Background Accelerated central arterial stiffening as represented by progression of aortic pulse-wave velocity (PWV) may be influenced by cardiovascular disease (CVD) risk factors. Little is known about the relationships between CVD risk factors and PWV progression among women transitioning through the menopause, or whether these relationships vary by ethnicity. To address this knowledge gap, we conducted a subgroup analysis of 303 African American and Caucasian participants in the Study of Women's Health Across the Nation (SWAN) Heart Study received PWV scans at baseline examination and at a follow-up examination an average of 2.3 years later. CVD risk factors were also assessed at baseline. Methods and Results Systolic blood pressure (SBP) and waist circumference were the strongest predictors of PWV progression, after adjustment for age, low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), diastolic blood pressure (DBP), glucose, and triglyceride levels. The magnitude of the influence of SBP, DBP, LDL-C, and glucose on PWV progression varied by ethnicity (difference in slopes: p=0.02 for SBP, p=0.0009 for DBP, p=0.005 for LDL-C, and p=0.02 for glucose). The positive relationship between SBP and PWV progression was significant among women of both ethnicities. LDL-C, DBP, and, to a lesser extent, glucose levels were positively associated with PWV progression only among African Americans. Conclusions Blood pressure, LDL-C, glucose, and excess body size may be important targets for improving vascular health and preventing clinical outcomes related to arterial stiffening, particularly among African American women.

BackgroundFamilial hypercholesterolemia is a genetic disorder mainly caused by defects in the low-density lipoprotein receptor gene. Few and limited analyses of familial hypercholesterolemia have been performed in Malaysia, and the underlying mutations therefore remain largely unknown.We studied a group of 154 unrelated FH patients from a northern area of Malaysia (Kelantan). The promoter region and exons 2-15 of the LDLR gene were screened by denaturing high-performance liquid chromatography to detect short deletions and nucleotide substitutions, and by multiplex ligation-dependent probe amplification to detect large rearrangements.ResultsA total of 29 gene sequence variants were reported in 117(76.0%) of the studied subjects. Eight different mutations (1 large rearrangement, 1 short deletion, 5 missense mutations, and 1 splice site mutation), and 21 variants. Eight gene sequence variants were reported for the first time and they were noticed in familial hypercholesterolemic patients, but not in controls (p.Asp100Asp, p.Asp139His, p.Arg471Gly, c.1705+117 T>G, c.1186+41T>A, 1705+112C>G, Dup exon 12 and p.Trp666ProfsX45). The incidence of the p.Arg471Gly variant was 11%. Patients with pathogenic mutations were younger, had significantly higher incidences of cardiovascular disease, xanthomas, and family history of hyperlipidemia, together with significantly higher total cholesterol and low density lipoprotein levels than patients with non-pathogenic variants.ConclusionsTwenty-nine gene sequence variants occurred among FH patients; those with predicted pathogenicity were associated with higher incidences of cardiovascular diseases, tendon xanthomas, and higher total and low density lipoprotein levels compared to the rest. These results provide preliminary information on the mutation spectrum of this gene among patients with FH in Malaysia.

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<.001). When the severity of CAD was expressed as 1‐, 2‐, and multiple‐vessel disease, there was a significant association between the severity of CAD and PWV. PWV differed significantly with different categorical severity of CAD even when age and total cholesterol were controlled for. In a univariable analysis, PWV was higher with higher systolic blood pressure (P<.004). The authors conclude that arterial stiffness measured through PWV is an independent and complementary cardiovascular risk marker.

Granulocyte colony-stimulating factor (G-CSF) is now widely used in patients with malignant disorders receiving intensive chemotherapy to increase leukocyte count and to upregulate phagocyte function during neutropenia. Monocytosis associated with G-CSF has been reported in anecdotal literature. We report two cases of pseudoleukemia secondary to G-CSF administration. Both patients initially presented with myelodysplastic syndrome with chromosome 7 abnormalities that evolved into acute myeloid leukemia. Case one had deletion 7q while case two initially had monosomy 7 and subsequently developed a balanced translocation between the short (p) arm of chromosome 1 and long (q) arm of chromosome 15. Following the induction chemotherapy and G-CSF administration, both of these patients developed pseudoleukemia. Patient 1 had white blood cell (WBC) count of 26 x 10(9)/l with 72% monocytes, while patient two had WBC of 14.1 x 10(9)/l with 30% monocytes. In both patients the monocytosis resolved after the discontinuation of G-CSF therapy. In summary, patients treated with G-CSF should be followed closely. In those cases with pseudoleukemia discontinuation of the drug with no supplemental chemotherapy is probably enough to control the atypical monocytosis.

Multiple myeloma (MM) is an exceptionally complicated and heterogeneous disease that is caused by the abnormal proliferation of malignant monoclonal plasma cells initiated in the bone marrow. In disease progression, a multistep process including differentiation, proliferation, and invasion is involved. Despite great improvement in treatment outcomes in recent years due to the substantial discovery of novel therapeutic drugs, MM is still regarded as an incurable disease. Patients with MM are afflicted by confronting remission periods accompanied by relapse or progression outcomes, which inevitably progress to the refractory stage. In this regard, MM may need new medications or modifications in therapeutic strategies to overcome resistance. A variety of genetic abnormalities (e.g., point mutations, translocations, and deletions) and epigenetic changes (e.g., DNA methylation, histone modification, and non-coding RNA) contribute to the pathogenesis and development of MM. Here, we review the significant roles of epigenetic mechanisms in the development and progression of MM. We also highlight epigenetic pathways as potential novel treatment avenues for MM, including their interplay, use of epigenetic inhibitors, and major involvement in immuno-oncology.

Blood transfusion is a fundamental and life-saving procedure where the consequence of errors can be fatal. Nurses’ knowledge plays an essential role in ensuring quality and safety in blood transfusion. The objective of this study was to assess blood transfusion-associated knowledge of tertiary hospital nurses on the east coast of Malaysia. This was a cross-sectional study with 200 registered nurses involved in blood transfusion procedures at Hospital Universiti Sains Malaysia. The knowledge of the nurses was evaluated by using the routine blood transfusion knowledge questionnaire based on five parts, and <50%, 50–74%, or ≥75% of the knowledge was considered as poor, moderate, or high, respectively. Based on the scoring system, the overall knowledge of blood transfusion among Malaysian nurses (33.2 ± 8.4 years) was estimated to be 54.9 ± 7.6%. In individual items, the scoring was 81.0%, 45.4%, 49.2%, 63.0%, and 90.0% in knowledge prior to blood transfusion, on pre-transfusion, on post-transfusion, on complications, and on transfusion policy, respectively. The findings of this study indicated that most of the nurses’ overall knowledge of blood transfusion was at a moderate level; therefore, training courses and continuous medical education are warranted to improve knowledge and skills of the nurses to ensure good practices of blood transfusion.

Venous thromboembolism (VTE), which encompasses deep venous thrombosis (DVT) and pulmonary embolism (PE), is a major public health concern due to its high incidences of morbidity and mortality. Patients who have experienced trauma with prolonged immobilization are at an increased risk of developing VTE. Plasma D-dimer levels have been known to be elevated in trauma patients, and they were closely correlated with the number of fractures. In other words, plasma D-dimer levels cannot be used as the only indicator of VTE in trauma cases. Given the limitations, further study is needed to explore other potential biomarkers for diagnosing VTE. To date, various established and novel VTE biomarkers have been studied in terms of their potential for predicting VTE, diagnostic performance, and improving clinical therapy for VTE. Therefore, this review aims to provide information regarding classic and essential haemostasis (including prothrombin time (PT), activated partial thromboplastin time (aPTT), D-dimer, fibrinogen, thrombin generation, protein C, protein S, antithrombin, tissue factor pathway inhibitor, and platelet count) and inflammatory biomarkers (C-reactive protein, erythrocyte sedimentation rate, and soluble P-selectin) as potential diagnostic biomarkers that can predict the risk of VTE development among trauma patients with prolonged immobilization. Thus, further advancement in risk stratification using these biomarkers would allow for a better diagnosis of patients with VTE, especially in areas with limited resources.

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