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Practical Diabetes Care, 3rd Ed., Excerpt #27: Hypertension Part 2 of 5

David Levy, MD, FRCP     

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Thresholds and targets for treatment

Type 2 diabetes
Thresholds and targets for treatment are shown in Table 11.1. There is general agreement that treatment should start once blood pressure is persistently greater than 140/90 mmHg. Targets for treatment have in some cases run ahead of the evidence; until ACCORD (Box 11.2), only one large clinical trial had achieved an SBP of less than 130 mmHg. While event rates were lower than anticipated in ACCORD, reducing its power, there are no clear benefits of intensive blood pressure lowering in high-risk hypertensive type 2 patients, and targeting SBP less than 140 mmHg is sufficient except in proteinuric patients.

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Management
Assess end-organ damage

Current microalbuminuria levels and retinopathy status should be known.
Macrovascular

  • Assess for peripheral vascular disease (foot pulses, carotid, renal and femoral bruits, abdominal palpation for aortic aneurysm). A bruit in the left flank is more likely to be splenic than renal.
  • LVH cannot be assessed clinically. Standard ECG criteria (SV1 + RV6 >35 mm; RV5 or RV6 > 25 mm; or SV1 or SV2 > 25 mm; ± ‘strain’ pattern) correlate poorly with echocardiography, which should be requested whenever there is ECG evidence of LVH. It is sometimes difficult to distinguish between LVH and ischemia on ECG (see Fig. 11.2).
  • Ultrasound scan of the common carotid artery for CIMT and the presence of atherosclerotic plaque. CIMT over 1 mm is a reliable indicator of cardiovascular risk, but the presence of plaque may be even more significant. In type 2 diabetes, increased CIMT is strongly associated with abnormal SPECT myocardial perfusion (Fig. 11.3).

Blood pressure measurement

Automated digital blood pressure devices are accurate and in widespread use, but manual measurements are still important, as an initial clinic reading may be misleading. Practical advice for blood pressure measurement, adapted from the British Hypertension Society guidelines (2004), is shown in Box 11.3.

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Home blood pressure monitoring
Affordable automated equipment is now widely available (recommended validated equipment only; the British Hypertension Society website has details of currently approved devices). Wrist monitors, while more convenient than upper arm monitors, are more difficult to use reliably because of the need to keep the wrist at heart level while the measurement is being taken. Home blood pressure measurements, like ambulatory blood pressure monitoring (ABPM), are lower than casual clinic readings by about 10/5 mmHg, but still correlate reasonably with echocardiographic estimations of left ventricular mass [5]. Home devices cannot be used for diagnosing hypertension, but they are of value in monitoring response to treatment when supported by clinic or office blood pressure measurements. Studies have shown significant reduction in medication and costs, and in some cases permanent discontinuation of treatment, with no significant worsening of blood pressure, though ambulatory pressures may be slightly higher [6]. Some patients will become anxious through measuring their blood pressure too frequently, the same problem posed by home blood glucose monitoring. Time spent explaining the physiological importance of minute-to-minute adjustment of blood pressure is worthwhile, and this can be shown more graphically using ABPM print-outs. Self-measurement of blood pressure opens up real possibilities for innovative programmes to improve blood pressure control, in combination with traditional and more time-consuming methods.

Ambulatory blood pressure monitoring
Mean 24-hour ABPM correlates better with cardiovascular risk and target organ damage than casual blood pressure readings. ‘Non-dipping’ (failure of nocturnal blood pressure to fall about 10%) is associated with increased left ventricular mass, and increased blood pressure variability is also associated with increased target organ damage independent of mean blood pressure. Box 11.4 lists some uses of ABPM.

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Diagnostic thresholds for ABPM in non-diabetic subjects have been updated in the light of important long-term prospective cardiovascular outcome studies [8] (Table 11.2). Though fewer than 10% of the subjects in the studies had diabetes, because of the higher cardiovascular risk in diabetes at any given blood pressure, they are worthwhile clinical targets; in patients with nephropathy, at the highest cardiovascular risk, optimal values, though daunting to achieve, should nevertheless probably be targeted.

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Sustained lifestyle interventions
While most hypertensive patients will need some pharmacological treatments, introducing a portfolio of lifestyle changes will enhance the benefits of existing medication (e.g. thiazide diuretics with dietary salt reduction), and possibly also reduce the need for additional medication. Individual responses vary, and there are few large interventional trials. Discuss and reinforce all the following [9].

  • Reducing salt intake. Average sodium intake in the USA is about 180 mmol/day, up to half consuming more than 300 mmol/day. Given these huge intakes, the recommendation to reduce intake to less than 6 g NaCl (< 2.4 g sodium or < 100 mmol/day) should have clinically important effects on blood pressure. Advise patients not to add salt to food at mealtimes, though prepackaged foods and salty snacks are major culprits, as well as monosodium glutamate. Response can be monitored, with valuable feedback to patients, by requesting urinary sodium with ACRs or 24-hour urinary albumin measurements. Reducing urinary sodium excretion by 30–45 mmol per 24 hours only modestly reduces blood pressure, but reduced cardiovascular events by 25% in a long-term follow-up, even though the original interventions lasted only 1.5–4 years. This legacy effect seems to be mediated in part through long-lasting reductions in sodium intake and awareness of dietary salt [10].
  • Dietary Approaches to Stop Hypertension (DASH). Consider implementing the DASH diet, with increased consumption of fruit (but in moderation in diabetes), vegetables, legumes, beans, nuts, whole-grains and soy, and decreasing saturated and total fat. This can reduce SBP by 8–14 mmHg.
  • Weight loss of 8 kg can reduce blood pressure by 7/3 mmHg (Look AHEAD study; see Chapter 5). Sustained weight loss of this magnitude with diet alone is rare in practice, though studies with exenatide and a mean weight loss of about 3 kg, more easily achievable, show propor- tionate blood pressure reductions, i.e. 2/0.5 mmHg (see Chapter 6).
  • Exercise: the standard recommendation of 30 min moderate exercise most days can reduce SBP by 4–9 mmHg.
  •  Limit alcohol intake: 21 units/week or less for men, 14 units/week or less for women can result in SBP reduction of 2–4 mmHg [11].
  • Vitamin D supplements and high-dose w-3 fatty acids (3 g daily) may reduce blood pressure slightly, but the evidence is not strong.

References:

  1. Cushman WC, Evans GW, Byington RP et al. Effects of intensive blood-pressure control in type 2 diabetes mellitus. ACCORD Study Group. N Engl J Med 2010; 362:1575–85. PMID: 20228401.
  2. Chew EY, Ambrosius WT, Davis MD et al. ACCORD Study Group and ACCORD Eye Study Group. Effects of medical therapies on retinopathy progression in type 2 diabetes. N Engl J Med 2010;363:233–44. PMID: 20587587.
  3. Brown MJ. Renin: friend or foe? Heart 2007;93:1026–33. PMID: 17488768.
  4. Rönnback M, Fagerudd J, Forsblum C, Pettersson-Fernholm K, Reunanen A, Groop PH. Altered age-related blood pressure pattern in type 1 diabetes. Finnish Diabetic Nephropathy (FinnDiane) Study Group. Circulation 2004;110:1076–82. PMID: 15326070.
  5. Shimbo D, Pickering TG, Spruill TM, Abraham D, Schwartz JE, Gerin W. Relative utility of home, ambulatory, and office blood pressures in the prediction of end-organ damage. Am J Hypertens 2007;20:476–82. PMID: 17485006.
  6. Verberk WJ, Kroon AA, Lenders JW et al. Self-measurement of blood pressure at home reduces the need for antihypertensive drugs: a randomized controlled trial. Home Versus Office Measurement, Reduction of Unnecessary Treatment Study Investigators. Hypertension 2007;50:1019–25. PMID: 17938383.
  7. Spence JD. White-coat hypertension is hypertension. Hypertension 2008;51:1272. PMID: 18378857.
  8. Kikuya M, Hansen TW, Thijs L et al. Diagnostic thresholds for ambulatory blood pressure monitoring based on 10-year cardiovascular risk. IDACO Investigators. Blood Press Monit 2007;12:393–5. PMID: 18277319.
  9. Sacks FM, Campos H. Dietary therapy in hypertension. N Engl J Med 2010;362:2102–12. PMID: 20519681.
  10. Cook NR, Cutler JA, Obarzanek E et al. Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). Br Med J 2007;334:885–8. PMID: 17449506.
  11. Tejada T, Fornoni A, Lenz O, Materson BJ. Nonpharmacologic therapy for hypertension: does it really work? Curr Cardiol Rep 2006;8:418–24. PMID: 17059793.
  12. Zillich AJ, Garg J, Basu S, Bakris GL, Carter BL. Thiazide diuretics, potassium, and the development of diabetes: a quantitative review. Hypertension 2006;48:219–24. PMID: 16801488.
  13. Jamerson K, Weber MA, Bakris GL et al. Benazepril plus amlodipine or hydrochlorothiazide for hypertension in high-risk patients. ACCOMPLISH Trial Investigators. N Engl J Med 2008;359:2417–28. PMID: 19052124.
  14. Yusuf S, Teo KK, Pogue J et al. Telmisartan, ramipril, or both in patients at high risk for vascular events. ONTARGET Investigators. N Engl J Med 2008;358:1547– 59. PMID: 18378520.
  15. Wright JT Jr, Bakris G, Greene T et al. Effect of blood pressure lowering and antihypertensive drug class on progression of hypertensive kidney disease: results from the AASK trial. African American Study of Kidney Disease and Hypertension Study Group. JAMA 2002;288:2421–31. PMID: 12435255.
  16. Nissen SE, Tuzcu M, Libby P et al. Effect of antihypertensive agents on cardiovascular events in patients with coronary disease and normal blood pressure: the CAMELOT study: a randomized controlled trial. JAMA 2004;292:2217–25. PMID: 15536108.
  17. Bakris GL, Fonseca K, Katholi RE et al. Metabolic effects of carvedilol vs metoprolol in patients with type 2 diabetes mellitus and hypertension: a randomized controlled trial. JAMA 2004;292:2227–36. PMID: 15536109.
  18. Ernst ME, Moser M. Use of diuretics in patients with hypertension. N Engl J Med 2009;361:2153–64. PMID: 19940300.
  19. Vrijens B, Vincze G, Kristanto P, Urquhart J, Burnier M. Adherence to prescribed antihypertensive drug treatments: longitudinal study of electronically compiled dosing histories. Br Med J 2008;336:1114–17. PMID: 18480115.
  20. Funder JW, Carey RM, Fardella C et al. Case detection, diagnosis, and treatment of patients with primary aldosteronism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2008;93:3266–81. PMID: 18552288.

 

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David Levy, MD, FRCP, Consultant Physician, Gillian Hanson Centre, Whipps Cross University Hospital; Honorary Senior Lecturer
Queen Mary University of London London, UK

This edition first published 2011, © 2011 by David Levy. 1st edition 1998 (Greenwich Medical Media/Cambridge University Press) 2nd edition 2006 (Altman Publications)