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  Alternative Medicine, (Zurich, Switzerland) (1986): 3, 241
Prevention and management of coronary heart disease by an indigenous compound Abana G.P. Dubey, Aruna Agrawal and K.N. Udupa, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.
 
 
 Abstract

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.


 Introduction

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.


 Materials and Methods

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 month’s 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.


 Results

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).

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


 Discussion

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.


 References
  1. 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.

  2. Feinleib, M. and Rifkind, B.M., Changing patterns of cardiovascular disease mortality in the United States. Isr. J. Med. Sci. (1982): 18, 1098, 1105.

  3. Griffith, J.C., Leung, F.Y.T. and McDonald, T.T., Fluorometric determination of plasma catecholamine. Clin. Chem. Acta. (1970): 30, 395.

  4. 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.

  5. 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.

  6. 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.

  7. 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.

  8. 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.