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  1. Salmi AA, Zaki NM, Zakaria R, Nor Aliza AG, Rasool AH
    VASA, 2012 Mar;41(2):96-104.
    PMID: 22403127 DOI: 10.1024/0301-1526/a000171
    This study aims to determine whether gestational diabetes mellitus (GDM) is associated with increased arterial stiffness, inflammatory and pro-atherogenic markers compared to age matched controls.
  2. Salmi AA, Nor Aliza AG, Nik Zaki NM, Wong AR, Aida HR
    Med J Malaysia, 2010 Jun;65(2):115-8.
    PMID: 23756794 MyJurnal
    Arterial stiffness is an index of vascular health; normal pregnancy is associated with reduced arterial stiffness. This cross sectional study compared arterial stiffness in older (≥35 years) and the younger (≤34 years) age groups of pregnant women. Arterial stiffness was assessed noninvasively in 66 pregnant women between 23 - 32 weeks gestation (41 women ≤ 34 years, 25 women ≥ 35 years) using the parameters pulse wave analysis and pulse wave velocity. Blood pressure (BP), body mass index (BMI), serum total cholesterol (TC) and fasting blood glucose (FBS) were also recorded. Mean ages of the younger and older age groups were 27.6±0.62 and 39.3±0.58 years; no significant difference was seen between the groups in their BMI, TC, FBS, SBP, DBP and gestational age. The older age group of women have increased arterial stiffness (augmentation index 19.4±1.9% vs 13.2±1.6%, p=0.015) and aortic stiffness (pulse wave velocity 8.7±0.3 vs 7.7±0.2 m/s, p=0.004) compared to the younger women. Linear regression analysis showed a positive significant correlation between age and augmentation index (R=0.278, p=0.026), and pulse wave velocity (R=0.350, p=0.004). We conclude that older pregnant women has increased arterial stiffness compared to a younger age group of pregnant women suggesting that vascular changes due to ageing occurs in pregnancy despite cardiovascular adaptations occurring in pregnancy.
  3. Marini M, Salmi AA, Watihayati MS, SMardziah MD, Zahri MK, Hoh BP, et al.
    Med J Malaysia, 2008 Mar;63(1):31-4.
    PMID: 18935728 MyJurnal
    Duchenne Muscular Dystrophy (DMD) is an X-linked recessive genetic disorder characterized by rapidly progressive muscle weakness. The disease is caused by deletion, duplication or point mutation of the dystrophin gene, located on the X chromosome (Xp21). Deletion accounts for 60% of the mutations within the 79 exons of the dystrophin gene. Seven exons (43, 44, 45, 46, 49, 50, and 51) were found to be most commonly deleted among the Asian patients. To detect the frequency of deletion of these 7 exons in Malaysian DMD patients, we carried out a molecular genetic analysis in 20 Malaysian DMD patients. The mean age of initial presentation was 60 months (SD 32 months, range 5-120 months). Fourteen patients were found to have deletion of at least one of the seven exons. The remaining six patients did not show any deletion on the tested exons. Deletions of exons 49, 50 and 51 were the most frequent (71.43%) and appear to be the hot spots in our cohort of patients.
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