systemic hypertension: some observations
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Systemic Hypertension: Some Observations
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n article from this pen 30 years ago provided someevidence that systemic hypertension was a greater risk
actor for development of other cardiovascular diseases thanreviously indicated.1 That evidence was primarily in-reased cardiac mass (�350 g in adult women; �400 g indult men) in a very high percentage of patients with non-raumatic sudden death; angina pectoris; acute myocardialnfarction and certain of its complications (rupture, leftentricular aneurysm, mitral regurgitation); fusiform, sac-ular and dissecting aneurysm of the aorta; cerbrovascularccidents; renal failure; and many cases of aortic valvetenosis and mitral anular calcium. These earlier observa-ions have been reinforced subsequently.
It is estimated in the USA that there are about 65 milliondults with systemic hypertension, 15 million who haveurvived �1 coronary events, 17 million with diabetes mel-itus, 5 million with heart failure, 5 million with strokes, and
million with atrial fibrillation. Thus, more adults in theSA have elevated (�140/90 mm Hg) systemic blood pres-
ure (BP) than all the patients with coronary heart disease,iabetes mellitus, heart failure, strokes, and atrial fibrillationombined. Yet, other than hyperlipidemia (low-density li-oprotein cholesterol �100 mg/dl), elevated systemic arte-ial BP is our most common cardiovascular condition,roper treatment of which prevents or certainly sharplyecreases strokes, aortic dissections, both systolic and dia-tolic heart failure, and chronic renal failure.
In the late 1970s, of every 100 US adults with high BP,nly 50 knew that they had it, only 30 of the 50 received �1ntihypertensive drugs, and only 15 of the 30 being treatedad their BP “controlled” (�140/90 mm Hg).2 Today,wareness, treatment, and control are not much better: ofvery 100 with elevated BP, 70 are aware that they have it,0 are receiving therapy, and 30 are controlled, a 50%ncrease in the “control” group in the last 30 years, but still0% are receiving inadequate antihypertensive therapy orone at all.2–4
Complications of elevated BP begin to arise when the BPasses 115/75 mm Hg.2 For every 20 mm Hg increase in theeak systolic pressure or 10 mm Hg increase in the end-iastolic pressure, the complication rate (stroke, heart fail-re, renal failure, aortic dissection) doubles. Thus, at 135/5 mm Hg, the risk is 2 times that at 115/75 mm Hg and yethat level is considered “normal.” At 155/95 mm Hg, theisk increases 4 times and at 175/105 mm Hg, the risk is 8imes that at the 115/75 mm Hg level. It is much lessxpensive to treat high BP than to treat a stroke, or heart orenal failure, or aortic dissection.
In the Western World, the systolic BP tends to rise withge such that by age 60, 50% of Americans have a systolicressure �140 mm Hg, and by age 100, 90% have an
levated systolic pressure.5,6 In other words, one’s age mi- o002-9149/05/$ – see front matter © 2005 Elsevier Inc. All rights reserved.
us 10% generally indicates theercent of older individuals inhe USA with systolic hyperten-ion. The diastolic BP works inhe opposite way. Most persons
50 years of age with hyperten-ion have the diastolic form, i.e.,iastolic BP �90 mm Hg. Fromge 50 to 60 years the diastolicP tends to level off, and afterge 60 it tends to gradually de-line. Because in older individuals the systolic BP tendso increase progressively with age and the diastolic BPends to decrease progressively with age, the pulse pres-ure, the difference between the peak systolic and the endiastolic systemic BP, tends to rise progressively withge.
Although many studies have shown the systolic BP to beore predictive of untoward events (stoke, heart failure,
enal failure, aortic dissection) than the diastolic BP, mosttudies examining the effects of “controlling” BP by �1ntihypertensive agents have focused on the diastolic ratherhan the systolic BP. (The Federal Drug Administrationntil the last decade or so also insisted on using the diastolicP as the marker of a drug’s effectiveness, despite thending in the Framingham study �30 years ago showing
he systolic pressure to be more predictive of untowardvents than was the diastolic BP.) Indeed, after the systolicP, the pulse pressure is more predictive of untoward eventsnd the diastolic BP, the least predictive.2
Although a blood pressure of 140/90 mm Hg has beensed as the cut off between normal and elevated BP, the BPevel, just like the low-density-lipoprotein cholesterol level,s a continium, the higher the level, the greater the risk. Theystemic BP at birth is about 90/60 mm Hg, a level oftenharacterized in adults in the USA as “shock”, but in soci-ties where no salt is eaten, or at least the salt level is so lowhat it cannot be measured, the BP does not rise with age andemains at about 90/60 mm Hg throughout life. Thus, aystolic BP of 140 mm Hg is 36% higher than what ourystolic BP probably should be. Fittingly, the Joint Nationalommittee (JNC) on prevention, detection, evaluation and
reatment of high BP (JNC 7) defined “normal” BP as that120/�80 mm Hg.Many things we do in living our lives effect our BP.7
eighing too much, smoking cigarettes, eating high-fat andigh sodium calories, drinking alcohol and caffeine, stress,nd taking non-steroidal anti-inflammatory medications allaise our BP. In contrast, bed rest, sleep, losing weight,elaxation, exercise, vegetarian-fruit (fiber) diet, garlic,
mega-3 polyunsaturated fatty acids , potassium, magne-www.AJConline.org
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1611From the Editor
ium, vitamin C, marital harmony, and owning a pet allower our BP.
Although systolic hypertension is more common thaniastolic hypertension, the latter is far more easily con-rolled by antihypertensive drugs than is the systolicressure. Isolated systolic hypertension (�160/�90 mmg) (stage 2 hypertension2) is particularly resistant to
ontrol and, with few exceptions, requires �2 antihyper-ensive drugs.
The JNC 7 report2 published May 21, 2003—a splendidocument—lists 66 individual oral antihypertensive agentsnd 27 combination oral antihypertensive agents containing
drugs in 1 pill. Of the 27 combinations, 24 contain aiuretic as 1 of the 2 drugs and the other 3 include a calciumntagonist with either an angiotensin-converting enzymenhibitor or an angiotensin receptor blocker. The latter 3ombinations can lower the systolic BP about 30 mm Hgnd the diastolic BP about 15 mm Hg. Few patients withypertension can have the elevated BP “controlled”�140/90 mm Hg) with a single antihypertensive drug;ost require �2 drugs. The type(s) of drug(s) chosen is not
early as important as administering �1 drug and convinc-ng patients that the best anti-stroke, anti-heart failure in-urance is taking the antihypertensive drug(s) every day.nd 70% of the hypertensive patients in the USA are not
eing “controlled. ” We all can do better.William Clifford Roberts, MDEditor in Chief
Baylor Heart and Vascular InstituteBaylor University Medical Center
Dallas, Texas
. Roberts WC. The hypertensive diseases. Evidence that systemic hyper-tension is a greater risk factor to the development of other cardiovas-cular diseases than previously suspected. Am J Med 1975;59:523–532.
. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, IzzoJL, Jones DW, Materson BJ, Oparil S, Wright JT Jr., Roccella EJ, andthe National High Blood Pressure Education Program CoordinatingCommittee. The seventh report of the Joint National Committee onPrevention, Detection, Evaluation, and Treatment of High Blood Pres-sure. JAMA 2003;289:2560–2572.
. Burt VL, Whelton P, Roccella EJ, Brown C, Jeffrey A, Higgins M,Horan MJ, Labarthe D. Prevalence of hypertension in the US adultpopulation: results from the third National Health and Nutrition Exam-ination Survey, 1988–1991. Hypertension 1995;25:305–313.
. Lloyd-Jones DM, Evans JC, Larson MG, O’Donnell CJ, Roccella EJ,Levy D. Differential control of systolic and diastolic blood pressure.Factors associated with lack of blood pressure control in the commu-nity. Hypertension 2000;36:594–599.
. Franklin SS, Gustin W IV, Wong ND, Larson MG, Weber MA, KannelWB, Levy D. Hemodynamic patterns of age-related changes in bloodpressure: the Framington Heart Study. Circulation 1997;96:308–315.
. Sagie A, Lason MG, Levy D. The natural history of borderline isolatedsystolic hypertension. N Engl J Med 1993;329:1912–1917.
. Kaplan KM. Kaplan’s Clinical Hypertension. 8th Ed. Philadelphia:
Lippincott Williams & Wilkins, 2002:550.