(Hypertension. 1999;34:1179.)
© 1999 American Heart Association, Inc.
Editorial Commentary |
Reappearance of the J-Shaped Curve
From the Alton Ochsner Medical Foundation, New Orleans, La.
Correspondence to Edward D. Frohlich, MD, Editor-in-Chief, Hypertension, Alton Ochsner Medical Foundation, 1516 Jefferson Hwy, BH-514, New Orleans, LA 70121.
Key Words: Editorial • myocardial infarction • blood pressure
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So soon after we believed that the issue had been resolved concerning the existence of a J-shaped curve relationship between myocardial infarction mortality and the level of blood pressure associated with antihypertensive therapy, this "curve" phenomenon has reappeared. The relationship was said to exist when a higher mortality rate from myocardial infarction was found in hypertensive patients with diastolic pressures <85 mm Hg which appeared to be greater than in those patients whose diastolic pressures were between 85 and 90 mm Hg. The steeper and higher aspect of the J-curve was demonstrated when pretreatment pressures exceeded 90 mm Hg.1 This report was confirmed by subsequent retrospective analyses.2 3 However, the issue seemed to have been resolved until several reports appeared indicating that hypertensive or normotensive patients who were elderly or who had ischemic heart disease failed to demonstrate such a J-shaped curve with treatment even if diastolic pressure was <90 mm Hg.4 5 6 7
In this issue of the journal, Voko et al8 once again revisit the subject by reporting that a J-curve relationship between stroke incidence and treatment of hypertension exists. In their paper, they demonstrated an increased risk of stroke in treated hypertensive patients having the lowest systolic and, more significantly, diastolic pressure elevations not seen in those patients who were untreated. To be sure, as might be expected, the issue is not totally clear and straightforward. Thus, the authors found that spontaneously occurring low arterial pressures are indeed beneficial, but in those patients who were treated and whose pressure was of the lower stratum, stroke incidence was greater. However, we do not know whether the low pressures were actually induced by antihypertensive treatment. The investigators had excluded isolated systolic hypertension as one explanation, but they did not totally exclude the possibility of selection bias or low pressures resulting from interim occult cardiovascular damage which could have predisposed those patients to stroke. It would have been helpful to see whether the excess of strokes at the lowest stratum of arterial pressure persisted in those patients under treatment than in those patients with whom other coexistent cardiovascular diseases were excluded. It is clear that the only way to resolve this important question is to conduct a prospective trial in which arterial pressure is lowered by treatment to different goal values in those patients with and without other cardiovascular conditions which could predispose them to stroke. Nevertheless, the authors have presented a very important consideration that merits publication, subsequent discussion, and further study.
Furthermore, this issue raises a very important concern for the practicing physician: given the identification and evaluation of a patient with hypertension as defined by the criteria stated in the Sixth Joint National Committee (JNC-6) report,9 particularly in those patients who may be predisposed to stroke, what should be the therapeutic goals? Perhaps this question has already been answered in JNC-6 and in the recent guidelines of the World Health Organization/International Society of Hypertension with their respective recommended therapeutic goal pressures.9 10 However, still demanding more clear-cut criteria is the issue of the immediate treatment of the hypertensive patients who present clinically with alarmingly high blood pressures and an acute stroke. JNC-6 cogently recommends that "Patients with acute ischemic stroke who are treated with fibrinolytic agents require careful blood pressure monitoring, especially over the first 24 hours after starting treatment." The report goes on to say that those patients with systolic or diastolic pressures of 180 and 105 mm Hg or greater, respectively, "may be controlled with intravenous agents with careful monitoring for worsening of neurological status."9 However, these recommendations are not concordant with the overall recommendation of reducing blood pressure in patients with hypertension whose pressures are >140 mm Hg or 90 mm Hg with less definite symptoms of stroke. Moreover, the recommendations are at some variance from those advanced in the neurological literature, American Heart Association (AHA) advisories, and in the package insert approved by the Food and Drug Administration for thrombolytic agents. These reports identify the levels of pressure at which antihypertensive therapy should be initiated in the patient with stroke (eg, systolic and diastolic pressures >220 and 130 mm Hg, respectively, in the AHA advisory). The recommended levels avoid the inconsistencies of the potential J-shaped curve; but they are less clear in defining the safest lower level of pressure elevation that requires therapeutic reduction or how aggressively arterial pressure should be lowered in this acute situation.
It is apparent that treatment of hypertension has been dramatically effective in preventing stroke.9 It is likewise clear that careful identification, evaluation, and treatment of patients with hypertension need intensive emphasis in order to reverse the recent decrease in national statistics for identifying and effectively treating patients with hypertension and to prevent severe disease outcomes including stroke. The present report in this journal brings to our attention the necessity of identifying the lower levels of blood pressure elevation that demand treatment in order to prevent stroke. If the answer is not available, then the time is at hand for us to learn these levels so that the clinician is not confused by a critical therapeutic pitfall. Nevertheless, these considerations should not deter physicians from seeking out and treating patients with hypertension to prevent strokes in elderly patients who predominantly have isolated systolic hypertension. This condition has been shown to be benefited by treatment in several prospective and randomized trials.4 11 12 13 14
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Footnotes |
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The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.
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References |
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TopIntroductionReferences |
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1. Cruickshank JM, Thorp JM, Zacharias FJ. Benefits and potential harm of lowering blood pressure. Lancet. 1987;1:581–584.[Medline] [Order article via Infotrieve]
2.
Alderman MH, Ooi WL, Madhavan S, Cohen H. Treatment
induced blood pressure reduction and the risk of myocardial infarction.
JAMA. 1989;262:920–924.
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Farnett L, Mulrow CD, Linn WD, Lucey CR, Tuley MR. The
J-curve phenomenon and the treatment of hypertension. JAMA. 1991;265:489–495.
4.
SHEP Cooperative Research Group. Prevention of stroke
by antihypertensive drug treatment in older persons with isolated
systolic hypertension: final results of the Systolic
Hypertension in the Elderly Program (SHEP). JAMA. 1991;265:3255–3264.
5. Hanson L, Zanchetti A, Carruthers SG, Dahlof B, Elmfeldt D, Julius S, Menard J, Rahn KH, Wedel H, Westerling S, for the HOT Study Group. Effects of intensive blood pressure lowering and low-dose aspirin in patients with hypertension: principal results of the hypertension optimal treatment (HOT) randomized trial. Lancet. 1998;351:1755–1762.[Medline] [Order article via Infotrieve]
6. Pfeffer MA, Braunwald E, Moye LA, Basta L, Brown EJ Jr, Cudy TE, Davis BR, Geitman EM, Goldman S, Flaker GC, Klein M, Lamas GA, Packer M, Rouleau J, Rouleau JL, Rutherford J, Wertheimer JH, Hawkins CM. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction: results of the survival and ventricular enlargement trial. N Engl J Med. 1992;327:669–677.[Abstract]
7. SOLVD Trial Investigators. Effects of enalapril on survival in patients with reduced left ventricular ejection fraction and CHF. N Engl J Med. 1991;325:293–302.[Abstract]
8.
Voko Z, Bots ML, Hofman A, Koudstaal PJ, Witteman JCM,
Breteler MMB. J-shaped relation between blood pressure and stroke in
treated hypertensives. Hypertension. 1999;34:1181–1185.
9.
The Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure. The Sixth Report of
the Joint National Committee (JNC-VI) on Prevention, Detection,
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Med. 1997;157:2413–2446.
10. Guidelines Subcommittee. World Health Organization – International Society of Hypertension Guidelines for the Management of Hypertension. J Hypertens. 1999;17:151–183.[Medline] [Order article via Infotrieve]
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The Systolic Hypertension in the Elderly
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12. MRC Working Party. Medical Research Council trial of treatment of hypertension in older adults: principal results. BMJ. 1992;204:405–412.
13. Dahlof B, Lindholm LH, Hansson L, Schersten B, Ekbom T, Wester PO. Morbidity and mortality in the Swedish Trial in Old Patients with Hypertension (STOP-Hypertension). Lancet. 1991;338:1281–1285.[Medline] [Order article via Infotrieve]
14. Staessen J, Bulpitt C, Clement D, De Leeuw P, Fagard R, Fletcher A, Forette F, Leonetti G, Nissinen A, O’Malley K, Tuomilehto J, Webster J, Williams BO. Relation between mortality and treated blood pressure in elderly patients with hypertension: report of the European Working Party on High Blood Pressure in the Elderly. BMJ. 1989;298:1552–1556.
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