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Congress Report: 26th Scientific Meeting of the International Society of Hypertension (ISH)

Congress Report: 26th Scientific Meeting of the International Society of Hypertension (ISH)
  • Cardiometabolic
  • Hypertension

26th Scientific Meeting of the International Society of Hypertension (ISH) Seoul, Korea 24 – 29 September 2016

This is the 50th anniversary year of the International Society of Hypertension (ISH), and its 26th Scientific Meeting was held in Seoul, Korea, attended by over 3,500 delegates.There were several hot topics generating interest and debate, including the procedure of blood pressure (BP) measurement in the SPRINT trial, as well as results from older and frail patients in this trial,  the lifetime risk of cardiovascular disease, pathophysiological mechanisms contributing to hypertension and the effect of time of day on antihypertensive dosing


Discussion of the SPRINT trial

Many sessions, including some sponsored symposia, featured continued discussion of SPRINT (Systolic Blood Pressure Intervention Trial)1 and these created some spirited discussion. Several of the SPRINT investigators were present at the meeting contributing to the debates and there were presentations featuring the recently published analysis of the older patients in the SPRINT trial2 by Professor Michael Weber (State University of New York, US) and others.

A major area of discussion was the procedure for BP measurement in the SPRINT trial using unattended automatic BP measurement devices in the absence of health professionals and how this would compare with usual office or home BP measurements. It has been suggested previously by Professor Sverre Kieldsen (Oslo, Norway) that the BP measurements in SPRINT were anything from 5 to 15 mmHg lower than usual BP measurements.3 It was reported by one of the SPRINT investigators that they were still in the process of checking that all of the trial centres did follow the required method of the trial for BP measurement. The unattended automated BP measurement is thought to control for any white coat hypertension effect and to reduce variability between BP measurements, but it has not been used in previous hypertension trials.  

The SPRINT outcome in 2636 participants ≥70 years old (mean age 79.9 years) showed a significant reduction of the primary composite outcome (nonfatal myocardial infarction, acute coronary syndrome not resulting in a myocardial infarction, nonfatal stroke, nonfatal acute decompensated heart failure and death from cardiovascular causes) as well as all-cause mortality in the intensive treatment group compared with the standard treatment group.2 There was also a significant reduction in non-cardiovascular mortality with intensive BP treatment. The investigators remarked this may really reflect cardiovascular mortality as many of the causes of non-cardiovascular mortality had not yet been adjudicated.

The study also addressed the outcome in hypertensive patients with different degrees of frailty. Patients who were most frail had the worst outcome but they still showed a similar benefit to less frail patients with intensive BP treatment, so frailty should not be considered as a contraindication to intensive BP treatment. Frailty was assessed using a 37-item frailty index and it was a comment that the frailest patients in the study were still ambulatory and able to attend the clinic for study visits. There was an increase in adverse events with intensive BP treatment but the overall rate of serious adverse events was not different between treatment groups. SPRINT also provided evidence that intensive treatment was useful in non-diabetic patients with chronic kidney disease with estimated GFR as low as 30 mL/min/1.73 m2.

Whilst many Europeans were skeptical that the results from SPRINT would influence BP guidelines it was noted that the SPRINT findings have already been incorporated into the new Canadian hypertension guidelines in 2016 with the comments that the target SBP <120 mmHg for selected patients at high cardiovascular risk would apply when BP is measured by automated office BP recordings taken without patient-health provider interaction.4

Morning or nighttime dosing of antihypertensives

Data were presented by Professor Neil Poulter (Imperial College London, UK, the incoming President of ISH) from the randomized crossover trial HARMONY (Hellenic-Anglo Research Into Morning or Night Antihypertensive Drug Delivery) trial which examined the timing of dosing of antihypertensive treatment.5 Some previous studies have suggested that nocturnal rather than daytime dosing of antihypertensive agents may have beneficial effects on BP control and cardiovascular outcomes. The HARMONY trial included 103 patients (age 18–80 years) from the UK and Greece with hypertension controlled on stable treatment with at least one antihypertensive agent, randomized to receive usual BP medication in the morning between 6 and 11 (n=51) or in the evening between 6 and 11 (n=52) for 12 weeks. The two groups then switched dosing times for an additional 12 weeks without any washout period. All the ambulatory BP monitoring (ABPM) recordings were completed in 95 (92%) patients. The most common class of antihypertensive used was renin-angiotensin-system blockers, followed by calcium-channel blockers.

The morning or night timing of dosing of antihypertensive drugs did not affect 24-hour ABPM systolic and diastolic BP levels or quality of life in these patients. The largest difference was for nighttime systolic BP at 122.76 mm Hg for morning dosing vs 121.08 for evening dosing, which at a 1.68 mmHg difference is not statistically significant, although it could be important with regard to CV events at a population level. The ongoing TIME [Treatment in Morning versus Evening] trial, involving 10,200 patients to be followed for 5 years, will hopefully provide definitive evidence of any preferential impact of nocturnal dosing of BP-lowering medication on major adverse cardiovascular events.

Pathophysiological mechanisms contributing to hypertension

Professor Rhian Touyz (Glasgow, UK), the outgoing President of ISH, discussed the pathophysiological mechanisms contributing to hypertension including endothelial dysfunction and altered vascular signaling.6 Changes in the characteristics of vascular cells to a pro-inflammatory, vasoconstrictory and proliferative phenotype, influenced by activation of the renin-angiotensin-system and oxidative stress are involved in these processes. Improved vascular function is associated with reduced hypertension-related target-organ damage and approaches to promote vascular health including conventional antihypertensive drugs and lifestyle modifications, which reduce oxidative stress and dampen activation of injurious signaling pathways, should be useful therapeutic strategies. The NADPH oxidase enzymes or NOX family of transmembrane proteins generate reactive oxygen species (ROS) which may result in oxidative post-translational modification of vascular proteins. Many NOX isoforms produce ROS in the vascular wall and recent findings show that NOX5 may be important in humans and may represent a new target for therapy.7

The Lancet Commission on Hypertension

Another highlight at the ISH meeting was the release of the first report from The Lancet’s Commission on Hypertension presented by a team under the leadership of Professor Michael Hecht Olsen (Denmark).8 This initiative aims to identify strategic actions to improve the management of BP at the population and the individual level and to develop a campaign to adopt the suggested actions at national levels to reduce the impact of elevated BP globally. The report introduces the concept of lifetime risk of cardiovascular disease and that early vascular ageing related to hypertension (or other cardiovascular risk factors) will result in the lifecourse curve crossing the thresholds for subclinical organ damage and cardiovascular disease at an earlier age (see figure).

The project was discussed by an expert panel and some members of the panel were concerned that some of the key actions could not be implemented in some parts of the world, such as improving the quality of BP measurement in rural areas of developing countries. The Commission will present some results of the initiative at the European Meeting on Hypertension and Cardiovascular Protection in Milan in June 2017.

Figure: Early-life effects and impact of preventive efforts in the management of elevated blood pressure8

The insert shows the effects of genetic susceptibility and epigenetic imprinting during fetal life. Preventive efforts (small grey arrows) result in downward shifts in the lifecourse curve, with earlier preventive efforts affecting lifecourse trajectory more than later preventive efforts

CV, cardiovascular; QOL, quality of life; BP, blood pressure

Reprinted from The Lancet, 388, Olsen MH, Angell SY, Asma S, et al. A call to action and a lifecourse strategy to address the global burden of raised blood pressure on current and future generations: the Lancet Commission on Hypertension, pages 2665-2712. Copyright 2016, with permission from Elsevier


References

1.            Cushman WC, Evans GW, Byington RP, et al. Effects of intensive blood-pressure control in type 2 diabetes mellitus. N Engl J Med. 2010;362:1575-1585. http://www.ncbi.nlm.nih.gov/pubmed/20228401

2.            Williamson JD, Supiano MA, Applegate WB, et al. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged >/=75 years: A randomized clinical trial. JAMA. 2016;315:2673-2682. http://www.ncbi.nlm.nih.gov/pubmed/27195814

3.            Kjeldsen SE, Lund-Johansen P, Nilsson PM, Mancia G. Unattended blood pressure measurements in the systolic blood pressure itervention trial: implications for entry and achieved blood pressure values compared with other trials. Hypertension. 2016;67:808-812. http://www.ncbi.nlm.nih.gov/pubmed/27001295

4.            Leung AA, Nerenberg K, Daskalopoulou SS, et al. Hypertension Canada's 2016 canadian hypertension education program guidelines for blood pressure masurement, diagnosis, assessment of risk, prevention, and treatment of hypertension. Can J Cardiol. 2016;32:569-588. http://www.ncbi.nlm.nih.gov/pubmed/27118291

5.            Poulter N, Anjum A, Cross M, et al. LBOS 01-01A Comparison of the impact of morning or night delivery of antihypertensive agents on 24 hour ABPM levels: A randomized cross-over trial (HARMONY)  J Hypertens. 2016;34:e547. http://journals.lww.com/jhypertension/Fulltext/2016/09001/LBOS_01_01A_COMPARISON_OF_THE_IMPACT_OF_MORNING_OR.1623.aspx

6.            Touyz RM. Ish Pre-2 the vascular phenotype in hypertension - molecular mechanisms and clinical implications. J Hypertens. 2016;34 Suppl 1. ISH 2016 Abstract Book:e384. http://www.ncbi.nlm.nih.gov/pubmed/27754201

7.            Montezano AC, Tsiropoulou S, Dulak-Lis M, et al. Redox signaling, Nox5 and vascular remodeling in hypertension. Curr Opin Nephrol Hypertens. 2015;24:425-433. http://www.ncbi.nlm.nih.gov/pubmed/26197203

8.            Olsen MH, Angell SY, Asma S, et al. A call to action and a lifecourse strategy to address the global burden of raised blood pressure on current and future generations: the Lancet Commission on Hypertension. Lancet. 2016;388:2665-2712. http://www.ncbi.nlm.nih.gov/pubmed/27671667

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