The contribution of raised blood pressure to all-cause and cardiovascular deaths and disability-adjusted life-years (DALYs) in Australia: Analysis of global burden of disease study from 1990 to 2019.

AIMS: In a high-income country, Australia, it is unclear how raised systolic blood pressure (SBP) ranks among other risk factors regarding the overall and cardiovascular disease (CVD) burden, and whether the situation has changed over time. METHODS: We analysed the 2019 Global Burden of Disease (GBD) data, with focus on Australia. We assessed ten leading risk factors for all-cause and CVD deaths and disability-adjusted life-years (DALYs) and compared findings with the Australian Burden of Diseases Study. RESULTS: From 1990 to 2019, raised SBP remained the leading risk factor for attributable all-cause deaths (followed by dietary risks and tobacco use), accounting for 29,056/75,235 (95% Uncertainty Interval (UI) [24,863 to 32,915]) deaths in 1990; 21,845/76,893 [17,678 to 26,044] in 2010; and 25,498/90,393 [20,152 to 30,851] in 2019. Contributions of raised SBP to cardiovascular deaths for both sexes were 54.0% [45.8 to 61.5] in 1990, 44.0% [36.7 to 51.3] in 2010 and 43.7% [36.2 to 51.6] in 2019, respectively. The contribution of raised SBP to cardiovascular deaths declined between 1990 and 2010 but exhibited an increase in males from 2010 onwards, with figures of 52.6% [44.7 to 60.0] in 1990, 43.1% [36.0 to 50.5] in 2010 and 43.5% [35.7 to 51.4] in 2019. The contribution of raised SBP to stroke deaths and DALYs in males aged 25-49 years were higher than other age groups, in excess of 60% and increasing steeply between 2010 and 2019. CONCLUSION: Raised SBP continues to be the leading risk factor for all-cause and cardiovascular deaths in Australia. We urge cross-disciplinary stakeholder engagement to implement effective strategies to detect, treat and control raised blood pressure as a central priority to mitigate the CVD burden.

Burden of Hypertensive Heart Disease and High Systolic Blood Pressure in Australia from 1990 to 2019: Results From the Global Burden of Diseases Study.

BACKGROUND: There is a dearth of comprehensive studies examining the burden and trends of hypertensive heart disease (HHD) and high systolic blood pressure (SBP) among the Australian population. We aimed to explore the burden of HHD and high SBP, and how they changed over time from 1990 to 2019 in Australia. METHODS: We analysed data from the Global Burden of Disease study in Australia. We assessed the prevalence, mortality, disability-adjusted life-years (DALY), years lived with disability (YLD) and years of life lost (YLL) attributable to HHD and high SBP. Data were presented as point estimates with 95% uncertainty intervals (UI). We compared the burden of HHD and high SBP in Australia with World Bank defined high-income countries and six other comparator countries with similar sociodemographic characteristics and economies. RESULTS: From 1990 to 2019, the burden of HHD and high SBP in Australia reduced. Age standardised prevalence rate of HHD was 119.3 cases per 100,000 people (95% UI 86.6-161.0) in 1990, compared to 80.1 cases (95% UI 57.4-108.1) in 2019. Deaths due to HDD were 3.4 cases per 100,000 population (95% UI 2.6-3.8) in 1990, compared to 2.5 (95% UI 1.9-3.0) in 2019. HHD contributed to 57.2 (95% UI 46.6-64.7) DALYs per 100,000 population in 1990 compared to 38.4 (95% UI 32.0-45.2) in 2019. Death rates per 100,000 population attributable to high SBP declined significantly over time for both sexes from 1990 (155.6 cases; 95% UI 131.2-177.0) to approximately one third in 2019 (53.8 cases; 95% UI 43.4-64.4). Compared to six other countries in 2019, the prevalence of HHD was highest in the USA (274.3%) and lowest in the UK (52.6%), with Australia displaying the third highest prevalence. Australia ranked second in term of lowest rates of deaths and third for lowest DALYs respectively due to high SBP. From 1990-2019, Australia ranked third best for reductions in deaths and DALYs due to HHD and first for reductions in deaths and DALYs due to high SBP. CONCLUSION: Over the past three decades, the burden of HHD in Australia has reduced, but its prevalence remains relatively high. The contribution of high SBP to deaths, DALYs and YLLs also reduced over the three decades.

Cost-effectiveness of ultra-low-dose quadruple combination therapy for high blood pressure.

OBJECTIVE: To determine the cost-effectiveness and cost-utility of a quadpill containing irbesartan 37.5 mg, amlodipine 1.25 mg, indapamide 0.625 mg and bisoprolol 2.5 mg in comparison with irbesartan 150 mg for people with hypertension who are either untreated or receiving monotherapy. METHODS: We conducted a within-trial and modelled economic evaluation of the Quadruple UltrA-low-dose tReaTment for hypErTension trial. The analysis was preplanned, and medications and health service use captured during the trial. The main outcomes were incremental cost-effectiveness ratios (ICERs) for cost per mm Hg systolic blood pressure (BP) reduction at 3 months, and modelled cost per quality-adjusted life year (QALY) over a lifetime. RESULTS: The within-trial analysis showed no clear difference in cost per mm Hg BP lowering between randomised treatments at 3 months ($A10 (95% uncertainty interval (UI) $A -18 to $A37) per mm Hg per person) for quadpill versus monotherapy. The modelled cost-utility over a lifetime projected a mean incremental cost of $A265 (95% UI $A166 to $A357) and a mean 0.02 QALYs gained (95% UI 0.01 to 0.03) per person with quadpill therapy compared with monotherapy. Quadpill therapy was cost-effective in the base case (ICER of $A14 006 per QALY), and the result was sensitive to the quadpill cost in one-way sensitivity analysis. CONCLUSIONS: Quadpill in comparison with monotherapy is comparably cost-effective for short-term BP lowering. In the long-term, quadpill therapy is likely to be cost-effective. TRIAL REGISTRATION NUMBER: ANZCTRN12616001144404.

May Measurement Month 2018: a pragmatic global screening campaign to raise awareness of blood pressure by the International Society of Hypertension.

AIMS: Raised blood pressure (BP) is the biggest contributor to mortality and disease burden worldwide and fewer than half of those with hypertension are aware of it. May Measurement Month (MMM) is a global campaign set up in 2017, to raise awareness of high BP and as a pragmatic solution to a lack of formal screening worldwide. The 2018 campaign was expanded, aiming to include more participants and countries. METHODS AND RESULTS: Eighty-nine countries participated in MMM 2018. Volunteers (≥18 years) were recruited through opportunistic sampling at a variety of screening sites. Each participant had three BP measurements and completed a questionnaire on demographic, lifestyle, and environmental factors. Hypertension was defined as a systolic BP ≥140 mmHg or diastolic BP ≥90 mmHg, or taking antihypertensive medication. In total, 74.9% of screenees provided three BP readings. Multiple imputation using chained equations was used to impute missing readings. 1 504 963 individuals (mean age 45.3 years; 52.4% female) were screened. After multiple imputation, 502 079 (33.4%) individuals had hypertension, of whom 59.5% were aware of their diagnosis and 55.3% were taking antihypertensive medication. Of those on medication, 60.0% were controlled and of all hypertensives, 33.2% were controlled. We detected 224 285 individuals with untreated hypertension and 111 214 individuals with inadequately treated (systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 mmHg) hypertension. CONCLUSION: May Measurement Month expanded significantly compared with 2017, including more participants in more countries. The campaign identified over 335 000 adults with untreated or inadequately treated hypertension. In the absence of systematic screening programmes, MMM was effective at raising awareness at least among these individuals at risk.

The Role of Sympatho-Inhibition in Combination Treatment of Obesity-Related Hypertension.

Obesity-related hypertension is commonly characterized by increased sympathetic nerve activity and is therefore acknowledged as a predominantly neurogenic form of hypertension. The sustained sympatho-excitation not only contributes to the rise in blood pressure but also elicits a vicious cycle which facilitates further weight gain and progression of associated co-morbidities. While weight loss and exercise remain at the forefront of therapy for obesity and obesity-related hypertension, the difficulties in achieving and maintaining long-term weight loss with lifestyle measures and the variable blood pressure response to weight loss often necessitate prescription of antihypertensive drug therapy. Remarkably, there are no specific recommendations for pharmacologic treatment for obese patients with arterial hypertension in any of the current guidelines and general principles of antihypertensive treatment are applied. The use of ß-blockers and diuretics is commonly discouraged as first- or second-line therapy due to their unfavorable metabolic effects. This review explores evolving therapeutic strategies which based on their interference with pathophysiologic mechanism relevant in the context of obesity may guide optimized treatment of obesity-related hypertension.

Assessment of endothelial function of the renal vasculature in human subjects.

BACKGROUND: L-Arginine, the substrate of nitric oxide (NO) synthase, and N(G)-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of endothelial NO synthase, are used to analyze endothelial function of the renal vasculature. However, little is known about the appropriate dose of L-arginine to be used and the duration of action of L-arginine and L-NMMA. METHODS: Twenty-nine healthy male subjects (age, 27+/-1 years) were examined. In protocol 1 (N = 17), L-arginine at low (100 mg/kg) and high dose (250 mg/kg), and high-dose L-arginine combined either with L-NMMA (total dose, 4.25 mg/kg; N = 9) or placebo (N = 8) were given. In protocol 2 (N = 12), L-NMMA was given before L-arginine infusion (100 mg/kg). Glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured at rest and at the end of each infusion step. RESULTS: In protocol 1, L-arginine dose dependently increased RPF and GFR (RPF: 599+/-19 v 630+/-18 v 690+/-24 mL/min, P <.05; GFR: 111+/-3 v 115+/-3 v 121+/-3 mL/min, P <.01; for baseline, L-arginine 100 mg/kg and 250 mg/kg, respectively). However, these changes could not be antagonized by coinfusion of L-NMMA to L-arginine 250 mg/kg: RPF and GFR remained unchanged in both the placebo and the L-NMMA group. In protocol 2, L-NMMA decreased RPF (492+/-18 v 567+/-27 mL/min, P <.01) and increased GFR (122+/-4 v 118+/-3 mL/min, P <.05). These changes could only be partially reversed by subsequent infusion of L-arginine (RPF: 533+/-15 mL/min; GFR: 121+/-4 mL/min; both parameters P = NS v L-NMMA and v baseline). CONCLUSIONS: L-arginine at a dose of 100 mg/kg is sufficient to analyze endothelial function of the renal vasculature. The prolonged effect of L-NMMA and L-arginine must be taken into account in study protocols using both substances. Thus, stimulation and blockade of NO synthase cannot be examined in the same protocol.