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Our
current knowledge regarding coronary heart disease (CHD) is primitive.
Recent studies have shown an increasing incidence of this disease
in most societies. Due to the complex aetiology, many risk factors
have been identified in the occurrence of coronary heart disease.
Many drugs have been introduced to manage coronary heart disease,
but due to adverse side-effects these drugs could not be used for
a long time. Several herbomineral drugs are traditionally used in
the prevention and management of cardiovascular disorders. Abana
is such a compound prepared on the basis of indigenous formulation,
advocated for the management of cardiovascular disorders.
Seventy-seven
diagnosed cases of essential hypertension, angina pectoris, stabilized
cases of ischaemic heart disease and sinus tachycardia were selected
for the present series of study. The routine drug treatment was
continued and patients were given Abana, two tablets twice a day
or an identical looking placebo for a period of 12 weeks. Considerable
improvement in clinical symptomatology was noticed after oral administration
of Abana. It reduced the frequency and intensity of anginal pain
and decreased the pulse rate. Similarly total lipids, triglycerides
and serum cholesterol levels also showed significant decreases.
Epinephrine and norepinephrine levels also fell in the treated group.
No adverse side-effects were noticed.
It
can be concluded that the herbomineral compound Abana may provide
a useful alternative remedy or act as an adjuvant in the prevention
and management of coronary heart disease.
Sudden death due to
coronary artery disease is a serious public health problem throughout
the world. Epidemiologic studies followed for many years have identified
numerous risk factors for coronary heart disease. A wide range of
study has provided strong support for the hypothesis that high lipid
levels increase the risk of CHD (Stamler, 1979; Levi, 1984)7,6.
Eighty per cent of cardiac deaths are due to atherosclerosis and
it is considered as a primary cause of cardiovascular disease. Grundy
(1984)4 emphasized over-production of lipoproteins as
being responsible for CHD. Recently, studies have shown that the
early identification and modification of risk factors may prevent
the occurrence of CHD. Tyroler (1984)8 suggested that
the incidence of CHD can be controlled by correcting lipids and
lipoprotein metabolism.
Many
new drugs have been introduced, which may demonstrate better efficacy
but also possess side effects. Recently attention has been directed
towards herbomineral drugs, which are traditionally used as potential
therapeutic agents in the prevention and management of CHD. However,
the scientific evaluation of such indigenous drugs is inadequate
and does not provide evidence regarding their clinical efficacy.
Keeping the above facts in view, it was decided to evaluate the
clinical significance of the known herbomineral compound Abana.
Abana
contains: Terminalia arjuna, Withania somnifera, Phyllanthus
emblica, Terminalia chebula, Asparagus racemosus, Centella asiatica,
Convolvulus pluricaulis, Ocimum sanctum, Cyperus rotundus, Piper
longum, Zingiber officinale, Syzygium aromaticum etc. in varying
doses. These drugs are commonly used by the traditional medical
practitioners in the management of cardiovascular disorders.
In
the present study an attempt has been made to study the clinical
significance of the herbomineral compound in the prevention and
management of essential hypertension, angina pectoris, stabilised
cases of myocardial infarction and sinus tachycardia.
Seventy-seven
diagnosed cases of essential hypertension, angina pectoris, stabilised
cases of myocardial infarction and sinus tachycardia were selected
for the present clinical trial. The diagnosis was confirmed on the
basis of routine clinical and laboratory investigations. The various
risk factors were identified in all cases. Thirty-four cases of
different types of cardiovascular disorders were given a placebo
and another thirty-three cases were administered the remedy Abana,
in order to compare the results. Those cases who had developed acute
clinical symptoms during the trial period were referred for conventional
therapy and discarded from this series.
Total
lipids including serum cholesterol and triglyceride levels were
measured in all cases. Epinephrine and norepinephrine levels were
estimated following the technique developed by Griffith et al.
(1970)3.
Abana
was given orally in the dose of two tablets twice a day continuously
for 3 months. Subjects on stable doses of medications for other
indications were permitted to continue them and their doses were
kept constant throughout the study. A laboratory profile, including
a complete blood count, ESR, urine analysis, blood sugar, blood
urea, creatinine, SGOT, SGPT and alkaline phosphatase was obtained
at the end of 1 month of the follow-up study. Electrocardiographic
recordings were also obtained at the end of one months therapy.
All the special investigations like total lipid profile, epinephrine
and norepinephrine levels were repeated for comparison in the treated
as well as the placebo groups.
Abana
brought about significant clinical improvement in cases of essential
hypertension, angina pectoris and ischaemic heart disease. Specific
clinical features, like palpitation, precordial discomfort and insomnia
were considerably reduced after the drug therapy. Abana did not
alter the resting haemodynamics of cardiac subjects. The angina
cases showed clinical improvement in frequency and intensity of
pain. Out of 20 cases, five did not show any clinical improvement.
There
was significant reduction in pulse rate following Abana treatment
(Table 1).
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Table
1: Mean pulse rates before and after 12 weeks of Abana treatment
Average pulse rate (mean ± S.D.)
|
| |
Essential
hypertension
|
Angina
pectoris
|
Ischaemic
heart disease
|
Sinus
tachycardia
|
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
| Placebo |
92.82
± 9.825
|
91.72*
± 12.085
|
90.72
± 12.23
|
86.96
± 9.36
|
86.42
± 13.29
|
82.77
± 9.77
|
122.72
± 16.85
|
120.72l
± 15.83
|
| |
(N=10)
|
(N=8)
|
(N=7)
|
(N=9)
|
| Treatment |
94.38n
± 10.29
|
80.72l
± 12.88
|
86.221*
± 10.21
|
79.77*
± 11.73
|
88.95n
± 14.33
|
78.22n
± 13.33
|
118.52n
± 16.83
|
93.72l
± 18.25
|
| |
(N=20)
|
(N=20)
|
(N=17)
|
(N=20)
|
| *
p<0.05 np<0.01 lp<0.001
|
The
effect of Abana on electrocardiographic patterns exhibited a significant
reduction in pulse rate. Abana produced a change in the electrocardiographic
pattern. In cases of ischaemic heart disease, improvement in ST
segment was noticed. However, the pattern of improvement was not
identical in all the cases. A slight increase in PR interval was
also noticed following Abana therapy in comparison with the placebo
group.
As
pointed out earlier, hyperlipidaemia, including hypercholestrolaemia,
is responsible for atherosclerosis.
There
was significant decrease in total lipids, triglycerides and cholesterol
levels as compared to the patients on placebo treatment (Tables
2-4).
|
Table
2: Mean lipid profiles and after 12 weeks of Abana treatment
Total lipids inmg% (mean ± S.D.)
|
| |
Essential
hypertension
|
Angina
pectoris
|
Ischaemic
heart disease
|
Sinus
tachycardia
|
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
| Placebo |
1122.08
± 139.56
|
1145.80l
± 158.82
|
1055.26
± 158.21
|
1128.97n
± 149.35
|
1340.70
± 210.78
|
1280.728*
± 224.39
|
995.32
± 130.82
|
892.33
± 130.38
|
| Treatment |
1105.57l
± 140.36
|
908.70l
± 142.55
|
1047.36*
± 140.39
|
930.32l
± 144.18
|
1291.15n
± 194.39
|
1074.815l
± 188.34
|
978.85*
± 157.21
|
861.55*
± 139.77
|
| *
p<0.05 np<0.01 lp<0.001 |
|
Table
3: Triglyceride levels before and after 12 weeks of Abana
treatment Average triglyceride levels inmg% (mean ± S.D.)
|
| |
Essential
hypertension
|
Angina
pectoris
|
Ischaemic
heart disease
|
Sinus
tachycardia
|
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
| Placebo |
268.50
± 37.40
|
285.87*
± 38.77
|
239.55
± 34.33
|
237.55
± 40.33
|
290.32
± 44.33
|
277.07
± 44.33
|
230.70
± 49.35
|
225.38
± 34.26
|
| Treatment |
271.55*
± 38.08
|
230.78*
± 49.39
|
246.22*
± 38.50
|
210.30*
± 30.31
|
287.85*
± 40.23
|
240.77*
± 38.71
|
240.55
± 46.85
|
212.40
± 44.29
|
| *
p<0.01 |
|
Table
4: Cholesterol levels before and after 12 weeks of Abana treatment
Average serum cholesterol levels inmg% (mean ± S.D.)
|
| |
Essential
hypertension
|
Angina
pectoris
|
Ischaemic
heart disease
|
Sinus
tachycardia
|
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
| Placebo |
258.92
± 46.38
|
248.92
± 39.29
|
246.70
± 35.11
|
242.32
± 39.09
|
274.78
± 48.73
|
267.28*
± 38.29
|
205.88
± 42.09
|
205.08*
± 43.33
|
| Treatment |
262.40n
± 39.29
|
218.77n
± 42.39
|
252.38*
± 40.03
|
220.87*
± 38.72
|
268.65n
± 40.33
|
224.29n
± 43.33
|
198.72*
± 48.33
|
168.55*
± 36.53
|
| *
p<0.05 n p<0.01 |
Epinephrine as well
as norepinephrine levels showed significant reduction after Abana
therapy in essential hypertension and ischaemic heart disease and
angina pectoris, but tachycardia cases did not show any change (Tables
5 and 6).
|
Table
5: Epinephrine levels before and after 12 weeks of Abana treatment
Average epinephrine level in ngml-1 (mean ± S.D.)
|
| |
Essential
hypertension
|
Angina
pectoris
|
Ischaemic
heart disease
|
Sinus
tachycardia
|
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
| Placebo |
5.38
± 1.132
|
4.53
± 1.33
|
4.30
± 0.94
|
4.21
± 1.93
|
4.28
± 1.87
|
4.50
± 1.84
|
4.87
± 1.39
|
4.75
± 0.98
|
| Treatment |
6.03*
±1.87
|
4.30*
± 1.89
|
3.98*
± 1.07
|
2.85*
± 1.87
|
4.77*
± 1.51
|
3.80*
± 0.97
|
5.20
± 1.71
|
4.50
± 0.99
|
| *
p<0.05 |
|
Table 6: Norepinephrine
levels before and after 12 weeks of Abana treatment Average
norepinephrine level in ngml-1 (mean ± S.D.)
|
| |
Essential
hypertension
|
Angina
pectoris
|
Ischaemic
heart disease
|
Sinus
tachycardia
|
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
Basal
|
12
weeks
|
| Placebo |
12.72
± 2.081
|
13.18n
± 2.802
|
10.50
± 1.95
|
9.77
± 1.875
|
9.22
± 2.708
|
8.50
± 2.372
|
8.80
± 1.825
|
8.37
± 2.028
|
| Treatment |
12.70n
± 2.88
|
10.51n
± 19.75
|
11.70l
± 2.728
|
8.57l
± 2.872
|
8.97*
± 2.325
|
6.68*
± 3.46
|
9.55
± 2.728
|
8.28
± 2.517
|
| *p<0.05
np<0.02 l p<0.01 |
Increased
understanding of the mechanism of coronary heart diseases has allowed
for development of new agents to treat them. The age-adjusted cardiovascular
mortality rate has decreased by 40% in the United States. Feinleib
and Rifkind (1982)2 presented a declining trend of mortality
rate from cardiovascular diseases, but this impressive 40% decrease
in the mortality rate due to CHD is not a world-wide phenomenon.
Many countries including India have shown increasing mortality rate
due to CHD.
Only
two cases of essential hypertension had exacerbation of clinical
symptoms. In stabilised cases of ischaemic heart disease only one
case showed deterioration and was then treated with digitalis and
Abana.
Dubey
et al., (1977)1 pointed out that the incidence
of ischaemic heart disease is increasing with the industrial development
of India.
Due
to varying aetiological factors, single drug therapy is inadequate
in the prevention and management of CHD. Similarly, in clinically
established cases of CHD the longevity may be increased by the modification
of various risk factors.
In
the recent past, serious attempts have been made to evaluate the
clinical significance of many herbal products especially in the
prevention and management of coronary heart disease. In preliminary
observations Abana showed a significant influence on clinical, biochemical
and electrophysiological levels. It is pointed out by Stein et
al., (1982)5 that psychological stress has a profound
influence on the occurrence of ischaemic heart disease. In this
series we noticed significant clinical improvement in psychological
symptoms like improvement in sleep, nervousness and precordial discomfort.
This suggests that Abana has a capacity to modify psycholgical risk
factors due to the presence of several ingredients like Brahmi,
Jatamansi, etc.
The
combined effects of this herbomineral compound brought about a significant
reduction in the heart rate.
In
the present series we noticed high lipid levels in cases of cardiovascular
disorders. Abana significantly reduced total lipids in essential
hypertension, angina pectoris and ischaemic heart disease cases.
Similarly, triglycerides and serum cholesterol were also reduced
following oral therapy.
Catecholamines
play a significant role in the aetiology and pathogenesis of essential
hypertension and ischaemic heart disease. Abana decreased the epinephrine
levels in hypertension and ischaemic heart disease cases, which
indicates that it reduces sympathetic hyperactivity.
Abana
is effective in the prevention and management of coronary heart
disease by modifying various risk factors. Abana appears to be a
well-tolerated, effective agent, hence Abana may also be used as
an alternative remedy for the management of certain cardiovascular
disorders.
-
Dubey, G.P. and Sharma, K., Incidence of ischaemic
heart disease in urbanized community of Northern India. Q.
J. Surgical Sci., Institute of Medical Sciences, Banaras
Hindu University, Varanasi, Vol. 13, Nos. 3 and 4, September
8, December 1977.
-
Feinleib, M. and Rifkind, B.M., Changing patterns
of cardiovascular disease mortality in the United States. Isr.
J. Med. Sci. (1982): 18, 1098, 1105.
-
Griffith, J.C., Leung, F.Y.T. and McDonald,
T.T., Fluorometric determination of plasma catecholamine. Clin.
Chem. Acta. (1970): 30, 395.
-
Grundy, S.M., Hyperlipoproteinaemia: Metabolic
basis and rationale for therapy. In: The American Journal of
Cardiovascular Mortality. Am. J. Cardiol. A Yorke Medical
Journal, Paul J. Carnese, New York, 27, August 1984.
-
Jonathan, H. Stein, John A. Ambrose and Michael
V. Herman, Psychosocial stress and coronary artery disease.
In: St. B. Day (Ed.), Life Stress, Vol. III, Van Nostrand
Reinhold Company, New York, 1982.
-
Levi, R.I., Causes of the decrease in cardiovascular
mortality. Am. J. Cardiol. A Yorke Medical Journal Paul
J. Carnese, New York, 27 August 1984.
-
Stamler, J., Diet, serum lipids and coronary
heart disease. The epidemiologic evidence. In: R.L. Levy, B.M.
Rifkind, B.H. Dennis and N. Erust, (Eds.), Nutrition, Lipids
and Coronary Heart Disease, A Global View, Raven Press,
New York, 1979.
-
Tyroler, H.A., Cholesterol and cardiovascular
disease. In: The American Journal of Cardiovascular Mortality.
Am. J. Cardiol. A Yorke Medical Journal paul J. Carnese,
New York 27 August 1984.
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