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Background: Treatment of the left ventricular thrombus (LVT) with Vitamin K antagonists (VKAs) such as warfarin may lead to longer hospitalization. Thus, the potential of non-VKA oral anticoagulants as alternative to warfarin need to be explored. This study aims to investigate the size reduction or resolution of LVT with apixaban compared to conventional warfarin. Materials and Methods: This is a pilot, prospective, single-center, randomized, single-blinded outcome study with patients diagnosed with LVT. Patients diagnosed with LVT by echocardiography were randomized into two treatment groups: apixaban or warfarin, with target international normalized ratio 2–3. Echocardiography was repeated at weeks 6 and 12 to assess the LVT size. The percentage of reduction or total resolution during the first 12 weeks was the primary endpoint. Repeated measure ANCOVA was used to evaluate the differences in left ventricular (LV) thrombus size between treatment groups. Results: Twenty-seven patients were recruited: 14 were treated with apixaban and 13 patients with warfarin. Thirteen patients completed treatment in the apixaban arm with one patient lost to follow-up, and one death observed. In the warfarin arm, nine patients completed the study follow-up, and four died during the follow-up. The mean (standard deviation [SD]) reduction in LV thrombus size in apixaban arm was 65.1% (SD 31.3) versus warfarin arm, 61.5% (SD 44.0) at the 12th week follow-up (P = 0.816). Safety outcomes were similar with both treatment arms. Conclusions: This pilot study suggests that apixaban may have similar effectiveness and safety to warfarin for LVT resolution.

A 47-year-old Malay man who presented with fever, poor oral intake and loss of weight for 1 month duration. Further work-up revealed evidence of disseminated Salmonella infection that was further complicated with pericardial and pleural empyema. Cultures from pericardial and pleural fluids grew Salmonella species with negative serial blood cultures. Contrast enhanced CT thorax showed pleural effusion with large pericardial effusion. The patient was treated with antibiotics and drainage of pericardial and pleural empyema was done and he was discharged well.

Objective: Assessment on platelet responsiveness to aspirin may be required in selected clinical conditions. So far, no standardization in laboratory practices for aspirin assessment using whole blood (WB) platelet aggregation based test. A study for method validation was performed to investigate the aspirin effects on platelets by comparing with a reference method. Methods: Forty patients taking aspirin were analyzed using WB by conventional platelet aggregometer (Chrono-Log Model 500CA/560CA). Among these patients, nine of them had their platelet rich plasma (PRP) tested by the same analyzer (reference method). Another WB specimens from 25 patients were tested on both ChronoLog and Multiplate® (Dynabyte GmbH), which is a newer generation platelet function analyzer. Results: There were good and moderate agreements between WB on the Chronolog analyzer vs the reference method and WB on Chronolog vs WB on Multiplate® analyzers respectively. Conclusions: There are agreements between PRP and WB aggregation (WBA) methods in detecting aspirin effects on platelets. It is recommended that the test validation for the assessment of platelet responsiveness to aspirin is interpreted and correlated with the reference method preferably PRP.

A b s t r ac t Background To assess potentially elevated cardiovascular risk related to new antihyperglycemic drugs in patients with type 2 diabetes, regulatory agencies require a comprehensive evaluation of the cardiovascular safety profile of new antidiabetic therapies. We assessed cardiovascular outcomes with alogliptin, a new inhibitor of dipeptidyl peptidase 4 (DPP-4), as compared with placebo in patients with type 2 diabetes who had had a recent acute coronary syndrome. Methods We randomly assigned patients with type 2 diabetes and either an acute myocardial infarction or unstable angina requiring hospitalization within the previous 15 to 90 days to receive alogliptin or placebo in addition to existing antihyperglycemic and cardiovascular drug therapy. The study design was a double-blind, noninferiority trial with a prespecified noninferiority margin of 1.3 for the hazard ratio for the primary end point of a composite of death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke. Results A total of 5380 patients underwent randomization and were followed for up to 40 months (median, 18 months). A primary end-point event occurred in 305 patients assigned to alogliptin (11.3%) and in 316 patients assigned to placebo (11.8%) (hazard ratio, 0.96; upper boundary of the one-sided repeated confidence interval, 1.16; P

To determine whether pulse wave velocity (PWV) as a measure of arterial stiffness is a marker of coronary artery diseases (CAD), the authors did a cross-sectional study in 92 patients undergoing coronary angiography for suspected CAD. Arterial stiffness was assessed through recording PWV from the left carotid-right femoral arteries using an automated machine. The mean PWV was higher in patients with CAD than in those without CAD (11.13+/-0.91 vs 8.14+/-1.25 m/sec; P

Background/aim: VKORC1 and CYP2C9 genetic polymorphisms may not accurately predict warfarin dose requirements. We evaluated an existing warfarin dosing algorithm developed for Malaysian patients that was based only on VKORC1 and CYP2C9 genes. Materials and methods: Five Malay patients receiving warfarin maintenance therapy were investigated for their CYP2C9*2, CYP2C9*3, and VKORC1-1639G>A genotypes and their vitamin K-dependent (VKD) clotting factor activities. The records of their daily warfarin doses and international normalized ratio (INR) 2 years prior to and after the measurement of VKD clotting factors activities were acquired. The mean warfarin doses were compared with predicted warfarin doses calculated from a genotypic-based dosing model developed for Asians. Results: A patient with the VKORC1-1639 GA genotype, who was supposed to have higher dose requirements, had a lower mean warfarin dose similar to those having the VKORC1-1639 AA genotype. This discrepancy may be due to the coadministration of celecoxib, which has the potential to decrease warfarin's metabolism. Not all patients' predicted mean warfarin doses based on a previously developed dosing algorithm for Asians were similar to the actual mean warfarin dose, with the worst predicted dose being 54.34% higher than the required warfarin dose. Conclusion: Multiple clinical factors can significantly change the actual required dose from the predicted dose from time to time. The additions of other dynamic variables, especially INR, VKD clotting factors, and concomitant drug use, into the dosing model are important in order to improve its accuracy.

Various factors may contribute to a hypercoagulable state and acute vascular thrombosis. A prospective study was conducted involving 165 coronary heart disease (CHD) patients from the Cardiology Unit, Hospital Universiti Sains Malaysia. The purpose of this study was to investigate the relationship among factor VIII (FVIII), prothrombin time (PT), activated partial thromboplastin time (APTT), and activated protein C resistance (APC-R) state among CHD patients and to look for potential clinical applications from these laboratory findings. There were 110 cases diagnosed as acute coronary syndrome (ACS), whereas another 55 were stable coronary artery disease (SCAD) patients. PT, APTT, FVIII, and APC-R assays were performed on all subjects. There was a significant difference between the FVIII level and the APTT results (P value0.0001). A negative relationship was found between the FVIII level and the APTT from linear regression analysis (R(2) = 10%, P value0.0001). For each 1% increase in the FVIII level, the APTT was reduced by 0.013 s (95% confidence interval (CI) between -0.019 and -0.007). Interestingly, none of the SCAD patients had abnormally short APTT. Approximately 68.4% of cases with a positive APC-R assay were found to have a high FVIII level. In conclusion, the APTT test is a potential hemostatic marker for hypercoagulable state including in arterial thrombosis.

Background Biomarkers play a pivotal role in the diagnosis and management of patients with acute coronary syndrome. This study aimed to investigate the differences in level of several biomarkers, i.e. C-reactive protein, myeloperoxidase, soluble CD40 ligand and placental growth factor, between acute coronary syndrome and chronic stable angina patients. The relationship between these biomarkers in the coronary circulation and systemic circulation was also investigated. Methods A total of 79 patients were recruited in this study. The coronary blood was sampled from occluded coronary artery, while the peripheral venous blood was withdrawn from antecubital fossa. The serum concentrations of C-reactive protein, soluble CD40 ligand and placental growth factor and plasma concentration of myeloperoxidase were measured using ELISA method. Results The systemic level of the markers measured in the peripheral venous blood was significantly increased in acute coronary syndrome compared to chronic stable angina patients. The concentrations of the C-reactive protein, myeloperoxidase and soluble CD40 ligand taken from peripheral vein were closely similar to the concentration found in coronary blood of ACS patients. The level of placental growth factor was significantly higher in coronary circulation than its systemic level. Conclusion The concentration of these C-reactive protein, myeloperoxidase, soluble CD40 ligand and placental growth factor were significantly increased in acute coronary syndrome patients. The concentration of the markers measured in the systemic circulation directly reflected those in the local coronary circulation. Thus, these markers have potential to become a useful tool in predicting plaque vulnerability in the future.