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Journal of the Anatomical Society of India

Anatomy of Human Coronary Arterial Lipid Accumulation

Author(s): Kumar, Keshaw

Vol. 52, No. 2 (2003-07 - 2003-12)

Department of Anatomy, M.L.N. Medical College, Allahabad, INDIA.

Abstract

To compare tunica intimal densities of lipid interrelating with pulse pressure of blood in left and right coronary arteries, tissue of anterior and posterior interventricular arteries was taken at constant levels from 50 human adults who had no history of any cardiovascular disease. Tissue was preserved in Baker's Calcium Cadmium Formal Solution (1944). Paraffin sections of 10 micron thickness were cut with the help of rotary microtome and stained with Sudan Black- B.

A ratio of 3 : 1 was observed between densities of reaction product of lipid in tunica intima of anterior and posterior interventricular arteries resembling with ratio between pulse pressures of blood in left and right coronary arteries i.e. 60mm of Hg in left coronary artery and 20mm of Hg in right coronary artery. It was concluded that pulse pressure of blood in an artery is directly proportional to tunica intimal density of lipid in that artery..

Key words: Coronary arteries, Anterior interventricular artery, Posterior interventricular artery, Pulse pressure.

Introduction:

In the past studies of lipid in tunica intima of arteries have been done by Gross et al (1934), Harvey et al (1963), Spiro and Wiener (1963). Clarification of relationship of systemic blood pressure with atherosclerosis has also been tried by Anitschkow (1913), Turnbull (1915), Davis and Klainer (1940), Bronte and Heptinstall (1954), Morgan (1956), Heptinstall et al (1958), Wilkins et al. (1959) Paterson et al, (1960) and Sacks (1960). Kumar (1996) reported the increasing pulse pressure of blood as a cause of arterial atherosclerosis. Kumar (2003) calculated pulse pressures of blood in left and right human coronary arteries. But exact anatomy of human coronary arterial lipid accumulation was uncertain to smoking, alcoholism, anxiety and hypertension.

Because arterial atherosclerosis begins with the increasing density of lipid in tunica intima, therefore, the present study is conducted to compare densities of tunica intimal lipid interrelating with pulse pressures of blood in these arteries.

Material and Method:

During autopsy, tissues of anterior and posterior interventricular arteries were taken from 50 human adults immediately after their death due to accidents after knowing history from their relatives that they were not suffering from any cardiovascular disease. Tissue of anterior interventricular artery was taken 2cm distal to its commencement (most effected site for myocardial infarction) while tissue of posterior interventricular artery was taken 1.25 cm distal to its commencement (least affected site for myocardial infarction).

Tissue was preserved in Baker's Calcium Cadmium Formal Solution (1944). Paraffin sections of 10 micron thickness were cut with the help of rotary microtome and stained with Sudan Black-B. Each layer of artery was graded for stain as +, ++, +++, ++++ according to density of reaction product of lipid with + representing the lightest and + + + + representing the darkest staining. Results were obtained by visual assessment by a single observer. The ratio of pulse pressures of blood in anterior and posterior interventricular branches of left and right coronary arteries (Kumar, 2003) was compared with ratio of their tunica intimal densities of reaction product of lipid.

Observations:

Tunica adventitia of anterior and posterior interventricular arteries showed + + + + density of reaction product of lipid. Tunica media of anterior and posterior interventricular arteries showed+ density of reaction product of lipid. Density of reaction product of lipid was + + + in tunica intima of anterior interventricular artery and + in tunica intima of posterior interventricular artery. (Fig. 1, 2)

Table - 1 Density of reaction product of lipid

Arteries Tunica adventitia Tunica media Tunica intima
Anterior Interventricular artery ++++ + +++
Posterior Interventricular artery ++++ + +

(Density of reaction product of lipid in tunica intima of anterior interventricular artery) / (Density of reaction product of lipid in tunica + 1 intima of posterior interventricular artery) = (+++) / (+) = 3/1

(Pulse pressure in anterior interventricular branch of left coronary artery) /(Pulse pressure in posterior interventricular 1 branch of right coronary artery) = (60 mm) / (20 mm of Hg) = 3/1

Table 2: Pulse pressure and tunica intimal density of reaction product of lipid

Arterial pressure and lipid density Anterior interventricular branch of left coronary artery Posterior interventricular branch of right coronary artery Ratio
Pulse pressure 60 mm of Hg 20 mm of Hg 3:1
Tunica intimal density of reaction product of lipd +++ + 3:1

Discussion:

On the basis of above observations, author proposes following theory of atherosclerosis.

"Tunica intimal density of lipid in an artery is directly proportional to pulse pressure of blood in that artery".

On the basis of above theory of atherosclerosis is established the mechanism of atherosclerosis as follows:

Pulse pressure of blood a Pinocytotic activity of endothelial cells of tunica intima a Amount of lipoproteins entering the tunica intima a Density of tunica intimal lipid a Relative inadequacy of metabolic removal of constituent lipids in tunica intima a Atherogenesis

Due to increased pulse pressure of blood pinocytotic activity of endothelial cells of tunica intima is increased which results into increased density of tunica intimal lipid due to increased amount of lipoproteins entering the tunica intima.

Due to which relative inadequacy of metabolic removal of constituent lipids is produced because inner 1/3 of tunica media and entire tunica intima is devoid of blood vessels and in this way atherogenesis occurs. The opinion of author that increasing pulse pressure of blood is the cause of atherosclerosis is supported by the findings of following workers.

1. Turnbull (1915) observed that atheromatous plaques were common in the pulmonary arteries of patients with mitral stenosis and he suggested that the high pulmonary pressure might be a factor in their production.

2. Davis and Klainer (1940) demonstrated a relationship between coronary disease severity and arterial pressure.

3. Paterson et al, (1960) established that the total extractable lipid in the coronary, cerebral and femoral arteries was related to blood pressure.

4. Wilkins et al (1959) and Sacks (1960) used heart weight as a guide to blood pressure and inadequacies of heart weight as an indicator of arterial pressure.

5. Antischkow (1913), Bronte-Stewart and Heptinstall (1954) Heptinstall et al, (1958) noticed that lesions found in cholesterol fed rabbits are not the same as those found in human arteries and the effects of experimental hypertension in these animals may not be relevant to human vascular disease. Because pulse pressure of blood is always increased with an increase in blood pressure therefore the theory produced by the author regarding atherosclerosis is supported by the findings of above workers who have observed the relationship of atheromatous plaques with increasing blood pressure in the past.

The mechanism of atherosclerosis laid down by the author on the basis of theory of atherosclerosis is supported by the findings of following workers :

1. Harvey (1963) presented some observations on the mechanism of arterial lipid accumulation in human coronary artery atherosclerosis. These observations supported the concept of plasma proteins entering the arterial wall from the lumen and because of localized relative inadequacy of metabolic removal of the constituent lipids, accumulated in selected areas of the arterial intima giving rise to the lesions of atherosclerosis.

2. Gross et al (1934) reported earlier appearance and more marked deposits of lipid crystals in the intima of anterior interventricular branch of left coronary artery in human beings.

3. Spiro and Wiener (1963) have laso observed membrane enclosed droplets and large vacuoles within the endothelial cells of rat coronary artery probably representing transport phenomenon within the cells. According to them pinocytotic activity might be of importance in certain pathological phenomenon, particularly the accumulation of lipid in atherosclerosis. Because the density of subintimal lipid, which is directly proportional to pulse pressure of blood, can not increase without increase in the pinocytotic activity of endothelial cells due to which amount of lipoproteins entering the tunica intima is increased which is responsible for producing relative inadequacy of metabolic removal of constituent lipids, therefore, mechanism of atherosclerosis established by the author is supported by the findings of above workers.

The theory proposed in the present study regarding arterial atherosclerosis is supported by following evidences also:

1. Normally atherosclerosis does not occur in pulmonary trunk and its branches unlike the ascending aorta and its branches unless there is pulmonary hypertension because pulse pressure of blood in pulmonary trunk is three times less than the pulse pressure of blood in ascending aorta.

2. In cases of myocardial infarction the anterior interventricular branch of left coronary artery is the most effected artery and posterior interventricular branch of right coronary artery is the least effected artery because density of lipid in tunica intima of anterior interventricular artery is three times more than the density of lipid in tunica intima of posterior interventricular artery.

3. Lower prevalence of atheromatous plaques in the neck arteries and upper aorta as compared with the higher prevalence in the distal aorta and iliac arteries in view of the fact that femoral to carotid pulse pressure ratio is approximately 3:2 as noted by Hurthle (1934, 1935, cited by Wehn 1957).

4. In the veins pulse pressure of blood is zero therefore these are never effected by atherosclerosis.

References:

  1. Antitschkow, N. (1913) : uber die veranderungen der Kaniuchenaorta bei experimentelle Cholesterinsteatose Beitr. path. Anat 56: 379.
  2. Bronte-stewart, B. & Heptinstall, R.H. (1954): The relationship between experimental hypertension and cholesterol induced atheroma in rabbits. Journal of Pathology and Bacteriology 68: 407.
  3. Davis, D. & Klainer, M.J. (1940): Studies in hypertensive heart disease. I The incidence of coronary atherosclerosis in case of essential hypertension. American Heart Journal 19: 185.
  4. Gross, L. Epstein, E.Z. and Kugel, M.A. (1934): Histology of coronary arteries and their branches in the human heart. American Journal of Pathology 253-274.
  5. Harvey, F. Watts, M.D. (1963): The mechanism of arterial lipid accumulation in human coronary artery atherosclerosis. Coronary Heart Disease, P-98.
  6. Heptinstall, R.H., Barkley, H. & Porter, K.A. (1958): Relative roles of blood cholesterol level and blood pressure level in the production of experimental aortic atheroma in rabbits, Angiology. 9: 84.
  7. Kumar, Keshaw (1996): Increasing pulse pressure of blood – A cause of atherosclerosis in arteries Journal of Anatomical Sciences. Vol. 15(1): 15-19.
  8. Kumar, Keshaw (2003) : Anatomy of human coronary arterial pulsation. Journal of Anatomical Society of India. Vol. 52(1) : 24-27.
  9. Morgan, A.D. : The pathogenesis of coronary occlusion Blackwell Scientific Publications, Oxford. (1956).
  10. Paterson, J.C., Mill, J. & Lockwood, C.H. (1960): The role of hypertension in the progression of atherosclerosis, Canadian Medical Association 82: 65.
  11. Sacks, M.I. (1960) : Aortic and coronary atherosclerosis in the three racial groups in Cape Town. Circulation 9: 533.
  12. Spiro, D. and Joseph, Wiener, M.D. (1963) : Fine structure of coronary artery. Coronary Heart Disease p-11.
  13. Turnbull, H.M. (1915): Alterations in arterial structure and their relation to syphilis. Quarterly. Journal of Medicine 8: 201.
  14. Wehn, P.S. (1957): Pulsatory activity of peripheral arteries. Scandinavian Journal of Clinical & Laboratory Investigation 9: Suppl. 30 :1.
  15. Wilkins, R.H. Roberts, J.C. & Moses, C. (1959): Autopsy studies in atherosclerosis Part III. Circulation 20: 527.

Fig. 1

Missing Image

(T.S. of anterior interventricular artery 2 cm distal to its commencement showing ++ + density of reaction product of lipid in its tunica intima (T.I.) (TM – Tunica media) (Sudan Black - 'B' 100)

Fig. 2

Missing Image

T.S. of posterior interventricular artery 1×25 cm distal to its commencement showing + density of reaction product of lipid in its tunica intima (T.I.) (TM - Tunica media; IEL-Internal Elastic Lamina) (Sudan Black - 'B' 100)

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