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Warfarin is the most commonly prescribed oral anticoagulant in Indonesia. However, the time in the therapeutic range (TTR) remains low across different countries worldwide. This study aimed to analyze the challenges associated with achieving optimal warfarin control. The analysis consisted of two distinct stages. The first stage was a prospective observational study that aimed to analyze anticoagulation control, dosing consistency, INR monitoring compliance, medication adherence, and knowledge of warfarin. Meanwhile, in the second stage, focus group discussion was used to propose strategies for overcoming the challenges. The result showed that the average TTR was 49.4 ± 32.1, where only 37.5% of patients had values = 65%. The average dosing consistency obtained was 62.33 ± 32.42%. The majority of patients with supratherapeutic INR values required a 1-month monitoring interval after dose adjustment. Further analysis indicated that only 43.8% of patients were classified as adherent and 39.5% had good knowledge of warfarin, suggesting the level of medication adherence and knowledge was not optimal. Approximately 14.6% of patients received other drugs that potentially interacted with warfarin, causing fluctuations in INR. In conclusion, this study found several challenges associated with achieving optimal warfarin control including barriers to dosing consistency, INR monitoring, medication adherence, and knowledge of warfarin, as well as drug interactions. The proposed solution is a holistic approach combining multifaceted strategies to address each barrier. [ABSTRACT FROM AUTHOR]

Coronary artery disease (CAD) is one of the main causes of death from cardiovascular disease, because heart attacks result in atherosclerosis which causes narrowing of the arteries. Atorvastatin has a pleiotropic effect as anti-inflammatory through one of the target levels of High Mobility Group Box-1 (HMGB-1). This prospective observational study aimed to analyze the effect of atorvastatin on serum HMGB-1 levels in CAD. Samples were collected from prospective observation pre–post study in May–July 2018 with consecutive sampling method. Serum HMGB-1 levels were measured in patients with CAD who were given atorvastatin for CAD with type-2 diabetes mellitus compared without type-2 diabetes mellitus in a patient ward. Blood was collected on admission day and before the patient left the hospital. After centrifugation, serum samples were stored at −80 °C before measurement. We used an ELISA kit (IBL International) to determine HMGB-1 concentrations. This research protocol has been approved by the Ethical Committee of Dr. Soetomo General Hospital, Surabaya. We enrolled 38 patients and divided them into two groups which 19 patients on CAD with type-2 diabetes mellitus and 19 patients without diabetes mellitus. Serum HMGB-1 levels in CAD with type-2 diabetes mellitus were increased significantly (p = 0.049) and not significantly decreased in CAD without type-2 diabetes mellitus (p = 0.480). The HMGB-1 level was not significantly different between the two groups (p = 0.210). HMGB-1 levels after providing atorvastatin in CAD with type-2 diabetes mellitus increased significantly, meanwhile, in CAD without type-2 diabetes mellitus did not decrease significantly. The HMGB-1 level was not significantly different between the two groups. Longer time and more point for the collected sample needed for further research. [ABSTRACT FROM AUTHOR]

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Background: Antiplatelet agents used in coronary heart disease (CHD) cause gastrointestinal side effects. Omeprazole can prevent and cure these antiplatelet side effects. Clopidogrel combined with aspirin increases the risk of gastrointestinal tract ulcers and bleeding. This research studied the effect of omeprazole on the antiplatelet effect of clopidogrel. Methods: CHD patients using clopidogrel and aspirin receive omeprazole 20 mg in a single dose for 10 days. Platelet antiaggregation point for clopidogrel was measured using VerifyNow P2Y12. The cutoff points used were: low on treatment platelet reactivity (LPR) <85 P2Y12 reaction unit (PRU), normal on treatment platelet reactivity (NPR) 85–208 PRU, and high on treatment platelet reactivity (HPR) >208 PRU. Results: Using the paired t-test PRU points pre- and post-omeprazole were 154 ± 85.89 PRU and 169.4 ± 56.15 PRU, respectively. The PRU points were consistent or decreased from the previous PRU points below the HPR cutoff (p: 0.215; >0.05). Before omeprazole use, five patients were categorized as NPR, two patients as LPR, and three patients as HPR. After omeprazole use, two patients, each from HPR and NPR category had a PRU point >208; the rest showed results below the HPR point. Conclusions: In this study the PRU points of clopidogrel after omeprazole use showed a PRU <208. The hypothesis that omeprazole may reduce the antiaggregation effect of clopidogrel as shown by the increase in PRU above the cutoff points >208 PRU (HPR) was not proven. [ABSTRACT FROM AUTHOR]

To analyze the differences in the effect of dual antiplatelet post PCI on the percentage of aggregation in myocardial infarction patients with DM and non DM. Percentage of aggregation were analyzed using light transmission aggregometry (LTA) before loading dose, after PCI, and after maintenance dose of dual antiplatelet (aspirin 100mg and clopidogrel 75mg). Total 22 patients were participated in this study divided into 10 and 12 patients in diabetic and non diabetic group. Percentage of aggregation after taking dual antiplatelet maintenace dose decrease significantly in both group (p=0.006 in diabetic group and p=0.002 in non diabetic group). Mean reduction of percentage of aggregation in diabetic group (3.30±2.91%) is less than non diabetic group (6.83±5.97%). Statistical analysis shows that the mean reduction of percentage of aggregation between two groups were not significantly different (p>0.05). Mean percentage of aggregation after dual antiplatelet maintenance dose was higher in diabetic group and mean reduction of percentage of aggregation was higher in non diabetic group, although statistically in both group it is not significantly different. [ABSTRACT FROM AUTHOR]

NT-proBNP is an amino terminal fragment of prohormone BNP released when there is cardiac wall stretch due to volume overload. The increase in NT-proBNP associated with the severity of heart failure and left ventricular ejection fraction. PCI can be improved cardiac function of patients with CHD who indicated an increase in ejection fraction. The purpose of this study to analyze changes in NT-proBNP levels and ejection fraction, and analyze correlation between ejection fraction as an indicator of cardiac function and NT-proBNP as cardiac stress marker in CHD patients undergoing PCI. An observational cross sectional study was conducted to analyze NT-proBNP levels and ejection fraction in patients with coronary heart disease who underwent PCI. The inclusion criteria were all patients aged ≥ 30 years with a diagnosis of CHD and underwent PCI. Exclusion criteria were all patients who had history of aortic stenosis, aortic regurgitation, pulmonary hypertension, hypertrophic cardiomyopathy, and kidney disease. The sample was drawn with consecutive sampling method. NT-proBNP levels was measured before and 96 hours after PCI. In pre-PCI, NT-proBNP levels was (909.66 ± 1360.56) pg/mL while ejection fraction was (56.40 ± 11.68) % and in post-PCI, NT-proBNP levels was (791.22 ± 1234.67) pg/mL while ejection fraction was (61.33 ± 11.09)%. There was a correlation between NT-proBNP levels and ejection fraction (r = -0.572, p = 0.001), showed that every decrease in the levels of NT-proBNP indicates a change in heart function associated with an increase in ejection fraction, and vice versa. In conclusions, there was significant difference neither in NTproBNP levels nor in ejection fraction. The significant correlation between NT-proBNP levels and ejection fraction can be used for prediction of heart failure post PCI. [ABSTRACT FROM AUTHOR]

Coronary heart disease (CHD) is a progressive disease and is closely related to the inflammatory response and acute thrombosis of atherosclerotic plaques. Use of loading dose Clopidogrel 300mg and aspirin 200 mg as anti-platelet aggregation reported to have responded quite well. Neointimal formation and restenosis are complications that arise in PCI action, triggered by the inflammatory process, IL-6 stimulates release of hsCRP in the liver. hsCRP as an inflammatory marker of cardiovascular events is still controversial. Of the 15 patients with prevalence of 80% male, with main risk factors are dyslipidemia, hypertension and smoking. All patients were found percent aggregation < 80% is included in hypoagregation. This suggests that loading dose Clopidogrel 300mg and Aspirin 200 mg is adequate as an anti-platelet aggregation. Seen positive ranks between hsCRP group pre (1.12 ± 1.34) and hsCRP post (2.34 ± 2.03), p = 0.001 (p < 0.05). This suggests that the inflammatory response occurs due to the PCI action. Seen negative correlation between hsCRP and percent aggregation r = -0.16, p = 0.56 (p > 0.05, r < 0.514). The use of Clopidogrel 300 mg loading dose and 200 mg aspirin as anti-platelet aggregation is adequate with hypoaggregation response. Identified inflammatory response occurs because of PCI with an increase in inflammatory factors hsCRP and no correlation with percent aggregation, so that hsCRP is only referred to as inflammatory factors and not a biomarkers of inflammation and is not is directly linked to the inflammatory process and reocclusion. [ABSTRACT FROM AUTHOR]