BLOOD SUPPLY TO THE HEART 



'523 



cardiac veins (64). Of greater concern, however, is the 

 existence of communications between the ventricular 

 cavities and the trabecular sinusoids via the The- 

 besian, arterioluminal, and arteriosinusoidal vessels 

 (153). Although dyes and particulate matter have 

 been recovered from ventricular myocardium follow- 

 ing intracavity injections (153), this has only occurred 

 experimentally with a) high ventricular end-diastolic 

 perfusion pressures, b) congenital aortic and pulmonic 

 valvular atresia with intact septa, and c) in the ar- 

 rested heart or one in which the heart stopped before 

 its removal. As a result of simple pressure differentials, 

 the dye or particle moves into the myocardium, while 

 for the same dynamic reasons only the reverse could, 

 and indeed does, occur in the actively beating heart 

 (i53. 404)- 



Congenital Anomalies 



Variations in the course and number of nutrient 

 vessels to the myocardium are not uncommon and, 

 as with other organ systems, are usually of no physio- 

 logic concern. However, the acceptance of the clinical 

 syndrome of the aberrant left coronary artery as part 

 of a group of congenital coronary arteriovenous 

 fistulae, and its recent physiologic documentation, has 

 prompted this brief digression into those embryologic 

 and phylogenetic ramifications relating to the coro- 

 nary arteries. 



The lowest orders of vertebrate hearts have no well- 

 defined myocardial blood supply. Thus, the single- 

 chambered ventricle of the lamprey nourishes its 

 myocardium via extensive intramyocardial sinusoids 

 in direct communication with the ventricular cavity 

 (142). The arterial supply to vertebrate orders below 

 reptiles arises from cranial and caudal vessels coursing 

 through the cardiac ligaments. Reptilia maintain a 

 single cranial supply of vessels which are related to the 

 fishes' epibranchial and hypobranchial vessels, the 

 latter disappearing and moving caudally with the loss 

 of the gills (8). 



Mammalian coronary arteries arise from primordial 

 buds in the truncus arteriosus during the 5th week of 

 gestation. At this time, the endocardial cushions and 

 longitudinal ridges are also forming, respectively 

 dividing the heart and truncus into two channels. The 

 heart has been actively beating and forcing blood 

 through the systemic circulation since the 3d week, 

 and the heart itself is nourished by the sinusoido- 

 luminal channels (8, 101, 140). In the fetal rabbit, 

 endothelial-lined trabecular spaces spiral toward the 

 surface forming capillaries and epicardial vessels. The 



latter join with venous cords growing caudally in the 

 epicardium from the sinus venosus to form the first of 

 the myocardial vessels. Arterial buds form a few days 

 later and spread as a solid column of cells to the 

 bulbus cordis, with subsequent extensions and branches 

 to the lateral areas. As these epicardial arteries 

 enlarge, the sinusoids decrease in size by a condensa- 

 tion and compression of the myocardial cortex, finally 

 becoming capillaries (140). In lampreys and lower 

 fishes, and in certain human congenital anomalies, 

 this condensation does not occur, the spongy trabecu- 

 lar network remaining undisturbed (141, 382). In 

 higher fishes and mammalia there is an outer, con- 

 densed, capillary-containing layer supplied by epi- 

 cardial vessels, and an inner trabecular layer with 

 retained cavitary communications. Thus, the varia- 

 tions in the number and site of the coronary ostial 

 anlagen will determine the final origin of the coronary 

 arteries, while variations in the epicardial course and 

 degree of myocardial condensation may determine the 

 eventual communications. These anomalies have 

 recently been presented as follows (101). 



a) Coronary arteries arising from the aorta and 

 supplying the heart in normal, albeit variable, fashion 

 without abnormal communications. This includes 

 those with single ostia and single coronary arteries, 

 common sinus, accessory ostia, and ostia elsewhere in 

 the aorta. In a recent large series, such anomalies oc- 

 curred in 52 cases of 18,950 autopsies for an incidence 

 of 2.75 per 1,000 (4). Reviews of single coronary 

 arteries in man have stressed the absence of clinical 

 symptoms except those related to associated cardio- 

 vascular anomalies (4, 308, 350). However, the 

 anomalous distribution seems to predispose to early 

 sclerotic changes and myocardial infarction, the 

 average age of death in adults being 45 years. In one 

 series (308), all cases of myocardial infarction, fibrosis, 

 or ischemia were related to the absence of a left 

 coronary artery, i.e., the presence of a single right 

 coronary artery. 



b) Coronary arteries supplying blood to grossly 

 abnormal hearts in which congenital pulmonary or 

 aortic atresia exists in conjunction with intact ven- 

 tricular septa and intact A-V valves. Ventricular 

 blood is forced from the cavities via myocardial 

 sinusoids which anastomose in the epicardium with 

 the coronary arteries. This type, fortunately, is rare. 



c) Coronary arteries distributing blood abnormally. 

 These may be via left-to-right arteriovenous shunts 

 into the right heart chambers, cardiac veins, or pul- 

 monary artery, or via arterioluminal shunts into the 

 left heart chambers (fig. 3). 



