JAW Vol. 16. No. I : 143-4
143
July I
s (6) correctly
increases
and renin
in both plasma
system
activity
volu
that
inhibitor captopril with minoxidil as the third drug choice in triple therapy of resistant hypertension and define the subtle differences in these two potent antihypertensive agents. The were patients in their hypertension if th stolic *Editorials published in Jorrrnal of rite Amc~ricnnCoLge ofCdio/og~ reflect tRe views of the autbohsand do not necessarily represent the views of
JACC or the American College of Cardiology. From the Division of Cardiology, Ohio Stare University Hospitals. Columbus Ohio. : Robert J. Cody, MD. Division of Cardiology, Ohio State University Hospitals. 611 Means Hall, 1654 Upham Hall. Columbus. Ohio 43210. 01990 by the American
eart rate m t point gut that t
College of Cardiology
rone was actually higher in the group treated with the angiote~si~-~onverti yme ~ah~bitor than in the group is well appreciated that urinary treated with minoxi aldosterone may be a better reflection of sodium intake and angiotensin-converting enzyme inhibition during long-term therapy; nonetheless. the absence of at least qualitative aldosterone suppression is somewhat surprising. The authors (6) are candid -ith respect to the effect of captopril on left ventricular mass. Although there was a of left ventricular mass in the overall
ass is more likely to decrease in resistant hy aptspril-based therapy, this response is not necessarily uniform. An additio.lal caveat to this s captopril was administered in co metoprolol. Thus, whether the captopril
alone
or to the combined
drug therapy cannot be differentiated
influence of this triple in this study. 07351097/90/$3.50
144
JACC Vol.16. No.I July 1990:143-4
CODYETAL. EDITORIALCOMMENT
Therapeuticimplications.As stated in a now classic clinical review (I), “truly resistant” hypertension is not that common in the era of effective pharmacologic therapy. Although practicingclinicians welcome reports of “effective monotherapy” of hypertension in the hope of achieving favorable blood pressure control at minimal cost and morbidity, the reality of clinical practice is that ,nany patients continue to require several agents for blood pressure control. The current study by Julien et al. (6) adds further convincing evidence to the concept that blood pressure reduction alone may not be a sufficientend point of antihy pertensive therapy. A combination of therapies that ameliorates target organ abnormalities may be preferable, particularly by blocking adverse contributions of neurohormonal pathways. The evidence for the adverse influence of the sympathetic nervous system and renin-angiotensin system on left ventricular hypertrophy continues to increase (B-10). Unfortunately, these abnormalities are often best addressed in experimental studies that do no: closely mimic human resistant hypertension. Nonetheless, the observations and implications from drug interventions specifically targeted toward neurohormonal pathways is very convincing. “Resistant hypertension,” defined as the requirement of two or more antihypertensive drugs for blood pressure control, will continue to include a significant proportion of the hypertensive population. Therefore, well defined and executed studies such as that by Julien and coworkers (6)
will help delineate pragmatic and clinically relevant a proaches to effective and antihypertensive the
I. Gifford
RW Jr, Tarazi RC. Resistant hypertension: diagnosis and management. Ann intern Med 1978:88:661-5:
2. Tarazi RC. Bravo EL. Fouad F . Omvik P. Cody RJ. Hemodynamic and volume changes associated with captopril. Hypertension 1980:2:576-85. 3. Dustan HP. Tarazi RC. Bravo EL. Dependence of arterial pressure on intravascular volume in treated hypertensive patienls. N Engl J Med 1972:286:861-8. 4. Tarazi RC. Dustan HP.Bravo EL, Niarchos AP. Vasodilating drugs: contrasting hemodynamic effects. Clin Sci Mol Med l976:51(suppl 111): 76S-84s. 5. Campese VM. Minoxidil: a review of its pharmacological properties and therapeutic use. Drugs 1981:22:257-78. 6. Julien J. Duiloux M-A. Prasquier R. et al. Etfecls of captopril and minoxidil on left ventricular hypertrophy in resistant hypertensive patients: a 6 month double-blind comparison. J Am Coll Cardiol 1990;16: 137-42. 7. Sen S. Tarazi RC. Bumpus FM. Cardiac hypertrophy and antihypertensive therapy. Cardiovasc Res 1977:11:427-33. 8. Devereux RB. Pickering TG. Cody RJ. Laragh JH. Relation of reninangiolensin system activity IOleft ventricular hypertropby and function in experimental and human hypertension. J Clin Hypertens 1987:3:87-103. 9. Frohlich ED. Cardiac hypertrophy in hypertension. N Engl J Med 1987:317:831-3. IO. Fouad-Tarazi F. Liebson PR.Echocardiographic studies of regression of left ventricular hypertrophy in hypertension. Hypertension 1987:9(suppl 11):11-65-8.
143
July I
s (6) correctly
increases
and renin
in both plasma
system
activity
volu
that
inhibitor captopril with minoxidil as the third drug choice in triple therapy of resistant hypertension and define the subtle differences in these two potent antihypertensive agents. The were patients in their hypertension if th stolic *Editorials published in Jorrrnal of rite Amc~ricnnCoLge ofCdio/og~ reflect tRe views of the autbohsand do not necessarily represent the views of
JACC or the American College of Cardiology. From the Division of Cardiology, Ohio Stare University Hospitals. Columbus Ohio. : Robert J. Cody, MD. Division of Cardiology, Ohio State University Hospitals. 611 Means Hall, 1654 Upham Hall. Columbus. Ohio 43210. 01990 by the American
eart rate m t point gut that t
College of Cardiology
rone was actually higher in the group treated with the angiote~si~-~onverti yme ~ah~bitor than in the group is well appreciated that urinary treated with minoxi aldosterone may be a better reflection of sodium intake and angiotensin-converting enzyme inhibition during long-term therapy; nonetheless. the absence of at least qualitative aldosterone suppression is somewhat surprising. The authors (6) are candid -ith respect to the effect of captopril on left ventricular mass. Although there was a of left ventricular mass in the overall
ass is more likely to decrease in resistant hy aptspril-based therapy, this response is not necessarily uniform. An additio.lal caveat to this s captopril was administered in co metoprolol. Thus, whether the captopril
alone
or to the combined
drug therapy cannot be differentiated
influence of this triple in this study. 07351097/90/$3.50
144
JACC Vol.16. No.I July 1990:143-4
CODYETAL. EDITORIALCOMMENT
Therapeuticimplications.As stated in a now classic clinical review (I), “truly resistant” hypertension is not that common in the era of effective pharmacologic therapy. Although practicingclinicians welcome reports of “effective monotherapy” of hypertension in the hope of achieving favorable blood pressure control at minimal cost and morbidity, the reality of clinical practice is that ,nany patients continue to require several agents for blood pressure control. The current study by Julien et al. (6) adds further convincing evidence to the concept that blood pressure reduction alone may not be a sufficientend point of antihy pertensive therapy. A combination of therapies that ameliorates target organ abnormalities may be preferable, particularly by blocking adverse contributions of neurohormonal pathways. The evidence for the adverse influence of the sympathetic nervous system and renin-angiotensin system on left ventricular hypertrophy continues to increase (B-10). Unfortunately, these abnormalities are often best addressed in experimental studies that do no: closely mimic human resistant hypertension. Nonetheless, the observations and implications from drug interventions specifically targeted toward neurohormonal pathways is very convincing. “Resistant hypertension,” defined as the requirement of two or more antihypertensive drugs for blood pressure control, will continue to include a significant proportion of the hypertensive population. Therefore, well defined and executed studies such as that by Julien and coworkers (6)
will help delineate pragmatic and clinically relevant a proaches to effective and antihypertensive the
I. Gifford
RW Jr, Tarazi RC. Resistant hypertension: diagnosis and management. Ann intern Med 1978:88:661-5:
2. Tarazi RC. Bravo EL. Fouad F . Omvik P. Cody RJ. Hemodynamic and volume changes associated with captopril. Hypertension 1980:2:576-85. 3. Dustan HP. Tarazi RC. Bravo EL. Dependence of arterial pressure on intravascular volume in treated hypertensive patienls. N Engl J Med 1972:286:861-8. 4. Tarazi RC. Dustan HP.Bravo EL, Niarchos AP. Vasodilating drugs: contrasting hemodynamic effects. Clin Sci Mol Med l976:51(suppl 111): 76S-84s. 5. Campese VM. Minoxidil: a review of its pharmacological properties and therapeutic use. Drugs 1981:22:257-78. 6. Julien J. Duiloux M-A. Prasquier R. et al. Etfecls of captopril and minoxidil on left ventricular hypertrophy in resistant hypertensive patients: a 6 month double-blind comparison. J Am Coll Cardiol 1990;16: 137-42. 7. Sen S. Tarazi RC. Bumpus FM. Cardiac hypertrophy and antihypertensive therapy. Cardiovasc Res 1977:11:427-33. 8. Devereux RB. Pickering TG. Cody RJ. Laragh JH. Relation of reninangiolensin system activity IOleft ventricular hypertropby and function in experimental and human hypertension. J Clin Hypertens 1987:3:87-103. 9. Frohlich ED. Cardiac hypertrophy in hypertension. N Engl J Med 1987:317:831-3. IO. Fouad-Tarazi F. Liebson PR.Echocardiographic studies of regression of left ventricular hypertrophy in hypertension. Hypertension 1987:9(suppl 11):11-65-8.
