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| 2. |
- Oldgren, Jonas, et al.
(författare)
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Myocardial damage, coagulation activity and the response to thrombin inhibition in unstable coronary artery disease.
- 2004
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Ingår i: Thrombosis and haemostasis. - 0340-6245. ; 91:2, s. 381-7
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Tidskriftsartikel (refereegranskat)abstract
- Unstable coronary artery disease is in most cases associated with plaque rupture, activation of the coagulation system and subsequent intracoronary thrombus formation which may cause myocardial cell damage. The aim of the present analysis was to assess the relation between troponin T, markers of coagulation activity, i.e. prothrombin fragment 1+2, thrombin-antithrombin complex, soluble fibrin and D-dimer, and ischemic events, i.e. death, myocardial (re-)infarction or refractory angina. 320 patients with unstable coronary artery disease were randomized to 72 hours infusion with inogatran, a low molecular weight direct thrombin inhibitor, or unfractionated heparin. Patients with elevated troponin levels had higher levels of prothrombin fragment 1+2, soluble fibrin and D-dimer before, during, and at 24 hours after cessation of anticoagulant treatment. These troponin-positive patients tended to have worse short-term clinical outcome, without relation to markers of coagulation activity. Troponin-negative patients with unchanged or early increased thrombin generation during treatment had a cluster of ischemic events within 24 hours after cessation of the study drug. The 30-day ischemic event rate was 19 % in troponin-negative patients with unchanged or early increased prothrombin fragment 1+2, and 5.7 % in patients with decreased prothrombin fragment 1+2, p=0.006, and similarly 15 % in troponin-negative patients with unchanged or early increased thrombin-antithrombin complex and 4.5 % in patients with decreased thrombin-antithrombin complex, p=0.02. In conclusion, in unstable coronary artery disease a troponin elevation indicates higher risk and higher coagulation activity. However, among the troponin negative patients, with a lower risk and lower coagulation activity, a part of the patients seem to be non-responders to treatment with a thrombin inhibitor expressed as unchanged or raised coagulation activity and a raised risk of ischemic events early after cessation of treatment.
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| 3. |
- Bräutigam, Malin, et al.
(författare)
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[Primary PTCA or thrombolysis in acute myocardial infarction?]. : Primär PTCA eller trombolys vid akut hjärtinfarkt?
- 2001
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Ingår i: Läkartidningen. - 0023-7205. ; 98:32-33, s. 3392-5
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Tidskriftsartikel (refereegranskat)abstract
- In acute ST-elevation infarction two different reperfusion strategies--thrombolytic medication and acute coronary angiography--have proved to improve the prognosis. The clinical course for patients with ST-elevation infarction is described in relation to whether they received thrombolytic medication or underwent acute coronary angiography with the aim of mechanical revascularization. The one-year mortality was high (20 percent) regardless of treatment strategy. In terms of morbidity there were no clear differences between the two treatment groups.
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| 5. |
- Montalescot, G, et al.
(författare)
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Recommendations on percutaneous coronary intervention for the reperfusion of acute ST elevation myocardial infarction.
- 2004
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Ingår i: Heart (British Cardiac Society). - 1468-201X. ; 90:6
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Forskningsöversikt (refereegranskat)abstract
- Little information is currently available from the various societies of cardiology on primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). Since primary PCI is the main method of reperfusion in AMI in many centres, and since of all cardiac emergencies AMI represents the most urgent situation for PCI, recommendations based on scientific evidence and expert experience would be useful for centres practising primary PCI, or those looking to establish a primary PCI programme. To this aim, a task force for primary PCI in AMI was formed to develop a set of recommendations to complement and assist clinical judgment. This paper represents the product of their recommendations.
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| 7. |
- Norgaard, B. L., et al.
(författare)
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Long term risk stratification of patients with acute coronary syndromes: characteristics of troponin T testing and continuous ST segment monitoring
- 2004
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Ingår i: Heart. - 1468-201X. ; 90:7, s. 739-44
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To examine the long term prognostic characteristics of troponin T testing and continuous multi-lead ST segment monitoring in combination with clinical and 12 lead ECG risk indicators in patients with acute coronary syndromes (ACS). PATIENTS AND DESIGN: Patients with suspected ACS (n = 213) were studied. Troponin T was analysed in blood samples collected during the first 12 hours after admission. Continuous vectorcardiography ST segment monitoring was performed for 24 hours and the number of ST vector magnitude episodes was registered. Patients were followed up for a median of 28 months. The end point was a composite of cardiac death and acute myocardial infarction. RESULTS: Thirty eight (18%) patients reached the composite end point. The median (interquartile range) time from study inclusion to the time of the composite end point was longer for patients predicted to be at risk by troponin T testing (n = 27) than for those predicted to be at risk by ST segment monitoring (n = 20) (8.4 (0.2-15) months v 0.3 (0.1-4.3) months, p = 0.04). Significant univariate predictors of the composite end point were age > or = 65 years, diabetes, previous myocardial infarction, congestive heart failure, use of beta blockers or diuretics at admission, 12 lead ECG ST segment depression at admission, troponin T concentration > or = 0.10 microg/l, and > or = 1 ST vector magnitude episodes. Age > or = 65 years, previous myocardial infarction, and troponin T concentration > or = 0.10 microg/l provided independent prognostic information after multivariate analysis of potential risk variables. The prognostic value of transient ischaemic episodes in ACS seems to be confined to the short term. CONCLUSIONS: Both biochemical and continuous ECG markers reflect an increased risk for patients with ACS; however, the methods exhibit different temporal risk characteristics.
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| 8. |
- Odell, Annika, 1960, et al.
(författare)
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One-year outcome after percutaneous coronary intervention for stable and unstable angina pectoris with or without application of general usage of stents in unselected European patient groups.
- 2002
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Ingår i: The American journal of cardiology. - 0002-9149. ; 90:2, s. 112-8
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Tidskriftsartikel (refereegranskat)abstract
- The outcome after percutaneous coronary intervention (PCI) of all patients treated for stable and unstable angina pectoris from July 1992 to June 1993 (group A [n = 590], of whom 3.7% received stents) was compared with the outcome in patients treated from July 1996 to June 1997 (group B [n = 768], of whom 64.7% received stents). All patients were followed up for at least 1 year. PCI was performed due to unstable angina in 34.1% and 33.5% of patients in groups A and B, respectively. More patients in group B than in group A had systemic hypertension, previous coronary artery bypass grafting, and PCI. Within 1 year, 42.2% of patients in group A versus 27.2% in group B (p <0.001) either died, had a nonfatal acute myocardial infarction (AMI), or underwent a new revascularization procedure. The difference between the groups persisted after correction for differences in baseline characteristics. No difference was seen in the subgroup that had previously undergone PCI. Mortality (2.0% vs 1.4%, p = NS) and the composite of death plus AMI (6.6% vs 6.1%, p = NS) was similar in groups A and B. The diagnoses of unstable angina and systemic hypertension at the time of the procedure were also predictors of adverse outcome. Thus, in a cohort of patients treated after the general acceptance of stenting, the composite of death, AMI, and/or revascularization procedures was significantly less than that in the cohort treated before this increase in stenting. However, this did not result in a reduced frequency of death or AMI.
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| 9. |
- Odenstedt, Jacob, 1968, et al.
(författare)
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Failure to demonstrate myocardial protective effects of the ultra short-acting calcium antagonist clevidipine in a closed-chest reperfusion porcine model.
- 2004
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Ingår i: Journal of cardiovascular pharmacology. - 0160-2446. ; 44:4, s. 407-15
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Tidskriftsartikel (refereegranskat)abstract
- Restoration of myocardial perfusion is essential in acute myocardial infarction for the salvaging of myocardial tissue. However, reperfusion per se can provoke myocardial necrosis within the jeopardized tissue. Yet, no intervention has been successfully applied to the clinical situation in this matter. Clevidipine, an ultra-short acting calcium antagonist, has, in open-chest animal models, shown to reduce the extent of reperfusion injury. In the present study we intended to reproduce those findings in a closed-chest porcine model with a clinically applicable set up. Pigs were subjected to balloon occlusion of the left anterior descending coronary artery (LAD) for 45 minutes. During 25 minutes, starting 1 minute prior to reperfusion, clevidipine, Intralipid, or saline was infused antegradely into the endangered myocardium. As no significant effects on infarct size were achieved, the model was modified. In a second phase, different anesthesias were evaluated addressing the same issue. Nonetheless no significant effects on infarct size were observed. Different techniques of occluding LAD, in an open-chest model, were investigated in a third phase, and revealed no significant differences between the techniques. However, when comparing all the closed- versus open-chest models, significant reduction in infarct size by the use of clevidipine was only obtained in the open-chest models. We could not demonstrate any significant myocardial protective effect with clevidipine in our porcine, closed-chest, acute infarct, and reperfusion model. However, in a modified open-chest model we obtained significant reduction in infarct size. Further studies are required to explain the discrepancies.
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