Dianzumba SB, Liebson PR, Grandits G, Prineas RJ, Grimm RH
Jr, Stamler J
Effects of long term antihypertensive therapy on left ventricular
remodeling: the treatment of mild hypertension study
11th Scientific Meeting, American Society of Hypertension
Am J Hypert
(Apr) 9:148A 1996
The impact of antihypertensive lowering therapy on left ventricular
hypertrophy (LVH) is a subject of intense interest in clinical
medicine in part because LVH is associated with increased cardiac
mortality risk. Not all antihypertensive drug regimens reduce LVH to
the same extent in patients with hypertension and LVH. A majority of
patients with hypertension have mild hypertension and the TOHMS study
was designed to investigate the efficacy and safety of both intense
lifestyle modification and drug therapy including placebo or one of
five first-line active agents in mild hypertensives.
To determine the impact of various agents on LVH, these investigators
studied 2-D echocardiograms in 844 TOHMS patients. They found that of
625 patients randomized to drug therapy, LV geometry was normal in
55.3% of placebo and 58.7 active drug treated patients and these
figures increased in both groups to about 75% at 48 months of
follow-up. Subanalysis of the active drug groups indicated that
amlodipine and acebutalol significantly reduced relative wall
thickness (RWT) early on in the study. However, only amlodipine
produced a significant reduction in RWT at 48 months as compared with
placebo. In contrast the other agents including chlorthalidone,
enalapril and doxazosin showed no differences as compared to placebo
at any time during the study.
The authors conclude that amlodipine and acebutalol are more effective
than placebo in normalizing LV geometry in stage I hypertension with
amlodipine showing more sustained long-term effects. This is a very
provocative finding because it has been suggested that ACE inhibitors
because of their effects on AII should be more effective at reducing
LVH. Also it has been suggested that thiazide diuretics like
chlorthalidone might worsen LVH by increasing angiotensin II.
Although not stated in the abstract, it seems likely that blood
pressure control was similar among these groups. Since comparisons of
effects, or control for lifestyle modifications is also not presented
one must assume that the degree of changes induced by lifestyle did
not affect these results.
Comment: This abstract suggests for the first time that a
dihydropyridine calcium channel blocker is superior to placebo, ACE
inhibition, -blockade, à1-blockade, thiazide diuretic therapy for
reducing left ventricular hypertrophy. If this is supported by other
studies it could lead to alterations in clinical practice. This area
will be watched with even greater interest in the future.
(Robert D. Toto, M.D., University of Texas Southwestern Medical
Center)
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11th Scientific Meeting, American Society of Hypertension
H: Drug therapy :
Calcium channel blockers
H: Pathophysiology :
Heart in hypertension