8. BP Treatment
Targets
Condition
160/100 Treatment threshold if no risk
factors,TOD or CCD
< 140/90 Treatment target for office BP
measurement
< 135/85 Treatment target for ABP or HBP
measurement
< 130/80 Treatment target for for Type 2
diabetics or non-diabetic
nephropathy
< 125/75 Treatment target for diabetic or
non-diabetic nephropathy with
proteinuria
Slide 5
Studies show that a multitude of diseases are attributable to hypertension.
They include:
âą Heart failure
âą Coronary heart disease
âą Myocardial infarction
âą Left ventricular hypertrophy and failure
âą Aortic aneurysm
âą Peripheral vascular disease
âą Retinopathy
âą Hypertensive encephalopathy
âą Chronic kidney failure
âą Cerebral hemorrhage
âą Stroke
With so many diseases linked to hypertension, prompt and effective treatments have the potential to reduce many complications.
Dustan HP, et al. Arch Intern Med 1996; 156:1926-1935.
Slide 6
Despite the advances that have been made in the treatment of hypertension over the last 50 years, it is clear that there is still room for improvement in the management of this condition. Less than 40% of of Canadians with hypertension are treated for their condition. Only 16% those receiving treatment have their blood pressure controlled (BP &lt; 140/90).
Joffres MR, et al. Awareness, Treatment, and Control of Hypertension in Canada. Am J Hypertens 1997; 10:1097-1102.
An aneroid sphygmomanometer found in my partnerâs medical bag â the needle was noted to be âoff â zeroâ
Subsequently, others have studied the BpTRU in both research and clinical settings.
This study was presented by Dr. Martin Myers of the U. of Toronto at the CHS meeting last October, and will be published in the American Journal of Hypertension next month. In comparing the BpTRU to a specialist BP, FP BP, research technician and ABP it shows the BpTRU to be as accurate as a research technician.
`
Slide 22
Hypertension increases the risk of target organ damage (i.e. cerebrovascular, cardiovascular and renal events).
Several studies have reported a closer relationship between target organ damage and blood pressure when blood pressure was recorded by 24-h ambulatory blood pressure monitoring (ABPM) compared with conventional measurements of blood pressure at the clinic (Mancia 1990; Devereux, et al 1987).
A consistent pattern is seen whether target organ damage is assessed by an overall score, left ventricular mass index (LVMI), left ventricular wall thickness, or retinopathy (Sokolow, et al 1966; Devereux, et al 1983; Parati, et al 1987).
Sokolow M, Werdegar D, Kain HK, Hinman AT. Relationship between level of blood pressure measured causally and by portable recorders and severity of complications in essential hypertension. Circulation 1966; 34:279-298.
Devereux RB, Pickering TG, Harshfield GA et al. Left ventricular hypertrophy in patients with hypertension: importance of blood pressure response to regularly recurring stress. Circulation 1983; 68:470-476.
Devereux RB, Pickering TG, Alderman MH, Chiken S, Borer JS, Laragh JH. Left ventricular hypertrophy in hypertension: prevalence and relationship to pathophysiologic variables. Hypertension 1987; 9: (Suppl II):1153-1160.
Parati G, Pomidossi G, Albini F, Malaspina D, Mancia G. Relationship of 24-hour blood pressure mean and variability to severity of target-organ damage in hypertension. J Hypertens 1987; 5:93-98.
Mancia G. Ambulatory blood pressure monitoring: research and clinical applications. J Hypertens 1990; 8 (Suppl 7): S1-S13.
Slide 24
Most patients with essential hypertension are âdippersâ - patients experience the same circadian pattern as normotensives with a night-time dip in blood pressure (Mancia, et al 1983).
The ânormalâ circadian pattern is lost in some patients with essential hypertension (ânon-dippersâ). There appears to be a greater prevalence of this phenomenon in patients with secondary hypertension, renal insufficiency, pre-eclampsia, in elderly hypertensives, and in the accelerated form of malignant hypertension (Redman, et al 1976; Kobrin, et al 1984; Baumgart, et al 1989; Imai, et al 1990; Portaluppi, et al 1991).
Redman CWG, Beilin LJ, Bonnar J. Reversed diurnal blood pressure rhythm in hypertensive pregnancies. Clin Sci Mol Med 1976; 51:687-688.
Mancia G, Ferrari A, Gregorini L et al. Blood pressure and heart rate variabilities in normotensive and hypertensive human beings. Circ Res 1983; 53:96-104.
Kobrin I, Oigman W, Kumar A et al. Diurnal variation of blood pressure in elderly patients with essential hypertension. J Am Geriatr Soc 1984; 32:869-879.
Baumgart P, Walger P, Gerke M, Dorst K-G, Vetter H, Raum K-H. Nocturnal hypertension in renal failure hemodialysis and after renal transplantation. J Hypertens 1989; 7 (Suppl 6):70-71.
Imai Y, Abe K, Munakata M et al. Does ambulatory blood pressure monitoring improve the diagnosis of secondary hypertension? J Hypertens 1990; 8 (Suppl 6):71-78.
Portaluppi F, Montanari L, Massari M, Di Chiari V, Capanna M. Loss of nocturnal decline of blood pressure in hypertensives due to chronic renal failure. Am J Hypertens 1991; 4:20-26.
Slide 27
Blood pressure falls during sleep and rises rapidly just before the time of awakening and arising (Millar-Craig, et al 1978; Mancia, et al 1983).
Millar-Craig M, Bishop CN, Raftery EB. Circadian variation of blood pressure. Lancet 1978; I: 795-797.
Mancia G, Ferrari A, Gregorini L, et al. Blood pressure and heart rate variabilities in normotensive and hypertensive human beings. Circ Res 1983; 53:96-104.
Slide 29
Epidemiological evidence shows that CHD morbidity and mortality are greatest in the morning waking period (Muller, et al 1985; Thompson, et al 1985; Muller, et al 1987; Rocco, et al 1987; Willich, et al 1987; Mulcahy, et al 1988), between 8 am and 12 noon (Rocco, et al 1987).
The peak incidence of cardiovascular events is associated with the BP surge that occurs as people arise and begin their routine daytime activities (Rocco, et al 1987).
Muller JE, Stone PH, Turi ZG, et al. Circadian variation in the frequency of onset of acute myocardial infarction. N Engl J Med 1985; 313:1315-1322.
Thompson DR, Blandford RL, Sutton TW, Marchant PR. Time of onset of chest pain in acute myocardial infarction. Int J Cardiol 1985; 7:139-146.
Muller JE, Ludmer PL, Willich SN, et al. Circadian variation in the frequency of sudden cardiac death. Circulation 1987; 75:131-138.
Rocco MB, Barry J, Campbell S, et al. Circadian variation of transient myocardial ischaemia in patients with coronary artery disease. Circulation 1987; 75:395-400.
Willich SN, Levy D, Rocco MB, Tofler GH, Stone PH, Muller JE. Circadian variation in the incidence of sudden cardiac death in the Framingham Heart Study population. Am J Cardiol 1987; 60:801-806.
Mulcahy D, Keegan J, Cunningham D et al. Circadian variation of total ischaemic burden and its alteration with anti-anginal agents. Lancet 1988; ii:755-759.
Willich SN, Goldberg RJ, Maclure M, Perriello L, Muller JE. Increased onset of sudden cardiac death in the first three hours after awakening. Am J Cardiol 1992; 70:65-68.