LITERATURE REVIEW
2.9. CORONARY ARTERIES: ETHNICITY AND SEXUAL DIMORPmSM
2.10.1. HISTOLOGIC FEATURES OF THE NORMAL CORONARY ARTERY
The histological picture ofthe coronary arteries is similar to that displayed by most arteries in that it has a concentric arrangement ofan intimal layer, a middle layer and an outer layer. The intimal layer or tunica intima, is composed ofa layer ofendothelial cells along with a subendothelial layer ofconnective tissue and smooth muscle cells. The endothelial cells are arranged longitudinally, in relation to the artery and are attached via occluding junctions and gap junctions, (Alexander et al., 1998). The intimal layer is separated from the media by the internal elastic lamina, a fenestrated sheet of elastic tissue.
The media is made up predominantly of smooth muscle cells and connective tissue. In the coronary arteries, there is a higher proportion ofmuscle than elastic tissue, (Baroldi, 1983). The media may consist ofup to 40 layers ofsmooth muscle tissue and ranges in thickness from 125J..I.m to 350J..l.m, (Waller et aI., 1992). Varying amounts ofcollagen and elastic fibers are also present within these layers.
lymphatics. The bundles of collagen are arranged longitudinally. According to Likoff et aI., (1972), this arrangement combined with the somewhat "loose" consistency of the adventitia, influences changes in the diameter of the coronary arteries. The adventitia is said to range from 30011m to 50011m in thickness.
2.10.2. ATHEROSCLEROSIS AND CORONARY ARTERY ANATOMY
Coronary artery disease is by far one of the most widely considered clinical subjects. Whilst investigations aimed at understanding the mechanisms involved in plaque formation and localization, and therapeutic possibilities continue to gain favor, there are also certain anatomical concepts worth considering. Fulton's (1965) account ofthe coronary arteries offers the following thought ofinterest, that" no matter what may be the true aetiology ofatherosclerosis it is evident that anatomical or dynamic factors must play a part in determining the localization ofthe lesionsin the heart. For the distribution ofcoronary atherosclerosis, though widespread and variable, is not entirely haphazard."
The extent of atherosclerotic changes that occur in an artery may range from stiffening of the vessel to diffuse or segmental dilatation or narrowing, (Gorlin, 1976); (Figures 46 and 47). The most significant, however, is the degree of atherosclerosis that ultimately impedes flow through the vessel. With regards to the coronary arteries, this disease may involve the entire epicardial length of the vessel. Under most circumstances however, such lesions tend to be confined to specific areas ofpredilection and is essentially segmental, (Gorlin 1976). The sites oflocalization
appear to be based on hydraulic factors subject to physiological and anatomical properties of the arteries.
The major curves of the RCA and LCX are said to be particularly prone to lesions as is the point ofdivision ofthe LCA. The sites oforigin ofthe first septal and diagonal branches from the LAD are considered uncommonly susceptible areas. Gorlin, (1976) goes on to describe an association between the branching formation and localization of lesions. He adds that vessels are usually spared segmental lesions in portions ofthe vessels beyond major bifurcations. This is commonly seen in the PDA, the distal branches of the LAD and terminal diagonal branches and also in the LCX system. Itis interesting to note that when the marginal branches are single and appear to be straight, they are found to be free of atheromata.
Much consideration appears to have been given to the branching pattern and length of the left main stem in terms oflesion distribution. Fulton, (1965) found such involvement to be located in an area of around 1cm in length, beginning about 2cm from the point of bifurcation.
In an attempt to explain this occurrence, Roberts, (1986) commented on the influence of mechanical stresses, anatomically determined by the length ofthe main trunk. He maintained that the maximum stress appeared to fall on the LAD just before it anchors by its first septal perforator. This portion ofthe artery, he termed the "pathological neck" and further added that a shorter length presented a predisposition to plaque distribution.
Fulton, (1965) discussed the influence of diminished caliber resulting from branching. He confirmed that whilst severe atherosclerosis was largely confined to themaincoronary vessels and
diseased parent vessel, were relatively if not totally free from lesions.
In addition to what has been described as far as the branching patters and morphometry of the coronaries are concerned, it is both anatomically and clinically interesting to consider what influence an anomalous path taken by an epicardial artery may have on the predilection of atherosclerosis.
Studies on the intra-mural coronary arteries seem indicate that such a disposition may offer a degree ifnot total immunity from sclerotic lesions, (Fulton, 1965; Geiringer, 1951; Polacek, 1961 Angelini et aI., 1983). Although a report by Edwards et aI., (1956) cast doubt on this "protective"
effect ofthe myocardial tissue, there appears to be stronger support in favor ofintra-mural vessels being relatively free from atherosclerosis.
Whilst the influence ofan intra-mural position in protecting a coronary artery from atherosclerotic changes is remarkable, there is no definitive account ofthe mechanism involved in this occurrence.
Fulton, (1965) suggests a relationship between lower gradients ofpressure during systole between the arterial lumen and the external layer resulting from peripheral myocardial compression. In addition, he adds that it may perhaps be related to the lower degree of shearing stresses during this cardiac phase where in the intra-mural position the artery may be splinted as opposed to lying
"unsupported" in an epicardial position. With the understanding ofcourse that in such a position, the degree ofkinking and buckling that accompanies each cardiac contraction is great.
Angelini et aI's., (1983) detailed review on myocardial bridges appears to support Fulton's, (1965) theories on the factors surrounding the syst6lic wave pattern. He adds, that by compressing an arterial segment, myocardial bridges may indeed oppose the detrimental effect of systolic action.
His comments are supported by evidence obtained from in-vivo animal studies using rabbits, whose major coronary arteries are typically intra mural. Conducted by Ying-han, in 1978, the study involved inducing atherosclerosis in the experimental group by means of cholesterol ingestion. Results showed that although sclerotic changes were recorded in the aorta, the proximal coronary arteries remained free ofdisease, even when extensive lesions occurred in the subendocardial arteries. Polacek and Zechmeister (1968) observed similar results in cholesterol- induced dogs, whose anatomical arrangement ofthe coronaries resembles that of man's.
Figure 46: Histological appearance of a normal coronary artery (A, B, C, D) (Adapted from Fareer-Brown, 1977)
Figure 47: Gross pathologic appearance of a diseased coronary artery (Adapted from Fareer-Brown, 1977.)