Coronary Angioplasty (cont.)
Daniel Lee Kulick, MD, FACC, FSCAI
Dr. Kulick received his undergraduate and medical degrees from the University of Southern California, School of Medicine. He performed his residency in internal medicine at the Harbor-University of California Los Angeles Medical Center and a fellowship in the section of cardiology at the Los Angeles County-University of Southern California Medical Center. He is board certified in Internal Medicine and Cardiology.
Melissa Conrad Stöppler, MD
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
In this Article
- Coronary balloon angioplasty and stents facts
- What is balloon angioplasty?
- How does coronary artery disease develop?
- How is coronary artery disease diagnosed?
- What medications treat coronary artery disease?
- What are the complications of percutaneous coronary intervention?
- How long is the recovery time after after percutaneous coronary intervention?
- What are the long-term results of percutaneous coronary intervention?
- Find a local Cardiologist in your town
How does coronary artery disease develop?
Arteries that supply blood and oxygen to the heart muscles are called coronary arteries. Coronary artery disease (CAD) occurs when cholesterol plaque (a hard, thick substance comprised of varying amounts of cholesterol, calcium, muscle cells, and connective tissue, which accumulates locally in the artery walls) builds up in the walls of these arteries, a process called arteriosclerosis. Over time, arteriosclerosis causes significant narrowing of one or more coronary arteries. When coronary arteries narrow more than 50% to 70%, the blood supply beyond the plaque becomes inadequate to meet the increased oxygen demand of the heart muscle during exercise. Lack of oxygen (ischemia) in the heart muscle causes chest pain (angina) in most people. However, some 25% of those with significant coronary artery narrowing experience no chest pain at all despite documented ischemia, or may only develop episodic shortness of breath instead of chest pain. These people are said to have "silent angina" and have the same risk of heart attack as those with angina. When arteries are narrowed in excess of 90% to 99%, people often have angina at rest (unstable angina). When a blood clot (thrombus) forms on the plaque, the artery may become completely blocked, causing death of a part of the heart muscles (heart attack, or myocardial infarction).
The arteriosclerotic process can be accelerated by smoking, high blood pressure, elevated cholesterol levels, and diabetes. Individuals are also at higher risk for arteriosclerosis if they are older (greater than 45 years for men and 55 years for women) or if they have a positive family history of coronary heart disease.
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