HEART ATTACK (Latin infarctus from infarcire to fill, fill, squeeze; synonym distsirkulyatorny necrosis) — the focal necrosis of body which is a consequence of sudden disturbance of local blood circulation.
The term «heart attack» was offered by R. Virkhov for designation of the devitalized site of fabric, infiltrirovanny («infartsirovanny») erythrocytes.
Proximate cause of development And. the obstacle to a blood-groove which is suddenly arising in the corresponding piece of an artery is. Assumed, as. develops only in bodies with the so-called trailer arteries which do not have an anastomosis. However further it was established that an anastomosis between final branchings of arteries is available in all bodies though degree of their expressiveness is not identical. The small caliber of vessels, individual options of branching and anomaly of their development, the insufficient quantity of a vascular anastomosis inherent to this body are premises for emergence And. in the conditions of the general circulatory disturbances. Only obstruction of large main arteries can lead to necrosis of fabric of body without the previous general hemodynamic frustration.
At incomplete closing of a gleam of a vessel with the reason of development And. discrepancy of need for food of functionally burdened body and insufficient blood supply of this site is. Such discrepancy can be observed, e.g., at a hypertension, heart diseases and is caused not so much by vasoconstriction, how many loss of elasticity by them and their inability to adaptation expansion. Ischemia (see) certain the site of body with the minimum blood-groove can arise also at sharp falling of the ABP. Development And. in this case is an indicator of insufficiency of general circulation (And. brain, myocardium). For development And. a cardiac muscle duration of ischemia, according to experimental data, makes 20 min., for education And. brain fabric — is there been enough by 5 — 6 min. Macroscopically and microscopically a necrosis of fabric in a zone I. a myocardium accurately comes to light on 2 days. At earlier stage (the so-called donekrotichesky period) it is possible to reveal disturbances of microcirculation, the centers of kontrakturny reduction of vascular myocytes or their lysis. Great value in the mechanism of development of fabric changes at And. belongs hypoxias (see). Disturbance of oxidation-reduction processes in fabrics in connection with a circulatory disturbance leads walls of vessels to accumulation of nedookislenny products of exchange which exert impact on colloids of fabrics, and bring to them to a necrosis (see).
Great value in development And. has sudden narrowing or closing of a vascular gleam therefore the most frequent reason And. is thrombosis (see) and embolism (see), more rare spasm (see). In these conditions of a collateral are insufficient, easily there are dystonic phenomena and obstruction of a vessel leads to
I. I. more often meet in heart (see), kidneys (see), to a spleen (see), lungs (see), brain (see), to a retina (see), intestines (see). And. in kidneys, a spleen, lungs has the wedge-shaped form that is connected with their angioarchitecture (the main type of the vessels going from gate to the periphery), takes the central part of the ischemic area; at this edge of a wedge it is sent towards an obstacle to a blood-groove (the place of obstruction or sharp narrowing of a vessel), and a wide part (basis) is turned on the periphery of body. In a muscle of heart And. has irregular shape, taking layer-by-layer various zones of a myocardium, beginning from subendocardial layers that is caused by loose type of branching of vessels; in intestines And. it is sharply delimited, its extent depends on caliber of the corked artery.
Against the background of the general and local circulatory disturbances in different bodies there can be small, sometimes the microscopic sizes, centers of a necrosis — the microheart attacks characteristic of a myocardium and a brain. In emergence pressure differences in small vessels, and also discrepancy between the increased need for food of fabric and an insufficient blood-groove in the conditions of emotional or physical can play their part. loadings, and also the metabolic disturbances caused by a hypoxia or ischemia.
Distinguish three look And.: white (ischemic, anemic), red (hemorrhagic), white with a hemorrhagic belt.
White (ischemic) And. are observed in kidneys, a spleen, a brain, a myocardium (tsvetn. fig. 1 and 3). They triangular shape, yellow-white color (from here the name «white»), are quite sharply delimited from surrounding fabric, a dense consistence. Arise in connection with complete cessation of a blood flow in this vessel and its branchings. The necrosis in such cases always has in the beginning character of dry coagulative.
Red (hemorrhagic) And. are observed in lungs (tsvetn. fig. 2), in intestines, sometimes in a spleen and a brain; arise, as a rule, in the conditions of a decompensation of blood circulation and venous stagnation: in lungs — at heart failure of various origin, in a spleen — at fibrinferment of her vein, in a brain — at fibrinferment of jugular veins or sine of a firm meninx. At the same time the reversed current of a venous blood in a zone I takes place., paralytic vasodilatation, increase in their permeability and treatment of a zone I. blood. Hemorrhagic And. triangular shape, on a section of dark red color that defines its name, it is quite sharply delimited from surrounding fabric. Over time And. turns pale owing to hemolysis of erythrocytes.
White And. with a hemorrhagic belt — white or light gray color with a dark red rim — it is observed in heart and a spleen, sometimes in kidneys. The zone of hemorrhage arises because a reflex spasm on the periphery And. quickly is replaced by paralytic expansion and overflow blood of capillaries with development of the phenomena of a prestaz, staza (see) and diapedetic hemorrhage (see. Emigration ).
In separate group it is necessary to allocate close to hemorrhagic so-called. congestive, or venous, And., caused by closing of a gleam and the termination of outflow of blood on rather large venous trunks or thrombosis of a large number of small veins. Stagnation of blood, hypostasis and massive hemorrhages create the conditions not compatible to life activity of fabrics — there is a heart attack. Such venous congestive And. are observed in intestines at fibrinferment of mesenteric veins, in kidneys at the accruing thrombosis of renal veins, in a spleen at obstruction of a gleam of a splenic vein.
At the same time or consistently in various bodies can arise multiple And. different localization, form and sizes. It is also possible to observe formation of the fresh centers of a necrosis on the periphery older, organized And., and also emergence of fresh necroses in the remained sites of a parenchyma in the thickness And. It can be caused by progressing of disturbance of blood circulation with capture of new vascular branches, napr, at distribution to their gleam of blood clot, deterioration in blood circulation in connection with falling of blood pressure or as it happens at myocardial infarction (see), with sudden inadequate physical. or emotional loading. It is preceded by changes at the level of intracellular organellas and macromolecules — swelling and destruction of cristas of mitochondrions, changes of ultrastructure of a sarcoplasmic reticulum, accumulation of lipoproteidny complexes.
Histochemical in a zone I. decrease and disappearance of a glycogen (in a myocardium, a liver, kidneys), decrease of the activity of oxidation-reduction enzymes, reduction of content of DNA and RNA, accumulation of neutral mucopolysaccharides of type sialine to - t, disturbance of ionic balance is defined. After short-term reflex narrowing vessels in a zone I. paralytic extend; in essence, in this area (in heart, lungs) there is not an anemia, but venous stagnation with a picture of a staz and small hemorrhages. The necrosis has coagulative character (kidneys, a spleen, a myocardium) or from the very beginning accepts character wet, kollikvatsionny (in a brain). At microscopic examination And. the structure of body is broken, kernels are not painted and all structural elements merge in homogeneous homogeneous mass (see. Necrosis ). On the periphery And. always there is a zone of a necrobiosis, dystrophic changes and a reactive inflammation. On cellular structure of inflammatory infiltration and proliferative reactions of a stroma on border And. it is possible to judge prescription of process. Small And. (microheart attacks) within 3 — 4 days are replaced with young connecting fabric. In extensive And. necrotic masses in the center of the center can remain within weeks and even months.
Outcome And. depends on conditions of its education, localization and the sizes. Under favorable conditions And. it is replaced with granulyatsionny, and then cicatricial fabric. In a brain on site of a wet necrosis the cyst develops. In necrotic masses adjournment of lime — petrification is possible And. In the presence of microbes And. can undergo purulent fusion. In hems on site hemorrhagic And. the pigment hemosiderin is found.
Value I. for an organism finally depends on its localization, the sizes, the functional importance of affected areas, regenerator and adaptation opportunities of body and fabrics. And. of a myocardium and substance of a brain can be a cause of death or cause heavy disturbances of functions of the struck body. Extensive And. cause intoxication of an organism products of fabric disintegration: temperature increase, a feverish state, dystrophic changes of internals are noted. Absorption of the denatured proteins from the center of defeat causes autoimmune reaction with formation of organospetsifichesky antibodies and plasmatization of lymphoid educations.
The term «heart attack» designate also the necroses developing in kidneys at treatment by their urate salts (see. Urate heart attack ) or bilious to-tami and gemoglobinogenny pigments (see. Bilirubinovy heart attack ).
Bibliography: Anbrokh Ya. M. To a question of a heart attack of a liver, Surgery, No. 1, page 114, 1965; Questions of morphology and a pathogeny of a heart attack (A myocardium, lungs, kidneys, a spleen), under the editorship of A. I. Struko-va, M., 1959, bibliogr.; Davydovsky I. V. General pathology of the person, M., 1969; The Multivolume guide to pathological anatomy, under the editorship of. A. I. Strukova, t. 1 — 9, M., 1956 — 1964; Delarue J. et Laumonier R. Anatomie pathologique, t. 1—3, P., 1969; General pathology, ed. by H. W. Florey, L., 1970, bibliogr.; Handbuch der allgemeinen Pathologie, hrsg. v. H. W. Altmann u. a., Bd 1-3, B. u. a., 1955-1972; K e t t-1 e r L. - H. Lehrbuch der speziellen Pathologie, Stuttgart, 1976, Bibliogr.; L e p a d a t P. Infarctul intestinal, Bu-cure§ti, 1973, bibliogr.; O g i 1 v i e R.F. Histopathology, Baltimore, 1962; Systemic pathology, ed. by G. P. Wright a. W. Sym-mers, L., 1966; Zollinger H.U. Pa-thologische Anatomie, Bd 1 — 2, Stuttgart, 1969.
S. A. Vinogradov.