To evaluate the suitability of two anticoagulants (heparin vs. argatroban) as adjunctive drugs during and after elective conventional percutaneous transluminal coronary angioplasty, we compared the changes in inflammatory, hemostatic, and endothelium-derived markers in groups of patients with stable angina treated with the two drugs during percutaneous transluminal coronary angioplasty. Twenty-seven patients were randomly allocated to either group 1 (15 patients who received an empiric dose of heparin and aspirin as anticoagulant), or group 2 (12 patients who received an alternative regimen of argatroban and aspirin). Both drugs were administered as a bolus followed by continuous infusion for 96 hours during and after percutaneous transluminal coronary angioplasty. There were no differences in the inflammatory response induced by percutaneous transluminal coronary angioplasty in both groups, but the fibrinogen concentration significantly decreased during percutaneous transluminal coronary angioplasty in group 2. Decreased platelet counts and increased mean platelet volume were observed during percutaneous transluminal coronary angioplasty in both groups. The levels of prothrombin fragment 1+2 and thrombin antithrombin III complex increased markedly during percutaneous transluminal coronary angioplasty. Group 2 showed a more rapid return to the baseline levels of these two markers than group 1. Secondary fibrinolysis was evidenced by a steep increase of D-dimer after percutaneous transluminal coronary angioplasty in both groups. In contrast to the significant decrease in antithrombin activities during percutaneous transluminal coronary angioplasty in group 1, no marked change in these markers was found in group 2. Although the levels of von Willebrand factor and plasminogen activator inhibitor-1 showed essentially the same changes in both groups during and after percutaneous transluminal coronary angioplasty, more markedly increased levels of tissue type plasminogen activator and type plasminogen activator-plasminogen activator inhibitor-1 complex after percutaneous transluminal coronary angioplasty were found in group 1 than in group 2. While neither drug had any effect on the percutaneous transluminal coronary angioplasty-induced inflammatory response, argatroban may more effectively inhibit the generated thrombin and prevent antithrombin consumption during and after percutaneous transluminal coronary angioplasty.
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http://dx.doi.org/10.1016/s0049-3848(99)00237-6 | DOI Listing |
J Invasive Cardiol
January 2025
Penn State Milton S. Hershey Medical Center, Hershey, Pennsylvania.
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View Article and Find Full Text PDFEur Heart J Case Rep
January 2025
Fondazione Toscana Gabriele Monasterio, Via Giuseppe Moruzzi 1, 56124 Pisa, Italy.
Background: Takotsubo syndrome (TTS) is characterized by transient left ventricular dysfunction, often triggered by emotional or physical stress. It usually presents with clinical features similar to acute coronary syndrome, making its occurrence following elective percutaneous coronary intervention (PCI) challenging to diagnose and treat.
Case Summary: A 67-year-old man with ischaemic heart disease and recurrent angina underwent elective PCI of the right coronary artery.
Cardiovasc Diagn Ther
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Department of Cardiology, Dokkyo Medical University Saitama Medical Center, Saitama, Japan.
Catheter Cardiovasc Interv
January 2025
Lancashire Cardiac Centre, Blackpool, UK.
Coronary calcification is a major factor leading to stent under-expansion, and subsequent adverse events. This meta-analysis aimed to evaluate the short and long‑term outcomes of rotational atherectomy (RA), followed by modified balloon (cutting or scoring) (MB) versus plain balloon before drug‑eluting stent implantation for calcified coronary lesions. We searched PubMed, Web of Science (WOS), Scopus, and the Cochrane Library Central Register of Controlled Trials (CENTRAL), from inception until 30 January 2024.
View Article and Find Full Text PDFJ Am Coll Cardiol
January 2025
Division of Cardiovascular Medicine, and Sulpizio Cardiovascular Institute, University of California-San Diego, La Jolla, California, USA. Electronic address:
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