Plasma brain derived neurotrophic factor level as a modifying factor for trans fat intake and hypertension.

BACKGROUND & AIM: Long-term consumption of trans-fat has been linked with its incorporation in brain neural membrane that could lead into alteration of signalling pathways, including Brain Derived Neurotrophic Factor (BDNF). As an ubiquitous neurotrophin, BDNF is believed to play a role in the regulation of blood pressure yet prior studies shown conflicting results to its effect. Moreover, direct effect of trans fat intake to hypertension has not yet been elucidated. This study aimed to investigate the role of BDNF and its association between trans-fat intake and hypertension. MATERIALS & METHODS: We conducted a population study in Natuna Regency which once reportedly has the highest prevalence of hypertension from Indonesian National Health Survey. Subjects with hypertension and those without hypertension were recruited for the study. Demographic data, physical examination, and food recall were collected. The level of BDNF from all subjects were obtained through analysis of blood samples. RESULTS: A total of 181 participants were included in this study, comprising 134 (74%) hypertensive subjects and 47 (26%) normotensive subjects. Median of daily trans-fat intake of hypertensive subjects was higher compared to normotensive subjects (0,013 [0,0003-0,07] vs 0,010 [0,0006-0,06] % of total energy/day, p = 0,021). Interaction analysis showed significant results for plasma BDNF level in relationship of trans-fat intake and hypertension (p = 0,011). Trans-fat intake association to hypertension in overall subjects showed odds ratio (OR) of 1,85 95%CI 1,05-3,26 (p = 0,034), while in those with low-middle tercile BDNF level the OR was 3,35 95%CI 1,46-7,68 (p = 0,004). CONCLUSION: Plasma BDNF level has a modifying effect in the association between trans-fat intake and hypertension. Subjects with high trans-fat intake, while having low BDNF level, have the highest probability for hypertension.

Oral Ferrous Sulphate Improves Functional Capacity on Heart Failure Patients with Iron Deficiency Anemia.

Background: Iron deficiency anemia (IDA) in heart failure (HF) is associated with poor functional capacity. Several studies reported the benefit of iron therapy in HF with IDA on improving functional capacity. Therefore, we attempt to investigate the effect of oral iron supplementation on functional capacity in HF patients with IDA. Results: A double blind randomized controlled trial was conducted in National Cardiovascular Center Harapan Kita Hospital Universitas Indonesia. A total of 54 HFREF patients with IDA were enrolled and randomized to either oral Ferrous Sulphate (FS) 200 mg three times a day or placebo with 1:1 ratio for 12 weeks. Primary outcome was functional capacity measured by a six-minute walk test. There were 41 participants completed the study (FS n = 22, placebo n = 19). Ferrous sulphate significantly improved functional capacity changes (46.23 ± 35 m vs -13.7 ± 46 m, p < 0.001, CI -86.8 to -33.2) compared with placebo groups respectively after 12 weeks intervention. Conclusions: Oral FS supplementation for 12 weeks significantly improved functional capacity in HF patients with IDA. Trial registration: clinicaltrials.gov, NCT02998697. Registered 14 December 2016 - Retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT02998697.

Hyperthyroidism in severe mitral regurgitation post mechanical mitral valve replacement: the effect on warfarin anticoagulation.

A 24-year-old male patient came to the emergency room with melena, gum bleeding and nosebleeds. This patient has a history of mechanical prosthetic mitral valve replacement for severe mitral regurgitation (MR) and consumed warfarin irregularly, but did not come back for regular check-up. Investigations showed greatly increased thyroid function and international normalised ratio (INR) was 15.8. Patients were diagnosed with thyroid storm and bleeding due to prolongation of INR. His hyperthyroid state might have caused increased rate of degradation of vitamin K-dependent clotting factor thereby increased sensitivity to warfarin. Concomitant acute decompensated heart failure, thrombocytopenia and hypoalbuminemia also contributed to his risk of bleeding. Treatment included anti-thyroid therapy as well as warfarin reversal therapy by stopping warfarin, low-dose intravenous vitamin K due to his mechanical prosthetic valve and fresh frozen plasma. In conclusion, hyperthyroidism could increase the response to warfarin so close monitoring is needed to balance the risk of bleeding and thromboembolism.