First Department of Cardiology, University Catheterization Laboratories, Medical University of Gdansk, Marii Skłodowskiej-Curie 3a, 80-210 Gdańsk, Gdańsk, Poland
Prof. Dr. Miłosz J. Jaguszewski
First Department of Cardiology, University Catheterization Laboratories, Medical University of Gdansk, Marii Skłodowskiej-Curie 3a, 80-210 Gdańsk, Gdańsk, Poland
Background: The monogenic defect in familial hypercholesterolemia (FH) is detected in ∼40% of cases. The majority of mutation-negative patients have a polygenic cause of high LDL-cholesterol (LDL-C). We sought to investigate whether the underlying monogenic or polygenic defect is associated with the response to rosuvastatin. Methods: FH Individuals were tested for mutations in LDLR and APOB genes. A previously established LDL-C-specific polygenic risk score (PRS) was used to examine the possibility of polygenic hypercholesterolemia in mutation-negative patients. All of the patients received rosuvastatin and they were followed for 8 ± 2 months. A propensity score analysis was performed to evaluate the variables associated with the response to treatment. Results: Monogenic subjects had higher mean (±SD) baseline LDL-C when compared to polygenic (7.6 ± 1.5 mmol/L vs. 6.2 ± 1.2 mmol/L; p < 0.001). Adjusted model showed a lower percentage of change in LDL-C after rosuvastatin treatment in monogenic patients vs. polygenic subjects (45.9% vs. 55.4%, p < 0.001). The probability of achieving LDL-C targets in monogenic FH was lower than in polygenic subjects (0.075 vs. 0.245, p = 0.004). Polygenic patients were more likely to achieve LDL-C goals, as compared to those monogenic (OR 3.28; 95% CI: 1.23–8.72). Conclusion: Our findings indicate an essentially higher responsiveness to rosuvastatin in FH patients with a polygenic cause, as compared to those carrying monogenic mutations.
Background: In light of a falsified medications pandemic, understanding the patient perspective on falsified medicines is warranted. Our study aimed to investigate the perspectives regarding falsified medicines among patients with cardiovascular diseases. Methods: Computer-assisted telephone interviews were conducted based on a questionnaire: (i) Respondents suffering from cardiovascular diseases and (ii) respondents not being chronically ill. Only participants below 50 years of age were included. Results: We enrolled 1200 respondents total, 800 in the study group and 400 in the control group (in cooperation with a professional public opinion research center). The vast majority of participants agreed that community pharmacies are the only place that ensures the secure purchasing of non-falsified drugs (67.01% study group and 65.25% control group; p < 0.01). The majority of respondents were convinced that purchasing medications on the Internet is associated with a higher risk of receiving falsified drugs. Patients diagnosed with cardiovascular diseases and those with “non-satisfactory financial situation” had significantly decreased likelihoods of obtaining a high score in general knowledge on falsified medications (OR = 0.64 and OR = 0.58, respectively). Conclusions: Awareness of the risks associated with falsified drugs among patients with cardiovascular diseases remains high but still insufficient.
Introduction: Patients with acute coronary syndrome (ACS) and atrial fibrillation (AF) treated with percutaneous coronary intervention (PCI) are at high risk of bleeding and thromboembolic events. Thus, optimal treatment strategies in this challenging subset have been controversial. Herein, we aim to investigate different triple antithrombotic treatment (TAT) strategies in patients with ACS and AF after PCI. Methods: This was a retrospective, single-center study based on all consecutive patients with the diagnosis of ACS and AF treated with vitamin K antagonists (VKA) or non-vitamin K antagonist oral anticoagulants (NOAC) plus dual antiplatelet therapy using a P2Y12 inhibitor (clopidogrel) and aspirin (for 1 to 3 months) and observed for 12 months for major adverse cardiac events (MACE) and major or clinically relevant non-major bleeding incidents. Results: MACE occurred in 26.6% of patients treated with the VKA and 30.9% with NOAC (p = 0.659). Bleeding occurred in 7.8% of patients treated with VKA and 7.4% with NOAC (ns). Conclusions: Among patients with ACS and AF who had undergone PCI, there was no significant difference in the risk of bleeding and ischemic events among those who received TAT with NOAC and VKA.