Early assessment and management of risk factors is known to have significant impact in preventing cardiovascular disease (CVD) and its associated burden. Cardiovascular disease risk assessment and management (CVDRAM) is best approached by teamwork across health care professionals. This study aimed at assessing health care students’ (HCSs) knowledge about the parameters needed for estimating CVD risk, their self-assessed preparedness/confidence and perceived barriers for the provision of CVDRAM services through a survey administered to third and fourth year pharmacy, medical, and nursing students in Qatar. Although all student cohorts achieved similar knowledge scores, less than half (n = 38, 47%) were able to identify all of the six main risk factors necessary to estimate absolute CVD risk, and a third (32%) were unable to identify total cholesterol as an independent risk factor necessary to estimate CVD risk. Training on the use of CVD risk assessment tools differed among the three student cohorts. All student cohorts also perceived similar levels of preparedness in CVDRAM. However, pharmacy students reported the highest preparedness/confidence with the use of the latest CVDRAM guidelines. The majority of statements listed under the barriers scale were perceived by the students as being moderate (median score = 3). Poor public acceptance or unawareness of importance of estimating CVD risk was the only barrier perceived as a major by nursing students. Future integration of interprofessional educational (IPE) activities in the CVDRAM curricula of HCSs may be a suitable strategy to minimize barriers and foster collaborative practice for the provision of CVDRAM services in Qatar.

A n at omy & P h y s io logy: C u r r e n t Re sear c h ISSN: 2161-0940 Shabana et al., Anat Physiol 2015, 5:4 http://dx.doi.org/10.4172/2161 Keywords: Doxorubicin; Etoposide; Topoisomerase II; Cardiomyocyte hypertrophy Introduction Doxorubicin (DOX), one of the most effective and used anthracyclines [1], has been used for several decades due to its potent broads spectrum antineoplastic activity [2]. DOX is heavily used to treat hematological malignancies such as multiple myeloma and hodgkin's lymphoma [3,4]. In addition, DOX has been used for the treatment of solid tumors like ovarian and breast cancer [5,6]. Despite the clinical application of DOX, it is well known to induce a dose-dependent cardiotoxicity, which limits its clinical usage [7]. DOX induced cardiotoxicity, early-onset or late onset, is characterized by a decline in left ventricular ejection fraction or the development of congestive heart failure [1]. In a retrospective analysis of three trials it has been demonstrated that 26% of all patients who receive a cumulative DOX dose of ≥ 550 mg/m2 develop DOX related congestive heart failure [8].The underlying molecular mechanism of DOX induced cardiotoxicity remains unclear. Zhang et al. reported that chronic DOX exposure induces functional and structural changes in the mitochondria; manifested by mitochondrial damage and vacuolization [9]. In addition, DOX was found to induce alterations in cardiac myosin and is responsible for nuclear membrane disruption [10]. Previous reports have associated DOX induced cardiotoxicity with its ability to produce reactive oxygen species (ROS) [11,12], which causes a release of iron and contributes to DNA damage and lipid peroxidation [13]. Recent reports have suggested that DOX-induced cardiotoxicity is mediated in part by topoisomerase II (TOPII) -β expression and activity [9,13,14]. TOPII is an enzyme that uncoils the supercoiled double stranded DNA and contributes to DNA replication. Two isoforms of TOPII exist, TOPII-a and TOPII-β, which are expressed in different tissue. TOPII-a is expressed in proliferating tissues including the bone marrow, spleen, and tumor cells and TOPII-β is expressed in adult mammalian cardiomyocytes [15]. Furthermore, an in vitro study showed that Dexrazoxane, which is the only approved iron-chelating agent to treat DOX induced cardiotoxicity, reduced the expression of TOPII-β enzyme [14]. Another study demonstrated that TOPII-β knockout mice had improved cardiac function compared to the control group [9]. In our study, we hypothesize that TOPII-β contributes to DOX induced cardiotoxicity.In our study we aimed to develop an in-vitro model in which DOX induces cardiotoxicity. In addition, we investigated the effect of inhibiting TOPII in attenuating DOX induced cardiotoxicity. Etoposide (ETO), a non-specific TOPII targeted anticancer drug and used in solid tumors such as lung cancer, lymphomas and sarcomas, was used in our study to inhibit TOPII [16]. Zhang et al. reported that ETO possess a time dependent degradation of both TOPII-a an...

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