Platelets and thrombolytic therapy
Article Abstract:
Platelets are disk-shaped structures in the blood that are important for blood clotting. If a small blood vessel is injured, platelets clump together at the site of the injury to plug the opening and stop the loss of blood. Platelets may also aggregate inside blood vessels that are lined with rough plaques in patients with coronary artery disease; platelets adhere to the uneven surface. If platelets and another substance, fibrin, accumulate to form a clot (thrombus), the artery can become blocked, resulting in a myocardial infarction, or heart attack. Clots can be prevented or dissolved with fibrinolytic or thrombolytic drug therapy, but fibrinolytic therapy is not always predictable or effective. Arteries may resist fibrinolytic therapy or respond to it but then become blocked again; another risk is serious hemorrhage. Platelets appear to be involved in delaying restoration of blood flow and creating new clots. Some thrombi may be difficult to dissolve because they contain a high concentration of platelets. The complex physiologic interactions between platelets and fibrinolytic therapy are discussed and therapeutic approaches are evaluated. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 1990
User Contributions:
Comment about this article or add new information about this topic:
Beneficial effects of cholesterol-lowering therapy on the coronary endothelium in patients with coronary artery disease
Article Abstract:
The cholesterol-lowering effect of lovastatin may cause improvements in the heart arteries of patients with atherosclerosis. Atherosclerosis is the irregular distribution of fat (lipid) deposits in medium and large arteries. A study of 23 patients given either lovastatin or placebo plus a lipid-lowering diet found that atherosclerosis patients who took lovastatin for six months had improved blood vessel dilator (vasodilator) responses in the lining of the heart (endothelium). Prolonged therapy may be needed to reverse heart endothelial dysfunction. Lipid lowering therapy may not produce changes in the short term but may improve heart endothelial function over the longer term in patients with fat deposits in the arteries of the heart. Aggressive lipid lowering may improve the regulation of the tone of heart arteries, diminishing blood vessel constriction and improving vasodilation. Aggressive lipid lowering may become one aspect of treatment for chest pain and syndromes in which blood flow to the heart is restricted.
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 1995
User Contributions:
Comment about this article or add new information about this topic:
Comparison of fondaparinux and enoxaparin in acute coronary syndromes
Article Abstract:
A study was conducted to assess whether fondaparinux would preserve the anti-ischemic benefits of enoxaparin while reducing bleeding, on a randomly assigned 20,078 patients with acute coronary syndromes. It was revealed that fondaparinux is similar to enoxaparin in reducing the risk of ischemic events at nine days, but it substantially reduces major bleeding and improves long-term mortality and morbidity.
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 2006
User Contributions:
Comment about this article or add new information about this topic:
- Abstracts: Breast conservation therapy: severe breast fibrosis after radiation therapy in patients with collagen vascular disease
- Abstracts: New challenges for thrombolytic therapy. Care of the patient and management of complications after percutaneous coronary artery interventions
- Abstracts: Catheter and surgical treatment of cardiac arrhythmias. Catheter ablation therapy for Supraventricular Arrhythmias
- Abstracts: New opportunistic infections - more opportunities. New genetic insights into Parkinson's disease
- Abstracts: Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure