1,721,059 research outputs found
Current status of activation markers in ischemic heart disease: Markers of coagulation activation
No full textInvasive coronary revascularisation is better than conservative treatment in patients with acute coronary syndromes
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Direct thrombin inhibitors for the treatment of acute coronary syndromes and during percutaneous coronary interventions
No full textAs acute coronary syndromes are principally sustained by plaque complication and subsequent thrombus formation, anticoagulant therapy plays a central role in avoiding ischemic events; its main targets are thrombin activity and generation. Despite its limitations, such as its scarce ability to activate bound thrombin and its unpredictable pharmacological response, heparin is the most widely uzed drug for this purpose. Direct thrombin inhibitors are biologically superior to heparin principally because they inhibit clot-bound and circulating thrombin without interacting with other plasma proteins. Their clinical role in acute coronary syndromes and during coronary intervention has been tested in several trials.
This article overviews the principal trials involving active-site direct thrombin inhibitors in acute coronary syndrome and during coronary intervention and compares their efficacy and safety with unfractionated heparin. It also describes ongoing trials and analyzes further clinical developments such as their use in addition to the glycoprotein Ilb/IIIa inhibitors and the potential advantage, possible with new agents orally administered
ABNORMAL CORONARY VASOCONSTRICTION AS A PREDICTOR OF RESTENOSIS AFTER SUCCESSFUL CORONARY ANGIOPLASTY IN PATIENTS WITH UNSTABLE ANGINA-PECTORIS
No full textBackground. High rates of restenosis after coronary angioplasty have been reported in patients with vasospastic angina. This study was designed to determine whether the occurrence of abnormal coronary vasoconstriction, detected by means of hyperventilation testing before angioplasty, influences the risk of restenosis after successful dilation.
Methods. Hyperventilation testing was performed 0 to 4 days before coronary angioplasty in 106 consecutive patients with unstable angina and single-vessel coronary artery disease. Abnormal coronary vasoconstriction was considered present if hyperventilation-induced myocardial ischemia occurred during the recovery phase of the test. All patients had follow-up angiography 8 to 12 months after angioplasty.
Results. Abnormal coronary vasoconstriction was observed in 48 patients (group 1), whereas 58 patients (group 2) had either a negative response throughout the test or a positive response only during the overbreathing phase of the hyperventilation test. Angioplasty was successful in 40 patients in group 1 and 51 in group 2. Restenosis was documented in 29 patients (73 percent) in group 1 and 13 (25 percent) in group 2 (relative risk of restenosis, 2.84; 95 percent confidence interval, 1.69 to 4.28; P < 0.001). In a multivariate analysis, the following three characteristics were independently related to the risk of restenosis (in descending order of importance): ST-segment elevation during spontaneous ischemic attacks (P < 0.001), hyperventilation-induced abnormal coronary vasoconstriction (P < 0.001), and the presence of a lesion more than 10 mm long in the left anterior descending coronary artery (P < 0.05).
Conclusions. In patients with unstable angina and single-vessel coronary artery disease who have been selected for coronary angioplasty, the presence of hyperventilation-induced abnormal coronary vasoconstriction identifies a subgroup at high risk for restenosis
Effect of transdermal nitroglycerin, oral N-acetylcysteine or both in the long term treatment of unstable angina pectoris
No full textTissue-factor antigen and activity in human coronary atherosclerotic plaques
No full textBackground Coronary atherosclerotic-plaque thrombosis is a key event in the pathogenesis of unstable angina and myocardial infarction. Although plaque rupture or fissuring frequently occurs in atherosclerosis, only a small proportion of ruptured plaques develop thromboses.
Methods Tissue-factor antigen and activity were measured in atherectomy samples from 50 consecutive patients with coronary artery disease (stable angina n=19, unstable angina n=24, and myocardial infarction n=7).
Findings Median tissue-factor antigen and activity concentrations were significantly higher in plaques from patients with unstable angina and myocardial infarction than in those from patients with stable angina (antigen: 66.1 pg/mg [interquartile range 43.8-82.5] vs 32.4 pg/mg [9.8-43.4], p=0.0001; activity: 0.22 mU/mg [0.17-0.41] vs 0.13 mU/mg [0.05-0.16], p=0.0004).
Interpretation Tissue-factor, an initiator of the coagulation cascade, may account for the different thrombotic responses to the rupture of human coronary atherosclerotic plaques
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