From Big Medical Encyclopedia

CORONARY INSUFFICIENCY (Latin coronarius coronal) — the discrepancy of blood supply of a myocardium to his metabolic requirements which is shown ischemia of a myocardium. A basis To. the N can be: 1) reduction of a coronary blood-groove (it is frequent in combination with disturbance of transport function of blood) at not changed metabolic requests of a myocardium; 2) strengthening of cardiac performance with increase of metabolic requirements of a myocardium at inability of coronal vessels to increase in a blood-groove; 3) combination of metabolic and vascular factors.

Concept K. N wider, than concept coronary heart disease (see) since atherosclerosis of coronal arteries is one of the possible reasons To. N.

To. N, caused by decrease in a coronary blood-groove (most often at stenosing defeat of coronal vessels of heart), usually call primary, and connected with sharp increase in metabolism in a myocardium (i.e. a nekoronarogenny origin) — secondary. On a wedge. allocate to a current acute and hron. To. N.

Acute K.n., or «coronary crisis» (on A. V. Smolyannikov and T. A. Naddachina's terminology, 1963), sometimes comes at not changed coronal vessels of heart. It is characterized by serious discrepancy of a coronary blood-groove to metabolic requests of a myocardium that is shown by an attack of stenocardia, quite often heavy frustration of a cordial rhythm and conductivity, changes of an ECG. Acute To. the N can lead to development myocardial infarction (see) and sudden death. Hron. To. the N is characterized by constant discrepancy of blood supply to metabolic requirements of a myocardium. Premises for its development are structural changes of coronal vessels (narrowing of a coronary bed).

Etiology and pathogeny

Acute and hron. To. N can cause the most various patol, processes. Most often it is atherosclerosis of coronal arteries of heart. Less often narrowing of coronal arteries is caused by vasculites of various etiology (see. Coronaritisis ), infiltration of vessels tumor cells, injury of a coronal artery. Various forms K. N are observed also at the acquired and inborn heart diseases and the main vessels (a stenosis of a pulmonary trunk, a hypoplasia and other anomalies of coronal vessels of heart), a bacterial endocarditis, a subaortic stenosis, trikhinozny myocarditis, gout, a syphilitic aortitis and the stratifying aortic aneurysm, an acute anaphylaxis and a serum disease, acute cholecystitis and pancreatitis, a polycythemia and anemias, acute disorders of cerebral circulation, severe injuries of a head and spinal cord, wet brain and at some other diseases.

Development acute To. by N it is connected most often with sudden disturbance of passability of a coronal artery owing to its spasm, thrombosis or an embolism. Metabolic requests of not ischemic sites of a myocardium at the same time increase that is followed by increase in a blood-groove in not changed adjacent coronal vessels. At the same time ischemia of a myocardium will mobilize mechanisms of coronary self-control: under the influence of metabolic mediators (ATP decomposition products, intermediat of a tricarbonic acid cycle, perhaps prostaglandins) first of all subendocardial vessels as much as possible extend. At functionally or integrally defective collaterals dilatation of not changed arteries can lead to redistribution of a blood-groove in favor of not ischemic sites and to strengthening of ischemia in a zone of the affected artery (a phenomenon of «burglarizing»).

A role of a vasomotor spasm in an origin acute To. to N it is proved, in particular, for special its wedge, versions — Printsmetal's stenocardias (see. Stenocardia ), edges is caused by periodically occurring spastic reduction of one of large coronal arteries without increase in metabolic requests of a myocardium before an attack. According to angiocardiography, the spasm is sometimes observed in not changed coronal arteries.

In an origin nekoronarogenny acute To. N can play a role patol, the processes which are followed by falling of minute volume of heart and decrease in perfused pressure in system of coronal arteries (the expressed arterial hypotension, considerable bradycardia, a hypovolemia) and also anemia, an arterial anoxemia and disturbance of dissociation of oxyhemoglobin at respiratory insufficiency, poisonings with carbon monoxide, nitro compounds of benzene etc. Even the maximum vazodilatation of absolutely normal coronal vessels cannot satisfy metabolic requirements of a myocardium in these conditions.

One of major factors of a pathogeny acute To. the N, connected with increase in metabolic requirements of a myocardium, is the increased allocation of catecholamines at excitement of a sympathetic part of century of N of page or their excess products adrenal glands. Under the influence of catecholamines oxygen consumption by a myocardium increases [W. Raab, 1963], intra myocardial pressure due to insufficient relaxation of heart in a diastole increases that leads to restriction of a coronary blood-groove, and, at last, perhaps spastic reduction of coronal arteries due to excitement of alpha adrenoceptors. The attacks of stenocardia of Printsmetal caused by a spasm of a large coronal artery were noted at stimulation of alpha adrenoceptors against the background of preliminary blockade of beta adrenoceptors. Also tachycardia, especially in combination with arrhythmias of heart has pathogenetic value. In such cases To. in N it is caused by a combination of the decrease in coronary perfusion (connected with shortening of a diastole and reduction of minute volume of heart) and increases in metabolic requirements of a myocardium. These mechanisms participate in emergence To. N at a Bouveret's disease, trembling and atrial fibrillation, at tachycardia against the background of inf. intoxications (even at children of early age), at a thyrotoxicosis, an emotional stress, and also at physical. to loading.

Normal at physical. loading or emotional pressure coronal arteries extend that provides constancy of a ratio between metabolism of a myocardium and a coronary blood-groove. Acute To. the N arises at sharp disturbance of this ratio. At excessive physical. tension at insufficiently persons prepared for it metabolism of a myocardium sharply amplifies. Cases of sudden death of the young low-trained athletes during the competitions are explained most likely by a hypoxia of a myocardium due to impossibility to provide sharply increased need of a myocardium for oxygen even at the maximum expansion of coronal arteries. According to Folkou (V. Folkow) and soavt. (1968), the sudden emotional pressure can triple an operational load on heart. Increase in cardiac performance plays a role in development acute To. N also at hypothalamic crises, considerable raising of the ABP (especially paroxysmal) at patients with an idiopathic hypertensia and at symptomatic forms of arterial hypertension. Raising of the ABP promotes strengthening of a coronary blood-groove, a cut not always compensates an excess metabolic cost of a myocardium, and premises for development acute are created To. N. At adrenal crises at patients with a pheochromocytoma acute ischemia of a myocardium can arise at at all not affected coronal arteries. Excess allocation of catecholamines in blood during such crisis causes acute increase in need of a myocardium for oxygen by means of the combined influence of several factors: a direct impact on metabolism of a myocardium, paroxysmal raising of the ABP, increase of cordial reductions. At the same time tachycardia reduces a pressure gradient in a coronary bed, and the irritation of a-adrenoceptors of coronal arteries interferes with the maximum expansion of the last and can even lead to their spasm. Preferential value of any pathogenetic factor in emergence acute To. the N manages to be established pe at all patients. So, acute To. the N at an embolism of branches of a pulmonary trunk can speak both an arterial anoxemia, and decrease in perfused pressure in a coronary bed owing to system arterial hypotension, and heavy frustration of a cordial rhythm and conductivity, and also the accompanying thrombosis of coronal arteries against the background of the hypercoagulation connected with the basic patol, process.

Hron. To. the N develops at damage of coronal arteries, their narrowing or reduction of expansivity. In absolute majority of cases hron. To. in N it is caused by atherosclerosis of coronal arteries, but it can be connected with an inflammatory sclerosis of their walls, cicatricial deformation, etc.

It is described typical a wedge, a picture of stenocardia of Printsmetal at periodic obturation of a gleam of the main coronal arteries by mobile polypostural educations on a leg or the limy masses which is hanging down from a semilunar valve of the aortal valve. Development acute and hron is known. To. N after not getting injury of bodies of a chest cavity (at blow, a prelum, action of a blast wave, falling from height). At an injury of pulmonary veins ischemia of a myocardium can be a consequence of an embolism of coronary vessels fresh unorganized blood clots, and at a contusion of heart — result of traumatic aneurism of heart, ruptures of a vascular wall with formation of aneurisms of coronal arteries or extensive hemorrhages. Sometimes To. the N is a consequence of existence of shunts between coronary arteries and branches of a pulmonary trunk.

Direct and strict dependence between extent of narrowing of coronary vessels and hron, manifestations To. the N does not exist. The progressing narrowing of a large coronal artery quite often leads to development in a myocardium of network of collaterals. In conditions functionally and integrally full-fledged collateral circulation a wedge, signs To. N can be absent even at total occlusion of a large coronal artery. At the same time and collaterals can be patholologically changed or individually underdeveloped.

The increased metabolic requirements of a myocardium are provided in essence only with increase in a coronary blood-groove as extraction of oxygen a myocardium is very big. Normal at power failure of oxygen the coronary blood stream can increase in a myocardium twice or even three times at the expense of a vazodilatation. However coronal vessels, rigid owing to atherosclerotic or inflammatory process, are not capable to so considerable expansion. Therefore against the background of hron. To. the N acute ischemia of a myocardium arises considerably more often than at not changed coronal arteries, it is frequent under the influence of small changes of cardiac performance, metabolic requirements, a gleam of coronal arteries.

Degree hron. To. the N increases in the presence of heart failure, anemia, an anoxemia, a thyrotoxicosis, arterial hypertension, at the heart diseases breaking an endocardiac hemodynamics. Hron. To. the N, observed at a coronaritisis, quite often is aggravated with hypostasis of a stroma of heart and the expressed hypertrophy of a myocardium in this connection diffusion of oxygen from blood in a myocardium is broken. Attacks of stenocardia upon transition to horizontal position at persons with heart failure are caused quite often by loading of heart volume due to increase in venous return. The mechanism acute is similar To. N, arising at an excess transfusion of blood substitutes.

Uneconomical cardiac performance as one of the major reasons hron. To. the N takes place at inborn or, a thicket, the acquired defects of mitral and aortal valves, a hypertrophy of a myocardium and dilatation of heart (first of all at hypertensia in a big or small circle of blood circulation), disturbance of synchronism in reduction of a left ventricle or change of a configuration of his cavity (generally at hron, aneurism of heart), a hyperthyroidism and hron, anemias. So, the expressed anginous attacks at patients hron, anemia are possible even at an insignificant stenosis of the main coronal artery. At the same time reduction of a coronary blood-groove at a stenosis of the mitral valve can be connected to some extent with a prelum an expanded left auricle of the place of an otkhozhdeniye of the left coronal artery, and at a stenosis of the aortal valve — with strengthening of a systolic ekstravazalny compression of intramiokardialny vessels, reduction of perfused pressure and volume of coronary haemo circulation.

A clinical picture

Clinically To. the N is shown by stenocardia (see) or its equivalents (e.g., a pristupoobrazny asthma), a myocardial infarction (see), heart failure at development of an ischemic myocardial dystrophy and a cardiosclerosis. Perhaps atypical and clinically asymptomatic current To. N before emergence of symptoms of heart failure or approach of sudden death. In the presence of stenocardia or its equivalents it is possible to estimate clinically approximately severity hron. To. N on character of attacks and their communication with physical. loading. The least heavy first degree hron. To. the N is characterized by rare attacks of stenocardia (or its equivalents), the arising hl. obr. at extraordinary physical or emotional pressure. At To. the N of the second degree is observed accurate clinic of an angina of exertion and decrease in tolerance to physical. to loading. The third degree To. and. it is characterized by frequent and heavy attacks of an angina of exertion with considerable decrease in tolerance to loading and accession of stenocardia of rest.

The diagnosis

the Diagnosis is based on a wedge, signs and on data of inspection by special methods, a prelude of all on indications electrocardiography (see). At the same time attempts of objective quality and quantitative standard of inadequacy of coronary haemo circulation to metabolic requirements of a myocardium become. For this purpose widely use test with dosed physical. loading on the stationary bicycle or the tredmil (tredbena). Other methods, including a method of bystry electric stimulation of auricles, were not widely adopted so far. Reliable electrocardiographic criterion To. the N at test with loading serves the depression of a segment of ST arising during maximum (submaximum) physical. loadings or nek-swarm a time later (2 — 5 min.). The disturbances of a cordial rhythm and conductivity arising in the course of performance of load tests also consider as the indirect evidence To. N.

Depth of a depression of a segment of ST is in direct correlation with oxygen consumption by a myocardium and increase in level of a lactate in a coronal venous sine. Along with it at a spontaneous attack of the stenocardia, and also during the performance dosed physical. loading or electric stimulation of auricles at patients To. N develop unambiguous hemodynamic shifts: rise in pressure in a pulmonary trunk, increase in end diastolic pressure in cavities of a left ventricle and increase in its final diastolic volume. The specified changes register both at coronary heart disease, and at To. and., connected with a rheumatic carditis, overdose of cardiac glycosides, a hyperthyroidism, etc. Test with dosed physical. loading reflects first of all funkts, frustration of coronary circulation or elektrolitnometabolichesky shifts in a myocardium.

Apply to direct assessment of a condition of arterial system of a myocardium and identification of localization, extent and expressiveness of occlusal defeat of coronal vessels, and also compensatory opportunities of collateral circulation coronary angiography (see), a stsintigrafiya with radiotracers (see. Blood vessels ). By comparison of data of coronary angiography to stsintigramma of a myocardium note at rest diffusion hypodispersion of drug in a myocardium, and against the background of a positive loading test — local decrease in accumulation of isotope in the zones corresponding to pools of okklyuzirovanny coronal arteries. Between changes of an ECG at dosed physical. to loading and results of coronary angiography or a stsintigrafiya of full compliance is not present. At funkts, the nature of acute ischemia of a myocardium patol, changes on koronarogramma quite often are absent or are expressed very slightly.

Positive loading tests indicate existence To. N and severity its wedge, manifestations, but do not characterize morfol, damages of coronal arteries. Negative takes of these tests do not exclude existence at all To. N. Leveling of an ischemic depression of a segment of ST is possible at the inadequate choice physical. loadings or a technique of registration of an ECG, at functionally full-fledged collateral circulation, despite a stenosis of the main coronal artery, and even in the presence of a zone of dyskinesia or an akineziya of a left ventricle.


Krom of purposeful treatment of a basic disease, therapy To. the N includes also stopping and prevention of anginous attacks. Lech. actions are directed at the same time to increase in volume of coronary perfusion (by means of special medicines or cardiac intervention) and restriction of metabolic requests of a myocardium with definition of specific therapeutic tactics according to a nosology of a basic disease.

Forecast it is always serious, especially if To. the N is shown by a myocardial infarction.

Prevention depends on an etiology of the disease which is the cornerstone To. N

See also Arterialization of a myocardium , Myocardial infarction , Coronaritisis , Coronary circulation , Stenocardia .

Bibliography: Gasilin V. S. Chronic forms of coronary heart disease, M., 1976, bibliogr.; Coronary insufficiency, under the editorship of E. I. Chazov, M., 1977; Smolyannikov A. V. and Naddachi of N and T. A. Questions of pathological anatomy and pathogeny of coronary insufficiency, M., 1963, bibliogr.; Shkhvatsaby I. K. Coronary heart disease, M., 1975, bibliogr.; Gannon P. J. Radioisotopic studies of the regional myocardial circulation, Circulation, v. 51, p. 955, 1975, bibliogr.; D an u b e r t J. Page of e. a. L'insuffisance coronarienne des pheo-chromocytomes, Arch. Mal. Coeur, t. 69, p. 49, 1976; Exercise testing and exercise training in coronary heart disease, ed. by J. Naughton a. H. K. Hellerstein, N. Y., 1973; F o 1 k o w B. o. Changes in cardiac output upon stimulation of the hypothalamic defense area and the medullary depressor area in the cat, Acta physiol, scand., y. 72, p. 220, 1968; Nogrette P. Physiopathologie de l’angine de poitrine, Coeur M6d. inter., t. 15, p. 83, 1976; R a-a b W. The nonvascular metabolic myocardial vulnerability factor in coronary heart disease, Amer. Heart J., v. 66, p. 685, 1963, bibliogr.; Y a s u e H. o. Prinzmetal's variant form of angina as a manifestation of alpha-adrenergic receptor-mediated coronary artery spasm, ibid., v. 91, p. 148, 1976.

A.S. Smetnev, V. D. Topolyansky.