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.
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What are the complications of percutaneous coronary intervention?
Percutaneous coronary intervention, using balloons, stents, and/or atherectomy can achieve effective relief of coronary arterial obstruction in 90% to 95% of patients. In a very small percentage of individuals, percutaneous coronary intervention cannot be performed because of technical difficulties. These difficulties usually involve the inability to pass the guide wire or the balloon catheter across the narrowed artery segments. The most serious complication of percutaneous coronary intervention results when there is an abrupt closure of the dilated coronary artery within the first few hours after the procedure. Abrupt coronary artery closure occurs in 5% of patients after simple balloon angioplasty, and is responsible for most of the serious complications related to percutaneous coronary intervention. Abrupt closure is due to a combination of tearing (dissection) of the inner lining of the artery, blood clotting (thrombosis) at the balloon site, and constriction (spasm) or elastic recoil of the artery at the balloon site.
When stents are placed patients are started on aspirin as well as a second agent for up to a year or more depending on the type of stent. These agents are clopidogrel (Plavix), prasugrel (Effient), and ticagrelor (Brilinta) may be given as an IV agent when the stent is placed for patients who cant take pills.
To help prevent the process of thrombosis during or after percutaneous coronary intervention, aspirin is given to prevent platelets from adhering to the artery wall and stimulating the formation of blood clots. Intravenous heparin or synthetic analogues of part of the heparin molecule is given to further prevent blood clotting; and combinations of nitrates and calcium blockers are used to minimize vessel spasm. Individuals at an increased risk for abrupt closure include:
- individuals with unstable angina, and
- individuals having heart attacks.
The incidence of abrupt occlusion after percutaneous coronary intervention has declined dramatically with the introduction of coronary stents, which essentially eliminate the problem of flow-limiting arterial dissections, elastic recoil, and spasm. The use of new intravenous "super aspirins", which alter platelet function at a site different from the site of aspirin-inhibition, have dramatically reduced the incidence of thrombosis after balloon angioplasty and stenting.
When despite these measures, a coronary artery cannot be "kept open" during percutaneous coronary intervention, emergency CABG surgery may be necessary. Before the advent of stents and advanced anti-thrombotic strategies, emergency CABG following a failed percutaneous coronary intervention was required in as many as 5% of patients. In the current era, the need for emergent CABG following percutaneous coronary intervention is less than 1% The overall acute mortality risk following percutaneous coronary intervention is less than one percent; the risk of a heart attack following percutaneous coronary intervention is only about 1% to 2%. The degree of risk is dependent on the number of diseased vessels treated, the function of the heart muscle, and the age and clinical condition of the patient.
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