Medical therapy for coronary artery disease works, even (especially) in the real world

2001 ◽  
Vol 110 (6) ◽  
pp. 497-498 ◽  
Author(s):  
Michael S. Lauer
2017 ◽  
Vol 20 (9) ◽  
pp. A626
Author(s):  
J Heiskanen ◽  
J Hartikainen ◽  
JA Martikainen ◽  
H Miettinen ◽  
M Hippeläinen ◽  
...  

2020 ◽  
Vol 8 (4S) ◽  
pp. 104-110 ◽  
Author(s):  
N. A. Kochergin ◽  
V. I. Ganyukov

Background. Today, a number of unresolved issues remain regarding vulnerable coronary plaques, one of which is the need for preventive revascularization.Aim. Evaluation of the appropriateness of preventive revascularization of functionally insignificant lesions of the coronary arteries with signs of vulnerability according to the virtual histology of intravascular ultrasound in patients with stable coronary artery disease.Methods. The prospective randomized study includes patients with stable coronary artery disease and isolated intermediate-grade coronary stenosis. The first step in patients is measured fractional flow reserve to confirm the hemodynamic insignificance of stenosis. Then an intravascular ultrasound is performed to verify signs of plaque vulnerability: a thin-cap fibroatheroma and / or minimum lumen area <4 mm2 and/or plaque burden >70%. After that, patients are randomized into two groups: preventive revascularization or optimal medical therapy. After 12 months, patients undergo repeated intravascular ultrasound and end-point analysis.Results. So far, 10 patients have been included in the study (6 in the preventive revascularization group and 4 in the optimal medical therapy group). No endpoints and complications were recorded in both groups in 30-days follow-up.Conclusion. Intravascular imaging methods can identify vulnerable coronary plaques, which allows you to use a personalized approach in determining treatment tactics, one of which can be preventive revascularization.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Andreas Schaefer ◽  
Sarah Weinberger ◽  
Martin Eigenthaler ◽  
Georg Ertl ◽  
Johann Bauersachs

Background: Incomplete inhibition of P2Y 12 -mediated platelet activation during clopidogrel treatment has been associated with increased cardiovascular morbidity and mortality after percutaneous coronary intervention. This study aimed to investigate the incidence of impaired individual clopidogrel-responsiveness using a P2Y 12 -specific and pre-treatment-independent assay in a real world situation. Methods: 100 consecutive patients with coronary artery disease on clopidogrel treatment (> 5 days including a loading dose of at least 300 mg) were screened for response to ADP-induced platelet signalling. We assessed the vasodilator-stimulated phosphoprotein-based platelet reactivity index (PRI) as the only P2Y 12 -specific assay to determine clopidogrel responsiveness. Insufficient inhibition of P2Y 12 by clopidogrel was defined as a PRI >50% based on previous studies indicating increased risk of stent thrombosis under this condition. The results were compared with conventional assays to assess ADP-induced P-selectin surface-expression and conventional turbinometric platelet aggregation to several concentrations of ADP. Results: Clopidogrel significantly lowered functional platelet reactivity in patients with coronary artery disease compared to untreated patients. However, insufficient individual response to treatment predisposing for adverse events and therefore previously described as “non-response” was diagnosed in 69% of clopidogrel-treated patients using PRI. Conventional aggregation failed to detect insufficient P2Y 12 -inhibition in 1/3of patients with a PRI>50%. Conclusion: Using the PRI as the only P2Y 12 -specific assay to evaluate the treatment effect of clopidogrel in patients with coronary artery disease, insufficient P2Y 12 -inhibition was present in the majority of patients in a real-world scenario. Insufficient P2Y12-inhibition could not be reliably detected by conventional aggregation More prospective studies are needed to evaluate the influence of the high prevalence of incomplete clopidogrel responsiveness to major adverse cardiac events.


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