Household financial burden associated with healthcare for older people in Viet Nam: a cross-sectional survey.

BACKGROUND: Population ageing and the associated increase in the healthcare needs of older people are putting pressure on the healthcare system in Viet Nam. The country prioritizes healthcare for older people and has developed financial protection policies to mitigate financial hardship due to out-of-pocket health expenditures (OOPHEs) borne by their households. This study examines the level and determinants of the financial burden of OOPHE among households with people aged ≥ 60 years in Viet Nam. METHODS: A cross-sectional household survey was conducted among a sample of 1536 older people living in 1477 households in three provinces representing the North, Central and South regions of Viet Nam during 2019-2020. The financial outcomes were catastrophic health expenditure (CHE), using WHO's definition, and financial distress due to OOPHE. Multivariate binary logistic regression analysis was employed to determine the factors associated with these outcomes. RESULTS: OOPHE for older household members accounted for 86.3% of total household health expenditure. Of households with older people, 8.6% (127) faced CHE, and 12.2% (181) experienced financial distress due to OOPHE. Households were at a higher risk of incurring financial burdens related to health expenditures if they had fewer household members; included only older people; were in rural or remote, mountainous areas; and had older members with noncommunicable diseases. There was no significant association between health insurance coverage and financial burden. However, when older people sought tertiary care or private care, the possibility of a household facing CHE increased. Regardless of the type and level of care, health service utilization by older people results in a higher likelihood of a household encountering financial distress. CONCLUSIONS: This study reveals that OOPHE for older people can impose substantial financial burdens on households, leading them to face CHE and financial distress. This study provides evidence to justify reforming financial protection policies and introducing policy interventions targeted at better protecting older people and their households from the financial consequences of OOPHE. There is also the need to strengthen the grassroots health facilities to provide primary care closer to home at lower costs, particularly for the management of noncommunicable diseases.

Bosentan versus nifedipine in the treatment of vasculopathy in systemic sclerosis patients: A randomized control trial.

BACKGROUND: Bosentan is effective agent in scleroderma vasculopathy. However, there are no studies evaluating effectiveness of bosentan in Vietnamese patients, where nifedipine is still the common treatment. OBJECTIVE: To compare the efficacy of bosentan versus nifedipine in scleroderma vasculopathy in Vietnamese patients. METHODS: We randomly assigned 70 patients in a 2:1 ratio to receive oral bosentan or oral nifedipine for 16 weeks, respectively. The primary outcomes were the change in Raynaud's Condition Score (RCS), appearance of new digital ulcers (DUs) and change in World Health Organization (WHO) functional class. Secondary outcomes were the change in the nailfold capillaries disease stage and systolic pulmonary arterial pressure (sPAP) value. RESULTS: At week 16, patients in bosentan group had no RCS imprvement, the mean difference was 0.8 ± 0.2 (95% CI, 0.4 to 1.1, p < 0.001) and improved WHO functional class, a mean treatment effect of 35.6% in favor of bosentan (95% CI, 13.4 to 57.7%, p < 0.05). Bosentan treatment was associated with a 58% reduction in the number of new DUs compared with nifedipine (mean ± standard error: 0.22 ± 0.42 vs 0.52 ± 0.59 new DUs, p < 0.05). sPAP was decreased by 4.1 ± 3.8 mmHg (95% CI, 3.0 to 5.3, p < 0.001) in bosentan group, versus 1.0 ± 2.9 mmHg (95% CI, -0.2 to 2.1, p > 0.05) in nifedipine group. Headache was the most common adverse event in both groups. CONCLUSIONS: Bosentan significantly limited the occurrence of new DUs, reduced symptoms of pulmonary arterial hypertension and sPAP value and all were better than nifedipine.

Alamandine Protects the Heart Against Reperfusion Injury via the MrgD Receptor.

BACKGROUND: Alamandine differs from angiotensin-(1-7) in a single N-terminal alanine residue. The aim of this study was to investigate whether alamandine protects the heart against reperfusion injury. Methods and Results: After euthanizing Sprague-Dawley rats, hearts were perfused with Krebs-Henseleit buffer for a 20-min pre-ischemic period with or without alamandine, followed by 20 min global ischemia and 50 min reperfusion. Alamandine (0.1 mg/kg) improved the postischemic left ventricular developed pressure and ±dP/dt, decreased the infarct size, and decreased the lactate dehydrogenase levels in the effluent. Alamandine increased the coronary flow and the amount of atrial natriuretic peptide (ANP) in the coronary effluent, and it decreased the expression of apoptotic proteins and increased the expression of antioxidative proteins. Pretreatment with the MrgD receptor antagonist or PD123319, but not the angiotensin type 1 receptor antagonist, attenuated the cardioprotective effects of alamandine. A similar cardioprotective effect with alamandine was also observed with high plasma ANP levels in an in vivo study. Alamandine directly stimulated ANP secretion from isolated atria, which was completely blocked by pretreatment with the MrgD receptor antagonist and was partially blocked by PD123319. CONCLUSIONS: These results suggest that the cardioprotective effects of alamandine against I/R injury are, in part, related to the activation of antioxidant and antiapoptotic enzymes via the MrgD receptor.

Comparative effects of angiotensin II and angiotensin-(4-8) on blood pressure and ANP secretion in rats.

Angiotensin II (Ang II) is metabolized from N-terminal by aminopeptidases and from C-terminal by Ang converting enzyme (ACE) to generate several truncated angiotensin peptides (Angs). The truncated Angs have different biological effects but it remains unknown whether Ang-(4-8) is an active peptide. The present study was to investigate the effects of Ang-(4-8) on hemodynamics and atrial natriuretic peptide (ANP) secretion using isolated beating rat atria. Atrial stretch caused increases in atrial contractility by 60% and in ANP secretion by 70%. Ang-(4-8) (0.01, 0.1, and 1 µM) suppressed high stretch-induced ANP secretion in a dose-dependent manner. Ang-(4-8) (0.1 µM)-induced suppression of ANP secretion was attenuated by the pretreatment with an antagonist of Ang type 1 receptor (AT1R) but not by an antagonist of AT2R or AT4R. Ang-(4-8)-induced suppression of ANP secretion was attenuated by the pretreatment with inhibitor of phospholipase (PLC), inositol triphosphate (IP3) receptor, or nonspecific protein kinase C (PKC). The potency of Ang-(4-8) to inhibit ANP secretion was similar to Ang II. However, Ang-(4-8) 10 µM caused an increased mean arterial pressure which was similar to that by 1 nM Ang II. Therefore, we suggest that Ang-(4-8) suppresses high stretch-induced ANP secretion through the AT1R and PLC/IP3/PKC pathway. Ang-(4-8) is a biologically active peptide which functions as an inhibition mechanism of ANP secretion and an increment of blood pressure.

Examining multiple funding flows to public healthcare providers in low- and middle-income countries - results from case studies in Burkina Faso, Kenya, Morocco, Nigeria, Tunisia and Vietnam.

Provider payment methods are traditionally examined by appraising the incentive signals inherent in individual payment mechanisms. However, mixed payment arrangements, which result in multiple funding flows from purchasers to providers, could be better understood by applying a systems approach that assesses the combined effects of multiple payment streams on healthcare providers. Guided by the framework developed by Barasa et al. (2021) (Barasa E, Mathauer I, Kabia E et al. 2021. How do healthcare providers respond to multiple funding flows? A conceptual framework and options to align them. Health Policy and Planning  36: 861-8.), this paper synthesizes the findings from six country case studies that examined multiple funding flows and describes the potential effect of multiple payment streams on healthcare provider behaviour in low- and middle-income countries. The qualitative findings from this study reveal the extent of undesirable provider behaviour occurring due to the receipt of multiple funding flows and explain how certain characteristics of funding flows can drive the occurrence of undesirable behaviours. Service and resource shifting occurred in most of the study countries; however, the occurrence of cost shifting was less evident. The perceived adequacy of payment rates was found to be the strongest driver of provider behaviour in the countries examined. The study results indicate that undesirable provider behaviours can have negative impacts on efficiency, equity and quality in healthcare service provision. Further empirical studies are required to add to the evidence on this link. In addition, future research could explore how governance arrangements can be used to coordinate multiple funding flows, mitigate unfavourable consequences and identify issues associated with the implementation of relevant governance measures.

How do healthcare providers respond to multiple funding flows? A conceptual framework and options to align them.

Provider payment methods are a key health policy lever because they influence healthcare provider behaviour and affect health system objectives, such as efficiency, equity, financial protection and quality. Previous research focused on analysing individual provider payment methods in isolation, or on the actions of individual purchasers. However, purchasers typically use a mix of provider payment methods to pay healthcare providers and most health systems are fragmented with multiple purchasers. From a health provider perspective, these different payments are experienced as multiple funding flows which together send a complex set of signals about where they should focus their effort. In this article, we argue that there is a need to expand the analysis of provider payment methods to include an analysis of the interactions of multiple funding flows and the combined effect of their incentives on the provision of healthcare services. The purpose of the article is to highlight the importance of multiple funding flows to health facilities and present a conceptual framework to guide their analysis. The framework hypothesizes that when healthcare providers receive multiple funding flows, they may find certain funding flows more favourable than others based on how these funding flows compare to each other on a range of attributes. This creates a set of incentives, and consequently, healthcare providers may alter their behaviour in three ways: resource shifting, service shifting and cost shifting. We describe these behaviours and how they may affect health system objectives. Our analysis underlines the need to align the incentives generated by multiple funding flows. To achieve this, we propose three policy strategies that relate to the governance of healthcare purchasing: reducing the fragmentation of health financing arrangements to decrease the number of multiple purchaser arrangements and funding flows; harmonizing signals from multiple funding flows; and constraining providers from responding to undesirable incentives.

Similarity and dissimilarity between angiotensin A and angiotensin II in cardiovascular functions in a rat model.

Angiotensin (Ang) A differs from Ang II in a single N-terminal alanine residue. The aim of this study was to investigate whether the effects of Ang A on postischemic cardiac injury and hemodynamics differ from Ang II. After euthanizing Sprague-Dawley rats, hearts were perfused with Krebs-Henseleit buffer for a 20 min preischemic period with or without Ang A or Ang II, followed by 20 min global ischemia and 50 min reperfusion. The blood pressure was measured in anesthetized rats. Ang A (0.1, 1.0, 10 µg/kg) deteriorated the postischemic left ventricular hemodynamics in a dose-dependent manner, which was similar to that by Ang II. Ang A (10 µg/kg) increased the infarct size and the lactate dehydrogenase level, and decreased the coronary flow, which were attenuated by the pretreatment with Ang type 1 receptor (AT1R) antagonist (losartan) but not by AT2R antagonist (PD123319). Ang A increased the expression of apoptotic proteins and decreased the expression of antioxidative proteins. Interestingly, Ang A increased the atrial natriuretic peptide (ANP) level in coronary effluent and in atrial perfusate but Ang II did not increase it. Ang A increased mean arterial blood pressure, which was less potent than Ang II. These results suggest that Ang A has a similar effect on postischemic injury via AT1R and less potent vasopressor effect but opposite effect on ANP secretion as compared to Ang II.

Angiotensin-(1-5), an active mediator of renin-angiotensin system, stimulates ANP secretion via Mas receptor.

Angiotensin-(1-5) [Ang-(1-5)], which is a metabolite of Angiotensin-(1-7) [Ang-(1-7)] catalyzed by angiotensin-converting enzyme (ACE), is a pentapeptide of the renin-angiotensin system (RAS). It has been reported that Ang-(1-7) and Ang-(1-9) stimulate the secretion of atrial natriuretic peptide (ANP) via Mas receptor (Mas R) and Ang II type 2 receptor (AT2R), respectively. However, it still remains unknown whether Ang-(1-5) has a similar function to Ang-(1-7). We investigated the effect of Ang-(1-5) on ANP secretion and to define its signaling pathway using isolated perfused beating rat atria. Ang-(1-5) (0.3, 3, 10µM) stimulated high pacing frequency-induced ANP secretion in a dose-dependent manner. Ang-(1-5)-induced ANP secretion (3µM) was attenuated by the pretreatment with an antagonist of Mas R (A-779) but not by an antagonist of AT1R (losartan) or AT2R (PD123,319). An inhibitor for phosphatidylinositol 3-kinase (PI3K; wortmannin), protein kinase B (Akt; API-2), or nitric oxide synthase (NOS; L-NAME) also attenuated the augmentation of ANP secretion induced by Ang-(1-5). Ang-(1-5)-induced ANP secretion was markedly attenuated in isoproterenol-treated hypertrophied atria. The secretagogue effect of Ang-(1-5) on ANP secretion was similar to those induced by Ang-(1-9) and Ang-(1-7). These results suggest that Ang-(1-5) is an active mediator of renin-angiotensin system to stimulate ANP secretion via Mas R and PI3K-Akt-NOS pathway.

Synthesis and Cytotoxic Evaluation of Artemisinin-triazole Hybrids.

Dihydroartemisinin was converted to its corresponding alkyne-functionalized esters, which were subsequently deployed as substrates for a 'click' chemistry-mediated coupling-with 3'-azido-3'-deoxythydimine (AZT) to furnish novel triazole-artesunate-AZT hybrid compounds. Moreover, various substituted triazole-artemisinin :hybrids were synthesized based on 'click' chemistry between propargyl-substituted derivatives and artemisinin containing a 2-hydroxypropane unit. Fourteen new hybrids were thus successfully prepared and evaluated as cytotoxic agents, revealing an interesting anticancer activity of four triazole-artemisinin derivative hybrids in KB and HepG2 cancer cell lines.

Assessment of systems for paying health care providers in Vietnam: implications for equity, efficiency and expanding effective health coverage.

Provider payment arrangements are currently a core concern for Vietnam's health sector and a key lever for expanding effective coverage and improving the efficiency and equity of the health system. This study describes how different provider payment systems are designed and implemented in practice across a sample of provinces and districts in Vietnam. Key informant interviews were conducted with over 100 health policy-makers, purchasers and providers using a structured interview guide. The results of the different payment methods were scored by respondents and assessed against a set of health system performance criteria. Overall, the public health insurance agency, Vietnam Social Security (VSS), is focused on managing expenditures through a complicated set of reimbursement policies and caps, but the incentives for providers are unclear and do not consistently support Vietnam's health system objectives. The results of this study are being used by the Ministry of Health and VSS to reform the provider payment systems to be more consistent with international definitions and good practices and to better support Vietnam's health system objectives.