The coronary arteries are frequently affected either at their orifices or in their course by lesions which interfere with the circulation through them. As these arteries are, at the most, possessed of very imperfect anastomosing communications, obstruction implies a very serious disturbance in the function of the heart, amounting, in the case of a sudden obstruction of a large branch, to sudden paralysis of its action and death.

Cohnheim asserts that the coronary arteries are end-arteries. Ligature of one of the larger branches in the dog produced first irregularity and then stoppage of the heart in from thirty seconds to' a minute. Wickham Legg and West believe that there are free anastomoses between the branches of the arteries, while Steven asserts that there are communications, but only among the finest arterioles. The author is convinced, from observation, of Steven's injections, that the communications are of the very finest vessels, partly capillaries and partly minute arteries.

Thrombus in right auricle. It is drawn up so as to be displayed, but in its natural position it fell down like a ball over tricuspid orifice.

Fig. 205. - Thrombus in right auricle. It is drawn up so as to be displayed, but in its natural position it fell down like a ball over tricuspid orifice.

Causes Of Obstruction Of The Coronary Arteries

These arteries are peculiarly liable to Atheroma. Perhaps the fact that, coming oft' directly from the aorta, they are exposed to higher pressure and greater variations of pressure than other arteries of their size, may account for this. Atheroma, as explained further on, leads to narrowing of the oalibre of the artery, and it often induces Thrombosis which may increase the stenosis or even lead to occlusion. This is most common where calcareous infiltration follows atheroma. After a prolonged stenosis there may be a sudden complete occlusion. Again, atheroma sometimes leads to a small aneurysm of the artery. Atheroma in the aorta leads not infrequently to Obstruction of the orifices of the coronary arteries. The aorta is the most frequent seat of atheroma, and as this condition leads to thickening of the internal coat there will sometimes be a bulging of this coat over the orifices of the coronary arteries. Not infrequently the prominent intima around the orifice coalesces and completely covers the aperture. Syphilis sometimes causes narrowing of the calibre of the coronary arteries, the condition resembling what occurs, with much greater frequency, in the arteries of the brain.

Embolism is also liable to occur in the coronary arteries. It used to be stated that during the systole of the ventricle the coronary arteries were closed by the curtains of the aortic valve falling against them. It is stated by recent observers, however, that this is not the case, and that the orifices are exposed during the systole, and hence, in cases of acute endocarditis, small portions of thrombi are liable to pass into the coronary arteries. The arteries obstructed will nearly always be small, and the obstruction is often multiple. In ulcerative endocarditis and pyaemia there may be septic embolism and the formation of abscesses.

Effects Of Obstruction Of The Coronary Arteries

The results vary somewhat according to the suddenness of the obstruction, the size of the vessel, and otherwise.

Sudden obstruction of a considerable branch, usually brought about by thrombosis occurring in consequence of atheroma, leads to Infarction of the heart. The affected area is usually in the wall of the left ven-tricle, the artery most frequently obstructed being the descending branch of the left coronary artery. If death occurs immediately after the obstruction the part will be found .of normal consistence, but pale yellow in colour. Very soon it becomes soft and yellowish white or brown in colour, and the part is depressed below the surface. In some cases the part; becomes almost fluid. This condition of softening, which' has been called by Ziegler Myomalacia cordis, may be associated with haemorrhage. Under the microscope the muscular fibre is found more or less broken up, its transverse strise have disappeared, and the fibres have assumed a hyaline or waxy appearance (waxy degeneration or coagulation-necrosis). There is often, at least in the peripheral part, a great infiltration of round cells, from inflammatory reaction.

The softened portion of the wall may give way before the pressure of the blood, and the result may be an Acute aneurysm of the heart or even Rupture. The condition under review is probably the most frequent cause of rupture of the organ.

If the patch of softening be small, then through time the muscular tissue is absorbed and the connective tissue is increased in the way to be described further on.

A more Chronic obstruction of a considerable branch or a sudden obstruction of a smaller branch, frequently leads to a condition which has been designated Fibrous transformation, or (less happily) fibroid degeneration. This condition is really that present in most cases of so-called Interstitial myocarditis. The gradual or more sudden deprivation of blood causes atrophy and degeneration of the muscular fibres, and the connective tissue comes to form the chief or entire constituent of the heart-wall, generally reinforced by a certain new-formation due to chronic inflammation. The patches of fibrous transformation vary greatly in size according to the artery obstructed. They may be simply small tendinous areas in the midst of the muscle (see Fig. 206), or they may affect extensive tracts. The tendinous or cicatricial appearance is sometimes visible in the musculi papillares when the ventricles are laid open, but it may only be discovered by slicing the muscular tissue, which is best done by sections parallel to the surface of the heart. Where an extensive area has undergone this transformation the wall of the heart may be bulged outwards, thus forming a Chronic aneurysm of the heart. Under the microscope the fibrous patch consists chiefly of wavy connective tissue, with very little appearance of inflammation. There may be no muscular tissue in the midst of the patch, but sometimes atrophied fibres may be visible (see Fig. 207). Fatty degeneration is also a result of obstruction of the coronary arteries. This is most pronounced in cases of obliteration of the orifice of one or both arteries by atheroma of the aorta.

Section of left ventricle and a musculus papillaris showing fibrous transformation.

Fig. 206. - Section of left ventricle and a musculus papillaris showing fibrous transformation.

Fibrous transformation of heart. The muscular tissue is seen interrupted by connective tissue, x 70.

Fig. 207. - Fibrous transformation of heart. The muscular tissue is seen interrupted by connective tissue, x 70.

In a case observed by the author where one orifice was completely occluded and the other somewhat narrowed, there was generalized and typical fatty degeneration, such as one sees in pernicious aniemia. There was here a slowly advancing deprivation of blood, which only proved fatal when very extreme. Greenfield has recorded a case in which both arteries were occluded, and in which he suggested that the heart might be partially nourished by imbibition.

It is clear that during life there will often be, in consequence of obstruction of the coronary arteries, serious functional disturbance of the heart. There may be urgent dyspnoea, pain and irregularity of the heart, leading up, it may be, to death more or less suddenly. Angina pectoris is a frequent feature in the cases of considerable interference with the circulation.


Cohnheim, Virch. Arch., lxxxv., 503, 1881; Wickham Lego, On cardiac aneurysms, Bradshaw leet., 1884; West, Path, trans., xxxv., 110, 1884; Qvaxn, On fatty heart, 1851; Weioert, Virch. Arch., lxxix., 1880; Huber, do., lxxxix., 1882; Turner, Trans. Med. Congress, London 1881, i., 427; Robin, Gaz. Hebd., 1885, No. 51; Paul, do., No. 10; Ziegler, Lehrbuch, and Deutsch. Arch, f. klin. Med., xxv.; Hilton Fagge, Medicine, ii., 32; Steven (with full literature), Lancet, Dec, 1887, Jour, of Path., ii., 190, 1893, and Glasgow Hospital Reports, vol. i., 1898.