in intensity, character or frequency is termed unstable. Unstable angina may precede myocardial infarction, and requires urgent medical attention. It is treated with oxygen, intravenous nitroglycerin, and morphine. Interventional procedures such as Percutaneous Transluminal Coronary Angioplasty may be done.

Prevention

Coronary heart disease is the most common form of heart disease in the Western world. Prevention centers on the modifiable risk factors: blood sugar, lipoprotein transport systems, obesity, homocysteine, hypertension, sedentary lifestyle, dietary choices, smoking, uric acid, omega 3 oils, and an increasingly growing and large number of other physiological markers and homeostatic mechanisms currently under scientific investigation.

Individuals with CHD are advised to avoid fats that are readily oxidized (e.g., saturated fats and trans-fats), limit carbohydrates and processed sugars to reduce production of all and especially Low density lipoproteins while increasing High density lipoproteins, keeping blood pressure normal, exercise and stop smoking. These measures limit the progression of the disease and may also help reverse it in some people.

Risk factor management is carried out during cardiac rehabilitation, a 4-phase process beginning in hospital after MI, angioplasty or heart surgery and continuing for a minimum of three months. Exercise is a main component of cardaic rehabiltation along with diet, smoking cessation and blood pressure and cholesterol management.

Recent research

Controversial research has recently suggested a link between the atherosclerosis-causing CHD and the presence of nanobacteria in the arteries. However, trials of currently available antibiotics known to inhibit or kill some of these microorganisms have not shown much benefit to patients. If an infectious role were found to be a significant factor, this could have important implications for treatment and prevention of the disease beyond the many current, proven strategies. See atheroma & atherosclerosis.