Implementation of the diabetes and hypertension guideline lifestyle recommendations in urban Mongolia: A qualitative study of primary care providers

Abstract
Background: Hypertension and diabetes, key risk factors for cardiovascular disease, are significant health problems globally. As cardiovascular disease is one of the leading causes of mortality in Mongolia since 2000, clinical guidelines on arterial hypertension and diabetes were developed and implemented in 2011. This paper explores the barriers and enablers influencing the implementation of these guidelines in the primary care setting.
Methods: A phenomenological qualitative study with semi-structured interviews was conducted to explore the implementation of the diabetes and hypertension guidelines at the primary care level, as well as to gain insight into how practitioners view the usability and practicality of the guidelines. Ten family health centres were randomly chosen from a list of all the family health centres (n = 136) located in Ulaanbaatar City. In each centre, a focus group discussion with nurses (n = 20) and individual interviews with practice doctors (n =10) and practice managers (n= 10) were conducted. Data was analysed using a thematic approach utilising the Theoretical Domains Framework.
Results: The majority of the study participants reported being aware of the guidelines and that they had incorporated them into their daily practice. They also reported having attended guideline training sessions which were focused on practice skill development. The majority of participants expressed satisfaction with the wide range of resources that had been supplied to them by the Mongolian Government to assist with the implementation of the guidelines. The resources, supplied from 2011 onwards, included screening devices, equipment for blood tests, medications and educational materials. Other enablers were the participants’ commitment and passion for guideline implementation and their belief in the simplicity and practicality of the guidelines. Primary care providers reported a number of challenges in implementing the guidelines, including frustration caused by increased workload and long waiting times, time constraints, difficulties with conflicting tasks and low patient health literacy.
Conclusions: This study provides evidence that comprehensive and rigorous dissemination and implementation strategies increase the likelihood of successful implementation of new guidelines in low resource primary care settings. It also offers some key lessons that might be carefully considered when other evidence-based clinical guidelines are to be put into effect in low resource settings and elsewhere.

Implementation of clinical guidelines on diabetes and hypertension in urban Mongolia: a qualitative study of primary care providers' perspectives and experiences

BACKGROUND: Hypertension and diabetes, key risk factors for cardiovascular disease, are significant health problems globally. As cardiovascular disease is one of the leading causes of mortality in Mongolia since 2000, clinical guidelines on arterial hypertension and diabetes were developed and implemented in 2011. This paper explores the barriers and enablers influencing the implementation of these guidelines in the primary care setting.

METHODS: A phenomenological qualitative study with semi-structured interviews was conducted to explore the implementation of the diabetes and hypertension guidelines at the primary care level, as well as to gain insight into how practitioners view the usability and practicality of the guidelines. Ten family health centres were randomly chosen from a list of all the family health centres (n = 136) located in Ulaanbaatar City. In each centre, a focus group discussion with nurses (n = 20) and individual interviews with practice doctors (n = 10) and practice managers (n = 10) were conducted. Data was analysed using a thematic approach utilising the Theoretical Domains Framework.

RESULTS: The majority of the study participants reported being aware of the guidelines and that they had incorporated them into their daily practice. They also reported having attended guideline training sessions which were focused on practice skill development. The majority of participants expressed satisfaction with the wide range of resources that had been supplied to them by the Mongolian Government to assist with the implementation of the guidelines. The resources, supplied from 2011 onwards, included screening devices, equipment for blood tests, medications and educational materials. Other enablers were the participants' commitment and passion for guideline implementation and their belief in the simplicity and practicality of the guidelines. Primary care providers reported a number of challenges in implementing the guidelines, including frustration caused by increased workload and long waiting times, time constraints, difficulties with conflicting tasks and low patient health literacy.

CONCLUSIONS: This study provides evidence that comprehensive and rigorous dissemination and implementation strategies increase the likelihood of successful implementation of new guidelines in low resource primary care settings. It also offers some key lessons that might be carefully considered when other evidence-based clinical guidelines are to be put into effect in low resource settings and elsewhere.

Dietary protein level interacts with ω-3 polyunsaturated fatty acid deficiency to induce hypertension

Background : Dietary ω-3 fatty acid deficiency can lead to hypertension in later life; however, hypertension is affected by numerous other dietary factors. We examined the effect of altering the dietary protein level on blood pressure in animals deficient or sufficient in ω-3 fatty acids.

Methods : Female rats were placed on one of four experimental diets 1 week prior to mating. Diets were either deficient (10% safflower oil; DEF) or sufficient (7% safflower oil, 3% flaxseed oil; SUF) in ω-3 fatty acids and contained 20 or 30% casein (DEF20, SUF20, DEF30, SUF30). Offspring were maintained on the maternal diet for the duration of the experiment. At 12, 18, 24, and 30 weeks, blood pressure was assessed by tail cuff plethysmography.

Results : At both 12 and 18 weeks of age, no differences in blood pressure were observed based on diet, however, by 24 weeks hypertension was evident in DEF30 animals; there were no blood pressure differences between the other groups. This hypertension in DEF30 group was increased at 30 weeks, with systolic, diastolic, and mean arterial pressure all elevated.

Conclusions : These results indicate that the hypertension previously attributed to ω-3 fatty acid deficiency is dependent on additional dietary factors, including protein content. Furthermore, this study is the first to plot the establishment of ω-3 fatty acid deficiency hypertension over time.

Isoflavones from red clover improve systemic arterial compliance but not plasma lipids in menopausal women

The possibility that the heightened cardiovascular risk associated with the menopause can be reduced by increasing dietary isoflavone intake was tested in 17 women by measuring arterial compliance, an index of the elasticity of large arteries such as the thoracic aorta. Compliance diminishes with age and menopause. An initial 3- to 4-week run-in period and a 5-week placebo period were followed by two 5-week periods of active treatment with 40 mg and then 80 mg isoflavones derived from red clover containing genistein, daidzein, biochanin, and formononetin in 14 and 13 women, respectively, with 3 others serving as placebo controls throughout. Arterial compliance, measured by ultrasound as a pressure (carotid artery) and volume (outflow into aorta) relationship, was determined after each period; plasma lipids were measured twice during each period. Urinary output of isoflavones was also determined. Arterial compliance rose by 23% relative to that during the placebo period with the 80-mg isoflavone dose and slightly less with the 40-mg dose (mean6SEM: placebo, 19.761.5; 40 mg, 23.760.7; 80 mg, 24.46 1.4). In the three women receiving continuous placebo, compliance was 16 6 2.2, similar to that during the run-in period for the remaining subjects (17 6 2.1). ANOVA showed a significant (P 5 , 0.001) difference between treatments; by Bonferroni multiple comparisons and by paired t test, differences were significant between placebo and 40- and 80-mg isoflavone doses (by paired t test: P50.039 for placebo vs. 40 mg; P 5 0.018 for placebo vs. 80 mg). Plasma lipids were not significantly affected. An important cardiovascular risk factor, arterial compliance, which diminishes with menopause, was significantly improved with red clover isoflavones. As diminished compliance leads to systolic hypertension and may increase left ventricular work, the findings indicate a potential new therapeutic approach for improved cardiovascular function after menopause.

Role of angiotensin II in the hypertension induced by renal artery stenosis

Identical degrees of renal artery stenosis were induced in 5 dogs on two separate occasions; once during continuous inhibition of angiotensin I converting enzyme with enalapril, and once with the dogs untreated. Arterial pressure rose about 25 mm Hg during 3 days of stenosis in untreated dogs, due to increased total peripheral resistance. When the dogs were treated with enalapril, blood pressure had risen 14.5 ± 3.4 mm Hg 24 hours after stenosis due to a 35% increase in cardiac output while total peripheral resistance fell by 16%. By the third day, blood pressure had returned to pre-stenosis levels, cardiac output was close to normal and total peripheral resistance had increased. The stenosis on the renal artery increased the resistance to blood flow of the kidneys in both untreated and enalapril treated dogs. This increase in kidney resistance in the untreated dogs accounted for about 30% of the change in total peripheral resistance. In the enalapril treated dogs, the increased kidney resistance helped offset the vasodilatation in the rest of the vasculature. These results suggest that angiotensin II mediated vasoconstriction of nonrenal vascular beds was responsible for about ⅔ of the hypertension following renal artery stenosis, and the resistance of the stenosis responsible for about ⅓.

Dietary salt loading impairs arterial vascular reactivity 1-3

BACKGROUND: Studies of sodium have shown improvements in vascular function and blood pressure (BP). The effect of chronic sodium loading from a low-sodium diet to a Western diet on vascular function and BP has been less well studied.

OBJECTIVE: The objective was to examine the effects of dietary salt intake on vascular function and BP.

DESIGN: Thirty-five hypertensive volunteers met the inclusion criteria. After a 2-wk run-in with a low-sodium diet (60 mmol/d), the participants maintained their diets and were randomly assigned to receive sequentially 1 of 3 interventions for 4 wk, with a 2-wk washout between interventions: sodium-free tomato juice (A), tomato juice containing 90 mmol Na (B), and tomato juice containing 140 mmol Na (C). The outcomes were changes in pulse wave velocity (PWV), systolic BP (SBP), and diastolic BP (DBP).

RESULTS: The difference in PWV between interventions B and A was 0.39 m/s (95% CI: 0.18, 0.60 m/s; P = 0.001) and between C and A was 0.35 m/s (95% CI: 0.13, 0.57 m/s; P = 0.01). Differences in SBP and DBP between interventions B and A were 4.4 mm Hg (95% CI: 1.2, 7.8 mm Hg; P = 0.01) and 2.4 mm Hg (95% CI: 0.8, 4.1 mm Hg; P = 0.001), respectively, and between interventions C and A were 5.6 mm Hg (95% CI: 2.7, 8.4 mm Hg; P = 0.01) and 3.3 mm Hg (95% CI: 1.5, 5.0 mm Hg; P = 0.001), respectively. Changes in PWV correlated with changes in SBP (r = 0.52) and DBP (r = 0.58).

CONCLUSIONS: Dietary salt loading produced significant increases in PWV and BP in hypertensive volunteers. Correlations between BP and PWV suggest that salt loading may have a BP-independent effect on vascular wall function. This further supports the importance of dietary sodium restriction in the management of hypertension. This trial was registered with the Australian and New Zealand Clinical Trials Registry as ACTRN12609000161224.

Exposure to a high-fat diet alters leptin sensitivity and elevates renal sympathetic nerve activity and arterial pressure in rabbits

The activation of the sympathetic nervous system through the central actions of the adipokine leptin has been suggested as a major mechanism by which obesity contributes to the development of hypertension. However, direct evidence for elevated sympathetic activity in obesity has been limited to muscle. The present study examined the renal sympathetic nerve activity and cardiovascular effects of a high-fat diet (HFD), as well as the changes in the sensitivity to intracerebroventricular leptin. New Zealand white rabbits fed a 13.5% HFD for 4 weeks showed modest weight gain but a 2- to 3-fold greater accumulation of visceral fat compared with control rabbits. Mean arterial pressure, heart rate, and plasma norepinephrine concentration increased by 8%, 26%, and 87%, respectively (P<0.05), after 3 weeks of HFD. Renal sympathetic nerve activity was 48% higher (P<0.05) in HFD compared with control diet rabbits and was correlated to plasma leptin (r=0.87; P<0.01). Intracerebroventricular leptin administration (5 to 100 μg) increased mean arterial pressure similarly in both groups, but renal sympathetic nerve activity increased more in HFD-fed rabbits. By contrast, intracerebroventricular leptin produced less neurons expressing c-Fos in HFD compared with control rabbits in regions important for appetite and sympathetic actions of leptin (arcuate: −54%, paraventricular: −69%, and dorsomedial hypothalamus: −65%). These results suggest that visceral fat accumulation through consumption of a HFD leads to marked sympathetic activation, which is related to increased responsiveness to central sympathoexcitatory effects of leptin. The paradoxical reduction in hypothalamic neuronal activation by leptin suggests a marked “selective leptin resistance” in these animals.

Central proopiomelanocortin but not neuropeptide Y mediates sympathoexcitation and hypertension in fat fed conscious rabbits

OBJECTIVE: High-fat diet (HFD)-induced hypertension in rabbits is neurogenic because of the central sympathoexcitatory actions of leptin. Hypothalamic melanocortin and neuropeptide Y (NPY) neurons are recognized as the major signalling pathways through which leptin exerts its central effects. In this study, we assessed the effects of specific antagonists and agonists to melanocortin and NPY receptors on HFD-induced sympathoexcitation and hypertension. METHODS: Rabbits were instrumented with intracerebroventricular cannula, renal sympathetic nerve activity (RSNA) electrode, and blood pressure telemetry transmitter. RESULTS: After 3 weeks HFD (13.5% fat, n = 12) conscious rabbits had higher RSNA (+3.8  nu, P = 0.02), blood pressure (+8.6  mmHg, P < 0.001) and heart rate (+15  b/min, P = 0.01), and brain-derived neurotrophic factor levels in the hypothalamus compared with rabbits fed a control diet (4.2% fat, n = 11). Intracerebroventricular administration of the melanocortin receptor antagonist SHU9119 reduced RSNA (-2.7  nu) and blood pressure (-8.5  mmHg) in HFD but not control rabbits, thus reversing 100% of the hypertension and 70% of the sympathoexcitation induced by a HFD. By contrast, blocking central NPY Y1 receptors with BVD10 increased RSNA only in HFD rabbits. Intracerebroventricular α-melanocortin stimulating hormone increased RSNA and heart rate (P < 0.001) in HFD rabbits but had no effect in control rabbits. CONCLUSION: These findings suggest that obesity-induced hypertension and increased RSNA are dependent on the balance between greater activation of melanocortin signalling through melanocortin receptors and lesser activation of NPY sympathoinhibitory signalling. The amplification of the sympathoexcitatory effects of α-melanocortin stimulating hormone also indicates that the underlying mechanism is related to facilitation of leptin-melanocortin signalling, possibly involving chronic activation of brain-derived neurotrophic factor.