Pathological anatomy of endocarditis

Morphologically endocarditis is a combination of the processes of alteration, proliferation and thrombosis. Exudative component due to poverty endocardial blood vessels is missing. Begins endocarditis with changes in the structural components of the connective tissue of the endocardium, due to the influence of pathogenic agents directly from washed by the blood. If the damage endocardial its borderline position with blood flow contributes to the formation of thrombi and often subsequent infection.
Localization endocarditis divided into valve (valvola), parietal (parietal), hardly, trabecular. Most often affected valve endocardium that depends on it to a higher functional load. Downstream endocarditis are acute, subacute and chronic. Depending on the morphological changes endocarditis can be divided into 5 types.
1. Simple, or primary, endocarditis occurs in rheumatoid arthritis, infectious diseases, intoxication, metabolic disorders and changes in the protein content in blood plasma. Usually attacked mitral valve, rarely aortic and tricuspid and parietal and hardly the endocardium. Alterative-proliferative inflammation of the deep layers of the endocardium is combined with the disorganization of the connective tissue (mukodni swelling, fibrinoidnogo swelling, fibrinoid necrosis) and proliferation gistiotitarnaya cells, rheumatism - with the formation typical of granulomas (see Rheumatism). Macroscopically valve normal or slightly thickened on line circuits, semi-transparent, grey color.
2. Warty endocarditis occurs in any part of the endocardium, often valve. Typical for rheumatism; also occurs as a complication of an infectious disease, severe cachexia, uremia, diabetes. Morphologically note alterative-proliferative changes in the thickness of the endocardium with involvement in the destructive process of endothelium and the subsequent formation of thrombi. I. Century Davydov and M. A. Skvortsov not make this endocarditis, attributing it to a variety of initial endocarditis. Macroscopically on the wings (atrial the surface of the mitral valve, ventricular - aortic) in line closures appear gray, translucent, the size of a pinhead, located chain warts (blood clots), easily removable. The endocardium under them rough, muddy, often thickened. Further warts grow in number, locating the ranks, becoming yellowish-grey, removed with difficulty. To atypical warty the endocarditis endocarditis include systemic lupus erythematosus (see). Characteristic is the location of warts on the basis of the valves, under them (for example, with ventricular surface of the mitral valve), and along with damage to other valves defeat of pulmonary valve stem.
3. Fibrous (fibroelastosis) endocarditis. This term implies rheumatic days, in which, along with the early fibrosis happen active alterative-proliferative fresh changes (see above simple endocarditis). Macroscopically valve slightly thickened, gray, semi-transparent.
4. Ulcer (septic) endocarditis occurs in various forms of sepsis. The essence lies in the dominance of alternative events over the processes of proliferation and reparations, which leads to the formation of large ulcers with several layers on them thrombotic overlays, often in the form of polyps. Clots of various sizes and fantastic shapes, yellowish or greenish color, friable consistence, often contain a large number of pyogenic bacteria (mycotic endocarditis). Microscopically this vast zone of necrosis in the thickness of the endocardium is separated from the healthy tissue leukocyte shaft. Sometimes leukocytic infiltration penetrates the entire thickness of damaged valve, reminding purulent fusion.
Often the process is localized to valve endocardium (the defeat of the mitral valve in acute septic endocarditis, aortic - in subacute septic endocarditis, isolated defeat tricuspid valve - with gynecologic sepsis). With valves process may spread to the wall the endocardium, the intima of the aorta, tendinous sutures adjacent infarction. Ulcerative endocarditis flowing sluggishly, subacute, or chronic, a dedicated Sutmoller in 1910 under the name of subacute bacterial endocarditis.
Currently, this endocarditis is considered one of the original forms of sepsis. Characterized by extensive destruction valves with a margin of chords, education aneurysms and perforation with massive thrombotic overlays containing greater part of the colony of Streptococcus viridans (printing. table, Fig. 1). The defeat of the endocardium in the early stages when sepsis lenta no different from other endocarditis (fibrinoid necrosis, the prevalence gistiotitarnaya reactions, amicrobic clots in the form of warts). To Express stages typically the presence in the blood clots colonies of microorganisms and very early deposition of lime. An important feature is the appearance epithelioid cells, sometimes forming granulomas, and giant cells, faguoqitirute cocci.
Sepsis lenta occurs more frequently as a serial disease already modified valve: rheumatism is 75%, with pneumococcus, Staphylococcus, gonococcal, syphilis endocarditis, congenital heart disease - in 3-5% of cases. Only 20-22% of cases of endocarditis with sepsis lenta - primary disease (A. M. Wiechert). The characteristic feature of sepsis lenta is hitting not only the endocardium, but also the entire arterial system in the form of arteritis - brain aneurysm, mesenteric, iliac, splenic artery, capillaries (osherovski nodules well tactile surface fingerprints, smudges Lukin on the lower eyelid conjunctiva from inner corner of eye, petechial rash on the skin and mucous membranes). When sepsis lenta often occurs focal (less diffuse) intercapillary, often hemorrhagic, glomerulonephritis, leading in some cases to the development of uraemia. In the arterial system, in addition to similar with the endocardium changes of the vascular wall (fibrinoid necrosis, proliferation gistiotitarnaya and endothelial elements, sometimes leukocytic infiltration), there are multiple embolism infected thrombotic masses (mycotic aneurysm) and slices of lime with heart valves. The pathognomonic for sepsis lenta multiple heart attacks (in the spleen, kidney, brain), small necrosis in various organs, bleeding. Subacute hyperplasia spleen emphasizes the septic nature of sepsis lenta.
5. Return endocarditis is the most typical form of the flow of endocarditis. There rheumatism, septicaemia (especially strep), in the initial stage of sepsis lenta. Affected mainly valve endocardium. Characterized by layering on old sclerotic processes (often posttraumatische) fresh alterative-proliferative changes with thrombosis. Return endocarditis, as a rule, is the true relapse prior to disease (see Rheumatism), rarely reflects new disease occurred on the background of the changed reactivity (subacute bacterial endocarditis, joined rheumatic disease valves). Characteristic of the newly formed vessels as a result of previous endocarditis. Macroscopically valves thickened, whitish, disfigured, on the inside of them there are warty small (unlike polyps) thrombotic overlay or ulcerous defects.
The outcomes of endocarditis dependent on a number of reasons: the duration of the process, the depth and extent alterative changes, possible reparations, volume thrombotic overlays and the content of microbes. The healing process is reduced to scarring, hyalinosis connective tissue structures in the thickness of the endocardium, to the formation of new blood vessels, resorption and organization of thrombotic masses. Mild form of endocarditis (simple endocarditis) can recover the endocardial the old-preserving function. More often, however, endocarditis ends gross scarring with a thickening, puckering, adhesion of valve cusps, their lack of agility that leads to hemodynamic disturbances with the gradual formation of valvular defect (see heart Defects). Fibrous endocarditis with a tendency to fibroplasia ends sclerosis, leading to valve insufficiency and stenosis of the corresponding holes. When warty endocarditis occurs organization thrombotic overlays, which increases the deformation of the valve. With the return endocarditis due multiple repetitions of an organization's processes and fibroplasia structural defects valve apparatus even more pronounced. Particularly severe deformation occur after ulcer (septic) endocarditis. Under the influence of antibiotic therapy on the affected endocardium almost completely disappears microbial flora, reduced thrombotic overlay increase dramatically the processes of proliferation and reparation. In the result of healing always remain severe scarring, massive calcification, leading to the emergence aneurysms and perforations that ends valvular disease (printing. table, Fig. 2) and cardiac decompensation.
The section in the differential diagnosis of attitude should be distinguished endocarditis from secondary changes valves (defects) with hemorrhages, deposition of lipids, pacificasia them, leading to ulcers and blood clots.

septic endocarditis
Fig. 1. Septic prepozna-ulcer endocarditis with perforation of the valves of the aortic valve. Fig. 2. Septic endocarditis aortic valve after antibiotic treatment; perforation of one of the doors, resorption and organization of thrombotic overlays.