Cardiosclerosis

CARDIOSCLEROSIS (from Greek cardia-heart and scleros-hard), "hardening" of the heart or more precisely of the heart muscle (myocardiosclerosis), is the result of proliferation of connective tissue in it and the transformation of the latter into scar tissue. Such enhanced development of connective, resp. scar tissue mostly occurs parallel to the death of muscular tissue. This process can be the result of 1) impaired blood supply to the heart muscle as a result of narrowing (resp. impaired patency) of the coronary arteries, or 2) an inflammatory process of the heart muscle, i.e., myocarditis, or 3) prolonged overstretching of the hypertrophied heart muscle and blood stasis in it when cardiac function is impaired. The most frequent type of C. is C. resulting from sclerosis of the coronary arteries. Since arteriosclerosis is the most frequent pathological change in the human organism in general, and sclerosis of the coronary arteries is one of the most frequent localizations of this process, it has a very unfavorable effect on such an important organ as the heart muscle, disrupting its nutrition, therefore C. as a result of arteriosclerosis belongs to the most important human diseases. Statistical data on morbidity and mortality from C. on the basis of arteriosclerosis are almost nonexistent. According to combined data from Moscow morgues for 1923-27, C. as the most important complication of arteriosclerosis (and as a cause of death) occurred in 30.4% of all cases of arteriosclerosis. The term C. in clinical practice at present is often used to denote precisely C. as a result of coronary arteriosclerosis and even to denote arteriosclerosis of the heart in general. Since the term C. is used to denote arteriosclerosis of the heart instead of the term "myocarditis", such designation can be considered more correct; the designation of arteriosclerotic changes of the heart as "myocarditis" widely used until recently is unacceptable because the primary and dominant process in this case is arteriosclerosis, while the inflammatory change is a secondary and relatively weakly expressed phenomenon. But from the point of view of the need for precise nomenclature, which is especially needed in the section on diseases of the heart muscle, it is more correct to denote cases where C. developed as a result of arteriosclerosis of the coronary arteries as arteriosclerotic (arterial) C., in contrast to myocarditic C., similarly to how one distinguishes between arteriosclerotic or arteriolosclerotic nephrosclerosis and glomerulonephritic nephrosclerosis. Cases of arteriosclerosis of the coronary arteries where there is no indication of sclerosis of the heart muscle itself should more correctly be denoted not as C., but as arteriosclerosis of the heart. Thus arteriosclerosis of the heart is a broader concept, while arteriosclerotic C. is only one of the consequences of arteriosclerosis of the heart. Both of these concepts are morphological concepts, while clinical concepts are of interest primarily insofar as they are associated with a certain impairment of the function of the given organ. Undoubtedly, arteriosclerosis of the coronary vessels reduces the working capacity of the heart even when it is not yet possible to establish the morphological manifestations of the impairment of blood supply to the heart muscle, in particular in the form of C. The latter is only the morphological expression of stronger degrees and more prolonged impairment of blood supply to the myocardium. Therefore, for clinical purposes and from a functional point of view, there is no actual boundary between arteriosclerosis of the heart and arteriosclerotic C. This to a certain extent justifies the fact that clinical practice does not strictly distinguish between these two concepts. Sclerosis of the coronary arteries by type belongs to atherosclerosis and affects the coronary arteries and their branches along their course from the mouth to the point where the branches penetrate into the heart muscle (see Arteriosclerosis), i.e., atherosclerosis affects only those parts of the coronary arteries that are located under the epicardium and usually only the larger of these branches. The small intramuscular branches of the coronary arteries are almost never affected by atherosclerosis, and in particular arteriolosclerosis of the heart is completely unknown.-Atherosclerosis of the coronary arteries of the heart, as is characteristic of this type of arteriosclerosis in general, differs in that it develops extremely unevenly, very often only in the form of separate foci-plaques. As a result of this, the impairment of blood supply to the heart muscle in coronary sclerosis is also very uneven and usually also has a focal character; the size of these foci depends on the caliber of the vessel narrowed or closed and to what extent it is possible for the blood supply of the area of heart muscle to be maintained through collaterals. As is known, the coronary arteries, although they are not terminal arteries in the sense of Congheim, still anastomose with each other only in the area of small intramuscular branches, and therefore when the lumen of a larger branch is occluded, restoration of blood supply in the area supplied by this branch occurs with difficulty and not completely. When the lumen of a large branch is occluded, e.g., ram. desc. art. coron. cordis sin., as a rule, an infarction of the heart muscle forms with stretching of this part of the muscular wall and sometimes with rupture of it or more frequently-with transformation of the corresponding place of the wall of the left ventricle into a scar, which subsequently, as it stretches, can form an aneurysm of the heart. Between such large scars and microscopic scars there are all possible transitional forms. The point is that macroscopic infarction of the heart muscle occurs only if the occlusion of the lumen of a large coronary branch occurs relatively quickly (e.g., as a result of thrombus formation on an atherosclerotic plaque). If only narrowing of the coronary artery develops or occlusion of its lumen occurs gradually and slowly, then in the area of heart muscle supplied by it, only diffuse but uneven development of connective tissue with scattered small scars occurs [see separate table (pp. 255-256), Fig. 6]. In some cases, such slowly progressing occlusion of the coronary arteries (mainly the left) is accompanied by the development of extensive scar fields and even aneurysmal dilatation of the heart in the complete absence in the anamnesis of any signs indicating acute cardiac weakness or angina pectoris, so characteristic of acute occlusions of the coronary arteries with development of infarctions. This unevenness and even the formation of small focal scars in such cases, despite the fact that blood supply to a large area of heart muscle is more or less impaired, is explained by the fact that blood supply to individual places of the heart muscle tissue is uneven even under normal conditions, since it varies depending on the distance of the corresponding place from the main feeding artery, on the number of anastomoses ensuring collateral blood supply, on the richness of this area with capillaries, etc.-This also explains in part the fact that development of infarctions in the heart muscle and development of connective tissue, more diffuse or in the form of scars, is observed predominantly in quite definite areas of the heart muscle. But of course the distribution of C. is also determined by the fact that atherosclerosis of the coronary arteries also has its favorite localizations. Thus, the left coronary artery and its branches are more frequently affected by atherosclerosis, in particular its descending branch. As a result of the influence of all these circumstances, both heart infarctions and more diffuse development of connective tissue and small scars in arteriosclerotic C. are most frequently observed in the lower third of the anterior wall of the left ventricle, in the anterior left papillary muscle, and in the upper third of the posterior wall of the left ventricle. C. of the right ventricle is a relatively rare phenomenon, even with significant changes in the right coronary artery.-Scars in the heart muscle in arteriosclerotic C. are often visible macroscopically on the surface of the section in the form of more or less small, slightly depressed spots or strips of pale-grayish color; because of these same scars, as well as more or less diffuse development of connective tissue, the heart muscle becomes denser, the heart wall bends with difficulty and crunches when cut. Small scars in arteriosclerotic C. are also visible on the outer and inner surfaces in the form of small, shallow retractions, in the area of which the endocardium or epicardium is mostly firmly fused with the heart muscle. However, it should be noted that the development of both scars and more diffuse connective tissue in arteriosclerotic C. occurs predominantly in the middle layers of the heart muscle wall, since obviously the blood supply to the outer and inner layers is better ensured.-Histological examination of the heart muscle in arteriosclerotic C. reveals an increase in connective tissue. As a result of this, in a certain volume of heart muscle, the amount of muscular tissue is reduced. The enhanced development of connective tissue occurs either diffusely-between the muscle bundles and around vessels-or in the form of larger or smaller foci. However, even diffuse development of connective tissue is never completely uniform. In some cases, the connective tissue has the character of scar tissue, while the muscle fibers located between its strands are completely unchanged.

These are cases where the process has temporarily stopped after a certain portion of muscular tissue has died and in its place connective tissue has developed and been transformed into a persistent scar. The cessation of the process occurred because atherosclerosis in the corresponding arterial branches also stopped, somewhat impairing the blood supply; but the diminished blood supply is sufficient to nourish the remaining portion of muscular tissue under the demands made upon it in this case. But for the most part, the microscope still detects one or another of the processes that occur in the heart muscle due to insufficient blood supply: atrophic, degenerative, and necrotic changes - in the muscle fibers, and inflammatory and organizational changes - on the part of the interstitial tissue. Depending on the degree and, above all, on the rapidity of development of the impairment of blood supply, these processes are expressed to a greater or lesser extent. If the impairment of blood supply occurs rapidly and extends over a considerable area of the heart muscle, then in the center - at least of this area - necrosis of the muscle fibers predominates: their cross-striation disappears, the nuclei do not stain, and the fibers undergo disintegration and resorption. At the edges of this area, where blood supply is maintained, albeit insufficiently, by collaterals, degenerative phenomena are observed: less frequently - vacuolar degeneration and hyaline-granular disintegration, more frequently - cloudy swelling and especially - fatty infiltration of the muscle fibers. The latter is regarded as a typical change in the tissue due to insufficient blood supply and is explained by the fact that the cells still retain the ability to absorb fatty substances from the surrounding tissue fluid, but due to lack of oxygen are unable to burn them (steatosis retentiva). - With less rapid and less extensive impairment of blood supply, necrotic processes are not observed, and fatty infiltration predominates, and with even weaker and slower restriction of blood supply - simple atrophy of the muscle fibers, usually accompanied by brown pigmentation. Parallel to these alterative processes and proportionally to them, depending on the rapidity and degree of impairment of blood supply, inflammatory processes are expressed to a greater or lesser extent. Around the necrotic area, dilation of capillaries (even development of new capillaries), edema of the tissue, and fairly significant cellular infiltration are observed. Among the cellular elements, histiocytes (epithelioid cells), lymphocytes, and fibroblasts predominate; eosinophilic and neutrophilic polynuclears are rarely encountered (only in large infarcts). These inflammatory changes, clearly expressed in cases of arteriosclerotic cardiosclerosis with a more rapid development rate, are the circumstance that at one time gave rise to classifying arteriosclerotic cardiosclerosis as myocarditis. With a slower developing impairment of blood supply, inflammatory phenomena are very weakly expressed or almost absent. In these cases, the microscopic picture consists of more or less diffusely or in foci of well-developed scar connective tissue, of muscle bundles with weakly expressed signs of brown atrophy, and of sparse cellular elements - mainly fibroblasts. - In comparison with the alterative and inflammatory processes and the proliferation of connective tissue, regenerative phenomena recede completely into the background. Regeneration of muscle fibers does not occur in any case; its rudimentary manifestation can perhaps be considered the presence of so-called myocytes. Sometimes muscle fibers among the proliferated connective tissue show signs of hypertrophy - increase in nuclei and number of fibrils. To what extent this hypertrophy existed before the development of cardiosclerosis, to what extent it developed together with it and is compensatory in response to the death of a portion of the muscular tissue and difficulty in its function due to its penetration by scar tissue - this is mostly impossible to determine. Theoretically, the development of hypertrophy of muscle fibers under conditions of insufficient blood supply, leading to atrophy of these same fibers, seems unlikely. As for the changes in the arteries of the heart muscle in arteriosclerotic cardiosclerosis, it has already been indicated above that the sclerotic changes leading to cardiosclerosis are located in the large subepicardial branches of the coronary arteries. Thus, these changes are as a rule located far from those areas of musculature in which cardiosclerotic changes occur due to impairment of patency of these large arterial branches. On microscopic examination of the sclerotic areas of the myocardium, small muscular arteries with thickening of the wall, narrowing or obliteration of the lumen are often found. These changes must be considered secondary, as they develop only in those areas of the heart muscle whose blood supply is impaired as a result of narrowing or closure of the lumen of the corresponding large arterial branch. Cardiosclerosis should cause a decrease in the working capacity of the heart both due to the reduction in the mass of muscular tissue and due to the difficulty of systole and diastole of the heart muscle due to the proliferation of scar connective tissue, which is less capable of contracting and elongating. Due to cardiosclerosis, the heart's ability to vary its work, mainly in the direction of increasing it, should be reduced. This reduction should correspond to the degree of development of connective tissue and atrophy of the muscle. However, it is difficult to practically establish a decrease in the working capacity of the heart specifically due to arteriosclerotic cardiosclerosis, since in this case the working capacity of the heart is reduced first of all already due to the sclerosis of the coronary arteries themselves. One can only imagine that the development of cardiosclerosis should further contribute to the decrease in the working capacity of the heart, since to the impairment of blood supply of the heart muscle are added also the physical changes of the heart muscle itself, which reduce its working capacity. - Clinically, it is in any case difficult to determine to what extent the various phenomena of cardiac insufficiency in sclerosis of the coronary arteries are caused by impairment of blood supply of the heart muscle without yet its anatomical changes, and to what extent they are already due to cardiosclerosis. The presence of cardiosclerotic changes will of course be indicated by the greater constancy and more severe degree of phenomena of cardiac insufficiency. The influence of age, sex, etc., on the development of arteriosclerotic cardiosclerosis, as well as other etiological factors, coincides with their influence on the development of atherosclerosis in general and of sclerosis of the coronary arteries in particular. Among the etiological factors contributing to the occurrence of cardiosclerosis, the profession of the patients must undoubtedly also be included. Unfortunately, to the present time there are no scientifically developed statistical data in this sense; this is a task for the nearest research. The subjective and objective manifestations observed in arteriosclerosis of the heart can be arranged according to their significance in terms of the degree of cardiac insufficiency they determine, starting from the weaker and proceeding to the more severe, in the following order: decrease in working capacity and endurance (physical and mental), shortness of breath on physical exertion, palpitations, attacks of cardiac asthma. As long as arteriosclerosis of the heart manifests itself only by a decrease in working capacity and sometimes already by shortness of breath appearing with intensified physical movements (climbing, walking), examination of the patient may not yet reveal any objective changes. - Cardiac asthma as a manifestation of arteriosclerotic cardiosclerosis already belongs to the grave symptoms and is usually accompanied by clear objective changes. Among them, the most important are: dilation of the left ventricle and (less frequently) gallop rhythm. It is necessary to state here that determining which symptoms should be considered characteristic specifically for impairment of blood supply of the heart muscle due to sclerosis of the coronary arteries, and which for arteriosclerotic cardiosclerosis, is difficult because sclerosis of the coronary arteries of the heart is usually combined with sclerosis of the aorta, often with hypertension, with sclerosis of the renal arteries, etc.; the manifestations of all these pathological conditions are added to those of coronary sclerosis and can influence them not only in the sense of their intensification but also in the sense of weakening. The greatest difficulties are caused by the question of the combination of arteriosclerosis of the coronary arteries with hypertension, since the first process should lead to atrophy, and the second - to hypertrophy of the cardiac musculature. If in fact hypertrophy of the cardiac musculature is often found in combination with arteriosclerotic cardiosclerosis, this can be explained as follows: as indicated above, sclerosis of the coronary arteries is characterized by uneven distribution: it can be comparatively strongly expressed in some branches, while in others it is weakly expressed or even absent altogether.

Then in the areas of the heart wall supplied by sclerotically changed arteries, K. will develop, while in the areas supplied by little changed or healthy branches—compensatory hypertrophy; sometimes, however, arteriosclerotic K. develops in already hypertrophied heart muscle (e.g., in the development of coronary sclerosis in hypertensives). Then we will also obtain, due to the same unevenness of the sclerotic process, a combination of K. with hypertrophy of the heart muscle. Due to these possibilities of combining heart hypertrophy and K., in the objective examination of the heart in arteriosclerotic K., the signs characteristic of K. as such are not always observed. Moreover, K. will manifest these characteristic signs only when it is strongly expressed and more diffusely developed. In these cases, upon palpation, weakening of the apical impulse or a double impulse with an additional weak beat at the beginning of diastole is determined (see below—determined upon auscultation as gallop rhythm). Percussion reveals dilation of the left ventricle; sometimes, if K. is complicated by atrial fibrillation (see below), dilation of the left atrium is determined, and later and more rarely, in already severe cardiac insufficiency, dilation of the right heart as well. X-ray methods of heart examination in pure cases of K. reveal a heart configuration characteristic of decreased tone of the heart muscle (the so-called flaccid heart) and greater or lesser dilation of the left ventricle, left atrium (in atrial fibrillation), and later of the right heart as well. Aneurysms of the left ventricle (as a result of large infarcts) can, in appropriate position, to such an extent and in such a way change the contour of the left ventricle that they can be recognized by fluoroscopy, resp. orthodiagraphy, resp. telecardiography.-Auscultation in mild K. reveals no deviations from normal. The generally accepted view that K. manifests as weakening of the intensity of heart tones must be recognized as generally correct. But one should not of course consider 'dull tones' in all cases as necessarily a manifestation of K., since this phenomenon can be the result of the most diverse physiological as well as pathological influences. In more severe cases, when the elastic extensibility of the heart muscle has been severely impaired, protodiastolic gallop rhythm is heard. Moreover, the very frequent disturbances of conduction in cardiosclerosis (see below) can also cause the appearance of one or another type of gallop rhythm. Very often in K., a systolic murmur is heard over the apex. Apparently in the origin of this murmur in K., the shortening of the aortic cusp of the mitral valve due to its sclerosis (Huchard) plays a lesser role than the decreased contractile ability of the left ventricular muscle and in particular of the left anterior papillary muscle, in which cardiosclerotic changes develop especially frequently (the artery supplying it makes a 180° turn).-Palpation of the pulse, besides changes in its rhythm (see below), in pure and already expressed arteriosclerotic K. reveals increased filling and tension of the pulse. Detection of sclerotic changes in peripheral arteries does not yet give the right to make a diagnosis of sclerosis of the internal organs' arteries and in particular of the heart, and the absence of such changes in peripheral arteries by no means excludes coronary arteriosclerosis. Changes in arterial pressure in arteriosclerotic K. as a rule show comparatively low figures for both maximum and minimum pressure; especially characteristic for severe K. is the decrease in pulse pressure. In view of the frequent association of K. with hypertension, in the presence of K. comparatively high figures for blood pressure are still often determined. If in such a patient it is possible to examine his blood pressure at a time when he still has only hypertension, and then already during the developing K., one can often observe as a very characteristic phenomenon more or less gradual fall in arterial pressure with decrease in its pulse oscillations. This fall in pressure occurs very often after attacks of angina pectoris and in parallel with the development of the picture of cardiac insufficiency. If K. develops in a case where there was previously expressed atherosclerosis of the aorta, then the increased pulse pressure characteristic of the latter is gradually replaced by normal or even decreased amplitude of pressure pulse oscillations.-In the further course of K., usually soon after the appearance of attacks of cardiac asthma, a picture of severe cardiac insufficiency develops with signs of congestion in the lungs, liver, kidneys, and with edema. Usually, dyspnea plays a dominant role in this picture, both constant and periodically intensifying. To this is often added disturbances of respiratory rhythm in the form of so-called Cheyne-Stokes breathing. Since sclerosis of the coronary arteries is the most important factor in the origin of angina pectoris, the development of arteriosclerotic K. is very often preceded and accompanied by various forms of angina pectoris. Between comparatively mild attacks of angina pectoris of the effort angina type and severe attacks (status anginosus), accompanied by the typical picture of myocardial infarction, all transitional forms are observed. It is impossible to establish a precise boundary between attacks that do not result in organic changes of the heart and those that are accompanied by necrosis of larger or smaller areas of the myocardium. Usually in cases where there were one or another signs of angina pectoris, they subside and recede into the background when cardiac asthma appears and the picture of cardiac insufficiency develops. Among the general phenomena observed in arteriosclerotic K., mention should also be made of increased temperature and leukocytosis. If these phenomena are observed in developing arteriosclerotic K., the question arises as to how much this process itself can cause them and how much they should be attributed to one or another complicating infection. There is no doubt that extensive infarcts of the heart muscle, if they are caused by more rapidly developing thrombosis of larger coronary arteries, as a rule are accompanied by high fever (up to 39°) and marked leukocytosis (up to 20,000). Between such large infarcts and disturbance of blood supply to small areas of heart muscle due to narrowing of the corresponding branch of the coronary artery, leading only to atrophy of the muscular tissue and development of connective tissue, all transitional forms exist. It is quite possible that multiple small infarcts of the myocardium, developing comparatively rapidly and accompanied by more acute reactive myocarditis, can give small increases in temperature and slight leukocytosis. Speaking of cardiac insufficiency as a manifestation of arteriosclerotic K., one has in mind more diffuse, widespread changes mainly of the heart ventricles in the form of more or less diffuse development of connective tissue or numerous, densely located scars, since the lesion of K. of individual areas of the heart muscle or a few scattered scars in it cannot have a substantial influence on the contractile ability of the heart muscle as a whole. But such cardiosclerotic foci, resp. such limited disturbances of blood supply to the heart muscle can have a substantial influence on the work of the heart if they, as is very often the case, develop in those areas of the heart wall that belong to the special system generating and conducting impulses for heart contraction. In view of this, arteriosclerotic K. often leads to various disturbances of heart rhythm, developing often before the appearance of pronounced signs of insufficiency or observed simultaneously with them. Arteriosclerosis of the heart, resp. arteriosclerotic K. can manifest with all types of heart rhythm disturbances: most often bradycardia and various types of heart block, extrasystole, and atrial fibrillation are observed. Arteriosclerosis of the heart is one of the main etiological factors of all these arrhythmias. In cases where arteriosclerotic K. develops the picture of cardiac insufficiency without special lesion of the impulse-generating and conducting system, tachycardia usual for cardiac insufficiency due to overstrain of the heart is observed. But besides that in K., sometimes periodically or for a long time regular or irregular tachycias are observed, which are the result of disturbances of atrial function of the flutter or fibrillation type. But more often, precisely in arteriosclerotic K., cases are observed when more or less persistent bradycardia, not disappearing even with cardiac insufficiency, is observed. This bradycardia is the result of suppression of impulse generation in the Kisch-Fick node, i.e., it is of sinus origin. More often bradycardia, correct or irregular, due to disturbance of conduction of the atrioventricular bundle is observed.-Sclerosis of the coronary arteries is the most frequent cause of various types of heart block, from lengthening of the interval between atrial and ventricular contractions (on the phlebogram a-c, on the electrocardiogram P-R) to complete block.

In more severe cases of heart block, predominantly incomplete block, manifestations of impaired cerebral blood supply are often observed, ranging from mild and transient dizziness to severe Morgagni-Adams-Stokes attacks. Arteriosclerotic C. also often shows disturbances in the conduction of the bundle of His branches: they clinically manifest only as splitting of heart tones, being easily detected electrocardiographically. Disturbance of conduction in the branching of the bundle of His (Arborization block) is also determined only electrocardiographically. Disturbance of conduction in arteriosclerotic C. is most often caused by anatomical changes in the form of scarred foci in the area of the atrioventricular bundle. Both the sinus node and the Ashoff-Tawara node and the bundle of His are supplied by special arterial branches, which in most cases arise from the right coronary artery (the branch supplying the Kis-Flakovsky node in 60% of cases arises from the right coronary artery, in 40% from the left, and the branch supplying blood to the Tawara node and the atrioventricular bundle in 92% arises from the right coronary artery, in 8% from the left). Sclerotic lesions of these branches or more often of the coronary arteries in the area of the origins of these branches are apparently a common cause of impaired blood supply and the development of scarred foci in the area of the heart's conduction system. Disturbances of conduction in the area of the branching of the bundle of His are most often the result of their destruction by scars due to sclerosis of the arterial branches supplying that area of the ventricular wall.-Special attention is deserved in coronary sclerosis by the so-called Czermak phenomenon, or Vagusdruckversuch, or Carotisphanomen: slowing of the pulse when pressure is applied to the area of the vagus nerve or carotid sinus, especially on the right side. In individuals with sclerosis of the coronary arteries, even slight pressure on this area sometimes causes a sharp slowing of the pulse, often accompanied by fainting and even collapse. This phenomenon is explained as the result of enhanced influence of the vagus nerve on the corresponding impulse-generating centers due to decreased functional capacity from impaired blood supply as a result of coronary sclerosis. Of even greater practical significance in arteriosclerotic C. than disturbances of conduction is the complication with atrial fibrillation, as it occurs more frequently and has a more adverse effect on the heart's work capacity. Arteriosclerosis of the heart is, after mitral valve defects, particularly mitral stenosis, the most common cause of atrial fibrillation. Treatment with quinine restores normal rhythm in atrial fibrillation due to arteriosclerosis of the heart as often as in atrial fibrillation due to mitral valve defects. This fact, as well as the often negative histological findings of the atria and particularly the sinus node in cases of atrial fibrillation and in cardiosclerotics, proves that functional, reversible changes in the atrial muscle may underlie atrial fibrillation in arteriosclerosis of the heart. In the origin of these changes in arteriosclerotic C., insufficiency of blood supply to the atria due to arteriosclerotic narrowing of the coronary vessels obviously plays a major role. In particular, one can think of narrowing of the origins of the branches of the coronary arteries that supply the atria, which all arise from the branches of the left and right coronary arteries located in the transverse groove of the heart. This impairment of blood supply to the heart, in connection with overexertion of the cardiac muscle and the special predisposition of the atrial muscle to fibrillation or flutter, explains the so frequent occurrence of atrial fibrillation in arteriosclerotic C. In C. due to coronary sclerosis, we more often than in mitral valve defects observe a relatively slow ventricular rhythm in atrial fibrillation. This is fully explained by the above-mentioned very frequent disturbance of conduction of the bundle of His in arteriosclerotic C.-Of least practical significance in arteriosclerotic C. is extrasystole, although it is the most common of all arrhythmias in arteriosclerotic C. But it disturbs the heart's work the least and is the result of the least widespread changes in the heart muscle. Ventricular extrasystoles are more often observed. The generally so frequent extrasystoles in old age are undoubtedly a manifestation of precisely cardiosclerotic foci.-All the above-mentioned rhythm disturbances in arteriosclerotic C. are best revealed by electrocardiography; but this method of research has recently acquired in diseases of the heart muscle in general and in C. in particular special significance, as it also reveals such changes in the myocardium that do not manifest as rhythm disturbances and are not detected by other research methods. Thus, it can now be considered established that macroscopic infarctions of the heart muscle as a result of occlusion of the lumina of the largest branches of the coronary arteries give very characteristic changes in the electrocardiogram. But even more diffuse changes in the heart muscle caused by C. are often accompanied by changes in the electrocardiogram: it is necessary to note the very low voltage, i.e. reduction of all waves, lengthening of the QR8 group, smoothing, biphasic or negative T wave; electrocardiograms characteristic of block of one or another branch of the bundle of His or so-called block of the branches are also not uncommon. The complete picture of arteriosclerotic C. consists of the following main features: cardiac insufficiency (often cardiac asthma attacks) or anginal pains and arrhythmia in old age in a man. Between these typical and fully expressed forms on the one hand and cases with poorly expressed manifestations of cardiac insufficiency or with one or another arrhythmia as the only sign on the other hand, all sorts of variations are observed. These not fully expressed forms often do not lend themselves to precise definition and cause differential diagnostic difficulties. It has already been indicated above how difficult it is to distinguish the manifestations of impaired blood supply to the heart muscle caused by coronary sclerosis in the sense of decreased functional capacity, but without anatomical changes, from the manifestations of proper C.-Furthermore, it is very difficult to distinguish the manifestations of myocarditic C. from the manifestations of arteriosclerotic C. These manifestations are in general identical, and the differential diagnosis can be correctly established only on the basis of indirect data, which however have only conditional significance, such as age, previous infectious diseases, presence or absence of typical anginal pains as a manifestation of coronary sclerosis, etc. The prognosis in arteriosclerotic C. depends on the degree and extent of the changes and their localization, but mainly on the rate of development of sclerosis of the coronary arteries and the degree, speed, and extent of the resulting impairment of blood supply to the myocardium. - Treatment of arteriosclerotic C. reduces to treatment of arteriosclerosis and symptomatic treatment of its manifestations from the heart side. In this symptomatic treatment, it is necessary to take into account certain special conditions existing in arteriosclerotic C. Thus, it is known that sclerotically changed arteries have a tendency to enhanced tonic, so-called spastic contraction of their musculature. Therefore, in coronary sclerosis it is advisable to long-term apply those means that can counteract this tendency, namely: preparations of caffeine and especially theobromine and theophylline (diuretin in doses from 0.5 to 1.0). Their great benefit in angina pectoris is beyond any doubt, but it is quite possible that they also in arteriosclerotic C. in the absence of expressed anginal attacks also act beneficially, promoting improvement of blood supply to the heart muscle. Preparations of digitalis, on the contrary, are contraindicated in the presence of angina pectoris, as they often cause intensification and more frequent attacks. But when there are no anginal pains and there is a picture of cardiac insufficiency, treatment with digitalis and similar preparations is quite permissible and often brings great benefit. In the presence of arrhythmia, digitalis is prescribed according to the already developed indications and contraindications for the use of digitalis in various types of arrhythmia. C. as a consequence of lesions of the coronary arteries of the heart of non-arteriosclerotic nature is rare. Syphilitic coronary arteritis is among these lesions comparatively the most frequent, if one does not consider special inflammatory and then scarred changes in the walls of small arteries of the myocardium in rheumatic myocarditis. Syphilitic arteritis has localization predominantly in the large branches of the coronary arteries, rheumatic in the small. Accordingly, as a result of the first, large macroscopic scars are obtained, as a result of the second, small microscopic ones. The consequences and clinical manifestations of C. developing as a result of syphilitic arteritis of the heart, as far as is known, are similar to those of arteriosclerotic C.

The clinical picture of cardiosclerosis resulting from damage to the heart's arterioles by a rheumatic inflammatory process merges with that of cardiosclerosis resulting from rheumatic myocarditis. It is difficult to determine to what extent damage and narrowing of only the coronary artery ostia due to atherosclerotic or syphilitic processes in the aortic wall can lead to cardiosclerosis by themselves, since in cases of damage to the coronary artery ostia, there is usually also damage to them by atherosclerosis along their course. Myocarditic cardiosclerosis can be the result of acute or chronic myocarditis. In the latter case, it can develop while the inflammatory process is still continuing or may be observed after its cessation, as a consequence of it. In the first case, it is impossible to distinguish between the manifestations of cardiosclerosis and those of chronic myocarditis. Myocarditic cardiosclerosis, like arteriosclerotic cardiosclerosis, appears as more or less uneven development of scar connective tissue in the myocardium, but in myocarditic cardiosclerosis, scarring occurs almost exclusively in the form of small microscopic foci. The only exception is cardiosclerosis resulting from syphilitic and specifically gummatous myocarditis, which can produce scars visible to the naked eye and even very large ones. The location of the scars varies depending on the etiology of the myocarditis of which they are a consequence. If the inflammatory process has not yet subsided, then along with scar connective tissue, various manifestations of inflammation are found, depending on the etiology and nature of the process, and all transitions between inflammatory and scar changes. Myocarditic cardiosclerosis proper can only be spoken of in those cases where the inflammatory process has led to the development of connective tissue in the form of more densely located foci over extensive areas of the heart muscle. In these cases, the heart wall is indeed thickened, so that it cuts with some crunching and is harder to bend; the muscle on cross-section has a mottled appearance. Of the acute myocarditises, diphtheritic myocarditis apparently most often ends in the formation of small scars in the myocardium; the localization of these scars is varied, but they are still most often observed under the endocardium and in the papillary muscles of the left ventricle. Acute myocarditis in influenza apparently very rarely leads to the development of cardiosclerosis; there are no data on the development of cardiosclerosis after typhoid myocarditis. From the point of view of the development of cardiosclerosis, myocarditis in typhus is of great interest. By its type, this myocarditis belongs to the productive form, and the characteristic localization of nodules is the small vessels, the lumen of which undergoes obliteration (Davydovsky). Judging by such a histological character of the process and by the fact that after typhus various manifestations of insufficiency and irregularity of cardiac activity are often observed, it can be assumed that acute typhus myocarditis relatively frequently passes into a chronic form, or rather, into cardiosclerosis. Such a transition of acute myocarditis into cardiosclerosis is also known in other forms of acute or subacute productive myocarditis, namely in rheumatic myocarditis. Aschoff's rheumatic nodules in the heart muscle are located predominantly subendocardially, and due to this localization, they often damage the branches and ramifications of the atrioventricular bundle; their localization is more often observed in the left heart, both in the atrium and in the ventricle, where the posterior and lateral walls up to the apex are most often affected. Another important point is the tendency of the nodules to perivascular location with spread to the middle and inner tunics of the vessels (Talalaev). As a result, obliteration of the lumen of arterioles due to thrombosis and the development of small infarcts occur. All these changes lead to the development of vascular and perivascular sclerosis. Accordingly, in persons who have had rheumatic infection, disturbances of cardiac activity are observed very often, either in the sense of its insufficiency, or in the sense of arrhythmia, or both together. Scarlet fever myocarditis is close in type to rheumatic, as it also gives perivascular granulomas. But there are no data on the development of cardiosclerosis as a result of scarlet fever myocarditis. In addition to these more or less definite myocarditides in etiology and form, there are also acute myocarditides of not strictly established etiology: focal interstitial, purulent and non-purulent; they can also lead to scar formation. But almost nothing more is known precisely about cardiosclerosis resulting from these myocarditides. Among chronic myocarditides, syphilitic myocarditis can undoubtedly lead to cardiosclerosis. Its gummatous form and a more diffuse form are distinguished. Gums give large scars, more rarely calcified nodes surrounded by a scar capsule. The forms of syphilitic heart disease that lead to cardiosclerosis in an expressed form are those where the productive inflammatory process develops more diffusely in the heart wall in the so-called 'gummatous infiltration' or 'gummatitis'. As a result of such a process, sometimes the entire heart muscle is found to be penetrated by scars. Syphilitic myocarditis is not necessarily associated with syphilitic arteritis of the large branches of the coronary arteries. Tuberculosis of the heart muscle is rare and as a cause of cardiosclerosis has no practical significance. The clinical picture of myocarditic cardiosclerosis has not yet been identified in sufficiently distinct forms. This is probably explained by the fact that the effect of the scar process in the heart muscle on its working capacity and on the heart rhythm, as a result of such diverse forms of heart muscle damage, and the manifestation of this disturbance of strength and heart rhythm are too varied and in themselves represent nothing typical. Here, as in arteriosclerotic cardiosclerosis, all variations and all stages of cardiac insufficiency and all kinds of rhythm disturbances are encountered. Only the painful phenomena characteristic of coronary sclerosis are usually absent. The diagnosis of myocarditic cardiosclerosis resulting from a specific form of myocarditis is based on anamnestic or other data indicating the past corresponding infection, and on the development of cardiac manifestations in connection with it. The manifestations of myocarditic cardiosclerosis by themselves are not sufficiently characteristic to make an etiological diagnosis. If one is dealing with older patients, they cannot even be distinguished from the manifestations of arteriosclerotic cardiosclerosis. The practical significance lies in resolving the question of to what extent the phenomena occurring in connection with a particular infection should be attributed to the manifestation of already completed scar changes in the heart muscle—cardiosclerosis, and to what extent to still active inflammatory changes in the myocardium. The more slowly and chronically these inflammatory changes proceed, the more difficult it is to resolve this question. In favor of the activity of the process will speak a certain variability of cardiac manifestations, the presence of elevated temperature, leukocytosis, and other manifestations of a chronic infectious process. The treatment of myocarditic cardiosclerosis, insofar as this implies only the scar process resulting from an already eliminated infection, can only be symptomatic. The third form of enhanced development of connective tissue in the heart muscle differs from the first two in that the development of connective tissue occurs completely uniformly and that it is not associated with either arteriosclerosis of the coronary arteries or with a definite myocarditic process, but is associated with hypertrophy, dilation, and insufficiency of the heart. This type of enhanced development of connective tissue in the heart was described by Merklen and Huchard as 'diffuse sclerosis' and was described especially thoroughly and accurately by Degio under the name 'myofibrosis of the heart.' Since this form should be strictly distinguished from arteriosclerotic and myocarditic cardiosclerosis in terms of its etiology, resp. pathogenesis, it is most appropriate to retain the term 'myofibrosis' proposed by Degio for it. The enhanced development of connective tissue in this case occurs completely uniformly, in the initial stages between the muscle bundles, and in more pronounced degrees also within the bundles, between the muscle fibers. This myofibrosis necessarily develops if the hypertrophied heart muscle undergoes dilation because it must withstand increased pressure during the diastolic period. At this time, there is already insufficiency of cardiac activity, which leads to venous congestion in the heart muscle, and congestion, if it is prolonged, causes enhanced development of connective tissue. From this point of view, it is also understandable that in more pronounced developments of heart myofibrosis in the hypertrophied musculature, degenerative changes are very often observed as a manifestation of those pathological, physicochemical processes in the heart muscle that occur in it during overexertion. This view of heart myofibrosis, partly already accepted by Degio, received final confirmation through the work of Stadler and displaced the theory of E. Albrecht, who considers both hypertrophy and degeneration of muscular tissue and proliferation of connective tissue as manifestations of an inflammatory process.

Myofibrosis complicates the work of the heart muscle and adversely affects its ability to vary tonic contractions, but perhaps due to the low extensibility of fibrous connective tissue, it prevents further expansion of the heart.