VIMS Journal: December 2017

Commentary

Managing HYPERTENSION --- Why, When, How Far?

Dr. Pranab Kr. Das

WHY:-
Hypertension- a Blood Pressure (BP) >140/90 is endowed with cardiovascular risks. It needs to be managed - as evidences suggest that treatment is beneficial in reducing CV risk. Such evidences evolve from (a) Epidemiological data (b) Experimental results (c) Analysis of Randomized Clinical Trials reports.
Epidemiological data put forth the rationale for reduction of elevated blood pressure because (i) cardiovascular mortality and morbidity are directly related to the elevated BP. The prospective studies collaboration[1] obtained data from more than nine and half lakh participants in 61 prospective studies of BP and mortality over a period of 12 years; these studies revealed ,from ages of 40 to 89 years, each increase 20/10 mm.Hg of BP is associated with a twofold increase in mortality from Ischemic Heart Disease (IHD) and more than twofold increase in stoke mortality.
(ii) BP rises most in those whose pressures are already high.In a more than 15 years longitudinal study of Welshman [2] and a 24 years follow up of American aviators[3], it was observed that hypertension begets hypertension. In both the studies the higher the BP, the greater was the rate of change of pressure pointing to an obvious conclusion: Progressive rises in BP can be prevented by keeping the pressure down.
(iii) In humans, there is less vascular damage where the BP is lower : eg. beneath a coarctation, beyond a renovascular stenosis and in the pulmonary Circulation.
The kidney with renal artery stenosis is exposed to a lower pressure than is the contralateral kidney without stenosis Arteriolar nephrosclerosis develops in the high pressure nonstenotic kidney.[4]
The vessels exposed to the high pressure above the coarctation develop atherosclerosis to a much greater degree than do vessels below the coarctation, where the pressure is low.[5]
The low pressure within the pulmonary artery ordinarily protects the vessels from damage. When patients develop pulmonary hypertension secondary to mitral stenosis or certain types of congenital heart disease, both arteriosclerosis and arteriolar necrosis often develop within pulmonary vessels.[6]
Experimental evidences in favour of treating hypertension sprout from animal experiments in which animals that were made hypertensive develop more atherosclerosis than do normotensive animals fed the same high cholesterol diet.[7]
Again, in animal the lesions caused by hypertension including accelerated atherosclerosis can be prevented by lowering the pressure with antihypertensive agents.[8]
The analysed reports from Randomized Clinical Trials (RCTs) is the most important evidence over last several decades, since antihypertensive therapy has become available, protection with anti hypertensive therapy has been demonstrated at progressively lower levels of pressure and more recently in the elderly.[9] The benefits of individual drugs against placebo are so compelling as to preclude performance of such trials and so attentions has turned to trials contrasting a set of one or two drugs against another set of one or two. The data in multiple meta-analyses[10,11,12,13] validate the conclusion of the European Societies guidelines that "main benefits of antihypertensive therapy are due to lowering of BP per se".[14] These guidelines cover disparate groups of patients with different pretreatment levels of BP.[10]

WHEN ?:-
Having an evidence-base of the cause of action against hypertension, next to address is the timing of such action.
Life style modification (eg. more of fruits, legumes, less of salt and calories and quitting smoking, moderation or avoidance of alcohol intake with increase of physical activities and exercises) should start even in the stage of Prehypertension (120-139/80-89mm Hg BP). This serves as the basal action for one with hypertension as it would do to one without it.
Before embarking on drug treatment one caveat should always be cleared off and that is, an initially elevated office BP above 140mm Hg systolic or 90 mm Hg. diastolic must always be confirmed by home or ambulatory BP monitoring as have been emphasized by both the New European guidelines and updated UK guidelines[15] or remeasured at least three times over at least 4 weeks to ensure that hypertension is present.
Drug treatment before any effort for clearing off the caveat mentioned above can be initiated only if (1) office level BP is very high(>180/110 mm. Hg) or (ii) symptomatic target organ damage is present.

Guidelines for the institution for therapy have been based solely on the level of BP, giving rise to major irrationalities and inconsistencies.[16].
All[other hypertension guidelines] but the US JNC-7 use overall risk assessment in determining the threshold to start therapy- No mention is made on overall risk assessment also in the 2014 report from the JNC-8 Committee[17], the 2013 guidelines from the American Society of Hypertension(ASH), International Society of Hypertension(ISH)[18,19], 2013 hypertension guidelines from ACC/AHA/CDC[20]. In contrast, the 2013 ESH/ESC guidelines[14]and the 2011 UK guidelines[15], use both global risk and BP level to decide when and how therapy should be started.
A BP. > 140/90 mm.Hg that does not tend to decrease with life style modifications is the threshold for antihypertensive therapy.
Though there is lack of trials on subjects with BP < 140/90 being given antihypertensive drugs, some have argued in favour of giving such drugs to people who are not yet hypertensive;
Arguments in favour are :-
(a) it would prevent the onset of elevated BP
(b) it would help to prevent the vascular damage that may develop before the level goes beyond 140/90 mm Hg threshold.
(c) The current therapy for persons with BP > 140/90 failed to provide more than partial protection eg. 40% against strokes and only 25% against heart disease. Stevo Julius conducted TROPHY (Trial of Preventing Hypertension) trial.[21] It was begun in 1999 using an ARB in half of 809 patients whose BP were 130-139/85- 89 mm Hg. During the two years on ARB, the number of those progressing to hypertension i.e. > 140/90 mm.Hg was 66% lower than in those on placebo; however, 2 years after ARB was discontinued, there was only a 16% lesser onset of hypertension in the previously tested group compared to the placebo group.
The Prehypertension group apart as discussed above, initiation of antihypertensives was suggested at a lower threshold for higher risk patient - The 2003 JNC report[22] recommended 130/80m.Hg for those with diabetes or CKD as these comorbidities are associated with very high CV risk.
Later on, 2008 AHA/ACC position statement on treatment of Hypertension in patients with coronary disease[23] expanded the 130/80 threshold to include patients with known or suspected coronary disease or peripheral arterial disease or those requiring primary prevention for a high global CV risk.
Still later, the BP lowering Treatment Trialist showed by meta-regression analysis that additional reduction in BP (Systolic or diastolic) produces additional reduction in CV risk regardless of the initial BP level, even at an initial SBP < 140mm Hg or an initial diastolic BP < 80 mm Hg.[10] These analyses support the utilization of BP lowering medication in high risk patients with and without hypertension. Most of the new evidence based guidelines have raised the threshold for invitation of drug therapy - (i) Hypertensive "elderly" to 150/90: the 2013 ESH/ESC guidelines[14] pushed it a bit up to 160mm Hg systolic. JNC 8 defines elderly as > 60 years whereas other guidelines define it > 80 years (ii) Hypertensive with diabetes or CKD from >130/80 to > 140/90 mm Hg by 2013 ESH/ESC guidelines. Canadian guidelines have kept the > 130/80 threshold .

HOW FAR ?
Logically the goal of therapy should be to lower BP below the threshold for starting therapy.
Till a few years back , the general attitude was "the lower the better". JNC 7 emphasized the impressive observational data from the Prospective Trialists Collaboration[1] showing that the risks of fatal coronary heart desease and of fatal stroke increase logarithmically bringing at a BP as low as 115/75 mm Hg.
The JNC 8 report concluded that RCTs do not support benefits of reducing BP to < 140/80 for patients > 60 years and < 130/80 for patients < 60 or those with diabetes or CKD.
On November 13,2017, Hypertension, AHA/ACC has published the 2017 Hypertension Clinical Guidelines[24]. This guidelines defines high blood pressure to be anyone with a systolic blood pressure (SBP) >130 mm Hg. or diastolic blood pressure (DBP) > 80 mm Hg. - Thus high BP redefined for the first time in 14 years. It is estimated that this new proposed SBP and DBP cutpoints for definition of hypertension compared to those recommended in 2003. JNC 7 guidelines will increase the prevalence of hypertension by about 14 %.

CONCLUSION :-
Because the new definition of hypertension is lower (130/80 mm Hg.), more people will be classified as having hypertension. However, most of these new patients can prevent hypetension - related health problems through life style changes alone.

References
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  2. Miall WE, Chinn S ; Blood pressure and ageing, results of a 15-17 years followup study in South Wales. Clin. Sci Mol Med Suppl 1973; 45(Suppl 1): 23s-33s

  3. Oberman A , Lane NE, Harlan WR et al. Trends in Systolic blood pressure in the thousand aviator cohort over a twenty four year period.Circulation 1967:36:812- 822.

  4. Thal AP, Grage TB, Vernier RL. Function of the contralateral kidney in rental hypertension due to renal artery stenosis. Circulation 1963; 27:36-43.

  5. Hollander W. Madoff I, Paddock J, et al.Aggravation of atherosclerosis by hypertension in a subhuman primate model with coarctation of the aorta, Circ. Res 1976;38:63-72.

  6. Heath D, Edwards JE. The pathology of hypertensive pulmonary vascular disease, a description of six grades of structural changes in the pulmonary arteries with special references to congenital cardiac septal defects.Circulation 1958;18:533-547.

  7. Chobanian AV 1989 Corcoran Lecture. Adaptive and maladapative response of the arterial wall to hypertension. Hypertension, 1990;15:666-674.

  8. Chobanian AV Haudenschild CC. Nickersion C et al. Trandolapril inhibits atherosclerosis in the Watanabe heritable hyperlipidemic rabbit. Hypertension 1992;20: 473-477.

  9. Beckett NS, Peters R, Fletcher AE, et al. Treatment of hypertension in patients 80 years of age or older. N Eng J Med 2008;358: 1887-1898.

  10. Czernichow S, Zanchetti A, Turnbull E, et al. The effects of blood pressure reduction and of different blood pressure-lowering regimens on major cardiovasular events according to baseline blood pressure. Meta-analysis of randomized trials. J.Hypertens 2011; 29:4-16.

  11. Staessen JA, Wang JG, Thijs L cardiovascular prevention and blood pressure reduction: A quantitative overview updated until 1 March, 2003. J Hypertension 2003; 21: 1055-1076.

  12. Turnbull F , Woodward M, Neal B, et al. Do men and women respond differently to blood pressure lowering treatment? Results of prospectively designed overviews of randomized trials. Eur Heart J 2008b;29:2669-2680.

  13. Wang JG, Staessen JA, Franklin SS, et al. Systolic and diastolic blood pressure lowering as determinants of cardiovascular outcome. Hypertension 2005; 45: 907- 913.

  14. Mancia G, Fagard R, NarkiewiczK, et al.2013 ESH/ESC.Practice Guidelines for Management of Arterial Hypertension. Blood Press 2014;23(1):3-16.

  15. Krause T, Lovibond K, Caulfield M, et al. Management of hypertension Summary of NICE guidance. BMJ 2011;343:d4891.

  16. Jackson R, Barham P, Bills J, et al. Management of raised blood pressure in New Zealand. A discussion document. BMJ 1993:307:107-110.

  17. James PA, Oparil S, Carter BL, et al. 2014 evidencebased guideline for the management of high blood pressure in adults. Report from the panel members appointed to the Eight Join National Committee (JNC8). JAMA 2014;311(5):507-520.

  18. Weber MA, Schiffrin EL, White WB, et al.Clinical practice guidelines for the management of hypertension in the community : A statement by the American Society of Hypertension and The International Society Of Hypertension. J. Hypertension 2014:32-15.

  19. Weber MA, Schiffrin EL, White WB, et al. Clinical practice guideline for the management of hypertension in the community a statement by the American Society of Hypertension and The International Society of Hypertension. J Clin Hypertens (Greenwich) 2014;16(1) 14-26 doi 10.11.11/jch 12237.

  20. Go AS, Bauman MA, Coleman King SM, et al.An effective approach to high blood pressure control.A science advisory from the American Heart Association, the American College of Cardiology and the Centers for Disease Control and Prevention. J. Am Coll Cardiol 2014; 63(12): 1230-1238.

  21. Julius S, Nesbitt SD, Egan BM, et al. Feasbility of treating prehypertension with an angiotensin- receptor blocker. N Engl. J Med 2006; 354; 1685-1697.

  22. Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood pressure. Hypertension 2003,42:1206-1252.

  23. Rosendorff C, Black HR, Canon CP, et al. Treatment of hypertension in the prevention and management of ischaemic heart disease:A scientific statement from the American Heart Association Council for High Blood Pressure Research and the Councils on Clinical Cardiology and Epidemiology and Prevention. Circulation 2007;115:2761-2788.

  24. Highlights : 2017 Guideline for the Prevention, Detection, Evaluation and Management of High Blood Pressure in Adults - A Report of the American College of Cardiology / American Heart Association Task Force on Clinical Practice Guidelines.

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