52 Group 3, 18%. Left coronary artery domi- nance. Apart from supplying the anterior and lateral aspects of the left ventricle and inter ventricular septum, it may also supply” the entire posterior aspect of the left ventricle, and part of the posterior right ventriele. Ectopic or Infarction at a Distance If the anterior descending branch of the left coronary artery becomes severely stenotic, or obstructed, the apical portion of the left ventricle may then derive its blood supply by anastomotic channels from the right coronary artery. If this tight coronary artery now becomes occluded, a fresh myocardial infarct may result in the apical region of the left ventricle (Saphir et al., 1935). The term “ec- topic infarction” has been applied by Bean in 1938, or “infarction at a distance” by Blumgart, (1939). SUBENDOCARDIAL INFARCTION This involves a thin rim of myocardium beneath the endocardium of the left ventricles occasionally it may involve the papillary muscle only. Severe stenosis—usually by atherosclerosis~of all three major coronary aiteries results in an increase in the subendocardial plexus of arte- ries. Should the patient go into a phase of hypotension as a result of shock, tachycardia, or transient imbalance of coronary flow, ot disturbance of blood supply by, for example, an occlusion of a smaller branch of the coro- nary arterial tree, the area furthest away from the major blood supply will suffer and a subendocardial infarct will result. The stenotic major vessels can barely supply their own territory and the anastomotic rearrangement can only achieve a more uniform distribution of blood. Regional infarction is therefore pre- vented This increase in vascularity in the subendo- cardial regions (and epicardial areas of the apex and atrio-ventticular groove) has been clearly demonstrated by Fulton (1956). Both arteries contribute to the plexus. In cases where the pattern of anastomosis between coronary arte- ries was normal, occlusion resulted in regional PATHOLOGY OF THE HEART infarction, whereas if the anastomotic pattern was increased and widely patent, focal or subendocardial damage resulted. MACROSCOPIC DATING OF MYOCARDIAL INFARCTION Inrespective of the distribution or type of myocardial infarction, the sequence of events of repair are similar. Lodge-Patch in 1951 listed these as follows, which in the writer's experi- ence is a reliable guide to dating infarction 15 hours: muscle pale and edematous. 36 hours: infarct center opaque oF yellowish, boréer hemorchagic. 34 days: rubbery border. 1 week: rubbery center, sight shrinkage of infart. 3 weeks: thinning of myocardium. 6-8 weeks: scarring; there may be a brownish tinge preceding this 3 months: white and firm sear, Eventually: tough, white scar center, distinct hemorrhagic Macroscopic dating of covonary arterial thrombus, if found, is often difficult. Fresh thrombi tend to be dark red-brown up to about fone week, or pale whitish yellowish in color after about two to three weeks. HISTOLOGIC GRADING OF MYOCARDIAL INFARCTION This is illustrated in Table 5.3 (after Lodge- Patch, 1951). [t can be seen that there is considerable overlap between the time sequence of organization of infarct, as shown in the table and accompanying diagram, Figure 5.4 shows a recent myocardial infarct. LOCALIZATION OF THROMBI IN CORONARY ARTERIES The most common site of coronary arterial occlusion is in the anterior descending branch of the left coronary artery. Harland and Holburn (1966) found them located in that site in 50% of patients, particularly in the first centimeter of the artery. In 20% the thrombus was located in the left circumflex artery and in 30% in the right coronary artery.Myocardial Infarction 53 TABLE 5.3. Histologic Grading of Myocardial Infarction ture Onset Maxieum Disappearance Comment Nuclear changes in S hours Karyalysis 23 days myocardial muscle Pyknosis fiber Necrosis and S hours 5-6 days 2weeks (edge) Necrotic muscle may phagocytosis (eosinophilic persist for X months of muscle eytoplasm) Edema 45 hours 36 hours 4Bhours Not reliable Neutrophil 6 hours 48 hours 1adays ——_Messad at periohery olymorpho: of infarct at 48 hours nuclears Degeneration starts a 48 hours Basaphilic extra 4th day 10th day 1ath day Not reliable cellular material onwards Macrophages ath day 6th week Xmanths May persist for month, Pigment laden: 9th day Small iyenphocytes 4th day 3rd week, X months Plasma cells Eosinophilic 7eh-Bth 68 Not reliable leukocytes day Fibroblasts 4th day 10 days 6th week 3rd week Collagen fibers ath day Increase Arranged parallel 10 adjacent muscle and visceral pericardium ath week Proliferation of Sr-ath 310-61h X months blood vessels day week © MOURS. 24 HOURS. 49 HOURS 3-S DAYS. 7-10 DmYS, (4-21 ORS. G WEEKS YEARS, NUCLEAR cKanges IN MUSCLE FIBRES, NECROSIS ANO puacoertons or muscle EE _—E—E ceDEMa NevTROFEIL POLYMORPHONUCLEADS aaxsopaic EXTRACELLULAR MATERIAL SMALL LeMpnocYTES, cosNOmL —= a SEE EEE MacnoPnaces a ———— a FIBBOBLAS, ‘BLOOD vesses a COLAGEN rae a emer Diagram: Dating of histologic events in myocardial infarction. (Lodge-Patch, 1951. By kind permission of the author and publishers of the British Heart Journal.)FIG. 6.4. Photomicrograph of recent myocardial infarction of 15 hours duration, Mainly neutrophils ccan be seen, between myocardial fibers which show early degenerative changes, Hematoxylin and eosin x 400, Localization of occlusion may be aided by coronary arterial injection by radio-opaque material. (See Chapter 1.) On macroscopic examination, identification of thrombi may be difficult, and reports of the frequency of identification have vatied widely (from 20 to almost 100%). It is often necessary to resort to histologic examination as the occlusion may be tiny and consist of fibrin and platelets only. However, careful examination of the coronary arterial tree will. usually be rewarded in locating the occlusion. Often the reason for low percentage yield on finding the occlusion is poor or inadequate technique, but one must not forget that infarction without thrombosis or occlusion does accu (see below). An interesting contribution came from Spain and Bradess in 1960, who correlated the inci- Gence of thrombosis to the length of survival after cardiac infarction: Death within 1 hour, 16%; death within 24 hours, 37%; death over 24 hours, 54%, This suggests that coronary artery thrombosis is @ secondary phenomenon upon such precipitating factors as lowered pressure and rate of blood flow. Another mechanism may be at operation, namely that increased fibrinolysis occurs after myocardial infarction and this may dissolve the thrombus if, small, only to reform at a later date: The sequence of events of organization of thrombi has been described by Imniger (1962-1963), from whose work the six phases recognized are freely translated, by the writer (with kind permission of the publishers and author). Phase 1: 2nd day (ist to 3rd day). No reaction between endothelium and thrombus, White blood cells, platelets and white blood corpuscles unchanged, Phase 2: Sth day (3rd to 8th day). Endothe- lial sprouts, beginning of central hyalinization. White blood cells pyknotic. Mononuclear cells enlarged and pale. Peripheral splits, “sinuses,” appear (due to thrombus contraction), Free