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The effect of Abana
and propranolol on left ventricular hypertrophy in hypertensive
individuals was studied by echocardiography. The study showed an
improvement in cardiac function as indicated by an increase in ejection
fraction and fractional shortening in both the Abana- and propranolol-treated
groups. A decrease in cardiac mass with propranolol was seen at
12 weeks and was maintained upto 36 weeks. With Abana, the reduction
in mass was seen from 18 weeks onwards and lasted up to 42 weeks.
In 5 patients on Abana and 2 on propranolol, the trial was continued
for a further period of 84 weeks, but the effects seen after 84
weeks were not significantly different from those at 60 weeks.
Left
ventricular hypertrophy (LVH) is a common sequel of hypertension1.
Blood pressure reduction may lower the risk of LVH2,
but drugs given to control blood pressure (BP) may not necessarily
halt the process of hypertrophy. Hypertensive patients with LVH
have higher plasma norepinephrine levels, indicating a trophic influence
of catecholamines on cardiac muscle mass3. Short-term
studies with propranolol have shown a regression of LVH in hypertensive
patients, along with a reduction in norepinephrine levels4.
Our earlier long-term study showed that though b-adrenergic
blockers like propranolol were capable of causing regression of
cardiac hypertrophy, the action did not last for the entire period
of the study5. A herbomineral preparation, Abana (The
Himalaya Drug Company, Bangalore, India), containing many useful
drugs in their optimum concentration, is used as an antihypertensive5
and hence, it would be worthwhile to study its effect on cardiac
hypertrophy.
A
60-week study was conducted on male hypertensive patients in the
age group of 50-65 years, having systolic blood pressure (SBP) 150-170
mmHg and diastolic blood pressure (DBP) of 90-100 mmHg. Written
informed consent was obtained from the patients before including
them in the trial. Hypertensive patients suffering from diabetes,
cardiac failure, cardiomyopathies and valvular diseases were excluded.
The criteria for hypertrophy were the following echocardiographic
parameters7.
i)
Left ventricular internal dimension in systole (LVIDs) 5 cm.
ii)
Left ventricular mass (LVM) 120 g/m2.
iii)
Posterior wall thickness 11 mm.
An
equal number of patients were assigned to either Abana, 2 tablets
3 times a day for 6 weeks, followed by 1 tablet 3 times a day, or
propranolol given in the antihypertensive dose range of 40-120mg/day.
Other drug treatments were similar in the 2 groups.
Assessments
of drug therapy on variables such as BP and echocardiography were
made every 6 weeks. Echoes were read by a person unaware of the
treatment given to the patient.
From
the measurement of ventricular dimensions, assessment of cardiac
function and volumes were made using the following formulae:
1
LVM = (LVIDd + 2 PWT)3 - (LVIDd)3 x 1.05
LVIDd - LVIDs
% FS = x 100
LFIDd
EDV - ESV
EF =
EDV
where
LVM is the left ventricular mass, LVIDd and LVIDs are the left ventricular
internal dimensions in diastole and systole respectively.
PWT
is the posterior wall thickness; FS is the fractional shortening;
EF is the ejection fraction; EDV is the end diastolic volume, and
ESV is the end systolic volume.
Statistical
analysis of the data was done by Student's 't'-test.
The
baseline parameters such as BP and echocardiography were similar
in the age-matched patients of both groups. Table 1 shows the assessment
parameters at the start of the trial, during the maximal effect
and at the end of therapy with Abana and propranolol. The extent
of decline in BP was greater and faster with propranolol, compared
with Abana. However, the reduction in LVID, LVM and improvement
in cardiac function, as noted by an increase in ejection fraction
and fractional shortening, were similar irrespective of the type
of therapy, although the maximal effect was seen at 12 weeks in
the case of propranolol and at 18 weeks with Abana. At the conclusion
of the 60-week trial, the improvement seen with drug therapy during
the trial declined considerably and the values were outside the
normal limits.
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Table
1: Effect of propranolol and Abana on different echocardiographic
parameters (mean ± SEM)
|
|
Propranolol
|
Abana
|
|
|
Before
|
30
weeks
|
60
weeks
|
Before
|
30
weeks
|
60
weeks
|
| SBP
(mm) |
154.00
± 5.00
|
122.00
± 6.00b
|
126.00
± 2.00b
|
152.00
± 7.00
|
134.00
± 3.00
|
136.00
± 6.00
|
| DBP
(mm) |
96.00
± 3.00
|
80.00
± 5.00
|
83.00
± 2.00
|
97.00
± 6.00
|
86.00
± 2.00
|
88.00
± 3.00
|
| LVIDd
(cm) |
5.60
± 0.00
|
4.20
± 0.30a
|
5.10
± 0.20
|
5.80
± 0.20
|
4.40
± 0.10b
|
5.20
± 0.40
|
| LVIDs
(cm)
|
4.80
± 0.70
|
3.70
± 0.80
|
4.20
± 0.60
|
4.70
± 0.90
|
3.60
± 0.70
|
4.40
± 0.30
|
| PWT
(mm) |
12.60
± 0.80
|
9.80
± 1.90a
|
11.60
± 0.90
|
13.00
± 0.70
|
10.10
± 1.30
|
10.80
± 1.00
|
| IVS
(mm) |
12.70
± 1.70
|
9.60
± 0.80a
|
11.30
± 0.60
|
12.90
± 2.00
|
9.90
± 1.10
|
11.70
± 1.50
|
| %
FS |
21.60
± 4.20
|
30.00
± 2.20
|
23.90
± 3.10
|
22.40
± 5.20
|
30.30
± 1.80
|
24.10
± 4.80
|
n=20
patients in each group
Statistical significance ap<0.05, bp<0.001
as compared with their respective initial readings.
SBP: Systolic blood pressure; DBP: Diastolic blood pressure;
LVID: Left ventricular internal dimensions;
PWT: Posterior wall thickness; IVS: Inter-ventricular septum;
FS: Fractional shortening. |
The single
most important parameter of cardiac hypertrophy is LVM. Figure 1 shows
that the decrease in cardiac mass at 12 weeks with propranolol was
maintained up to 36 weeks. With Abana, the reduction in mass seen
from 18 weeks onwards, lasted up to 42 weeks. In both groups, from
42 weeks onwards, the cardiac mass started increasing above normal.
The DBP remained below 90 mmHg (both during and after the period of
reduction) but the LVM started increasing. In 5 patients on Abana
and 2 on propranolol, the trial was continued for a further period
of up to 84 weeks, but the effects seen at 84 weeks were not significantly
different from those at 60 weeks.
Mode
echocardiography is an accurate method of assessing left ventricular
function8. Echocardiographic estimates correlate well
with those laid down by the American Society of Echocardiography9
and left ventricular function in these patients improved with drug
treatment, according to the criteria laid down10. Cardiac
hypertrophy is dependent on increased sympathetic tone and sympatholytic
drugs have been reported to cause reduction in hypertrophy. Abana
is an Ayurvedic herbal preparation containing several important
herbs (Table 2) and its overall effect is to cause down regulation
of b-receptors6. Hence, the
trophic influence of the sympathetic system on cardiac mass and
size is reduced. If a decrease in BP is taken as an indicator of
decrease in sympathetic tone, then regression of hypertrophy does
not depend solely on decrease in sympathetic tone11 as
even with good blood pressure control, improvement in cardiac function
and reduction in cardiac volumes and mass throughout the study were
not permanent.
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Table
2: Ingredients of Abana
|
|
Ingredients
|
Mg
|
Ingredients
|
Mg
|
| Terminalia
arjuna |
30
|
Shankh
bhasma |
10
|
| Withania
somnifera |
20
|
Makardhwaj |
10
|
| Nepeta
hindostana |
20
|
Cyperus
rotundus |
5
|
| Dashamoola |
20
|
Acorus
calamus |
5
|
| Tinospora
cordifolia |
10
|
Embelia
ribes |
5
|
| Emblica
officinalis |
10
|
Syzgium
aromaticum
|
5
|
| Terminalia
chebula |
10
|
Celastrus
paniculatus |
5
|
| Eclipta
alba |
10
|
Santalum
album |
5
|
| Glycyrrhiza
glabra |
10
|
Elettaria
cardamomum |
5
|
| Asparagus
racemosus |
10
|
Foeniculum
vulgare |
5
|
| Boerhaavia
diffusa |
10
|
Rosa
damascene
|
5
|
| Shilajeet |
20
|
Cinnamomum
cassia |
5
|
| Centella
asiatica |
10
|
Abhrak
bhasma |
5
|
| Convolvulus
pluricaulis |
10
|
Pearl
pishti |
5
|
| Ocimum
sanctum |
10
|
Agata
pishti |
5
|
| Nardostachys
jatamansi |
10
|
Jade
pishti |
5
|
| Piper
longum |
10
|
Ruby
pishti |
5
|
| Carum
copticum |
10
|
Coral
pishti |
5
|
| Zingiber
officinale |
10
|
Crocus
sativus |
2
|
| Jaharmohra |
10
|
|
|
We
convey our sincere thanks to The Himalaya Drug Company, Bangalore,
India, for sponsoring the trial.
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