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Article Review/Hyperlink
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Rossi GP, Sacchetto A, Visentin P, Canali C, Graniero GR,
Palatini P, Pessina AC
Changes in left ventricular anatomy and function in
hypertension and primary aldosteronism
Hypertension
(May) 27:1039-1045 1996

The role of the renin-angiotensin system in the pathogenesis of
cardiac hypertrophy has been the subject of intense investigation over
the past 5 years. One hypothesis is that angiotensin II may directly
stimulate myocardial cell hypertrophy directly, as experimental models
have shown, thereby leading to left ventricular hypertrophy. These
observations have led to the hypothesis that reducing left ventricular
hypertrophy by interfering with angiotensin II formation or blockade
of the AII type 1 receptor may in turn reduce mortality in subjects
with left ventricular hypertrophy, a powerful risk factor for sudden
cardiac death. Indeed, a major clinical trial utilizing the AII type
I receptor blocker losartan, is now underway. Recent observations
also suggest the possibility that aldosterone may directly influence
cardiac function through growth promoting effects on cardiac
connective tissue, specifically cardiac fibroblasts which produce
collagen type III.
In this regard, Rossi and colleagues compared cardiac mass (2D
echocardiograph) and estimates of left ventricular filling (color
doppler) in 34 patients with primary aldosteronism (PA) and 34
patients with essential hypertension (EH) matched for age, sex, BMI,
degree and duration of hypertension and potassium intake. They also
measured these parameters before and one year after surgical
correction in 19 patients and after 1 year of medical therapy alone in
6 patients with PA. They found that patients with PA had greater
degree of left ventricular hypertrophy and lower intracardiac flow
velocity as compared to EH patients. Moreover, impaired ventricular
diastolic filling was noted in PA patients and the atrial contribution
to LV filling was noted to be increased in PA as compared to EH
patients. After one year, LV mass was significantly reduced in
post-surgically treated but not in medically treated PA patients. The
increased LVH and reduced flows were positively correlated with plasma
aldosterone concentration, diastolic and systolic blood pressures.
The authors concluded that hyperaldosteronism with suppression of the
renin-angiotensin system is associated with increased degree of LVH
and impaired diastolic function. They speculate that high
concentration of aldosterone may contribute to this effect possibly by
altering cardiac extracellular matrix through changes in fibroblast
and collagen.
Comment: The study raises the intriguing possibility that
aldosterone could alter cardiac function independent of angiotensin II
as previous studies have suggested. It is noteworthy that patients
with PA had longer mean duration of hypertension (111 vs 77 months,
NS) and that sodium excretion rates were not compared. It is possible
that differences in duration of hypertension and/or differences in
volume could have produced these effects. Still, the comparison of
post-op versus medically treated patients showing the regression of
LVH in the former but not in the latter is quite interesting. It will
be interesting to see if indeed aldosterone emerges as an important
hormone in cardiac remodeling in humans.
(Robert D. Toto, M.D., University of Texas Southwestern Medical
Center)
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