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Резюме Рецензент: д.мед.н., проф. Л.М. Іванова УДК 616-085:616.12-008.318 Вищий державний навчальний заклад України «Українська медична стоматологічна академія» (Полтава) Высшее государственное учебное заведение "Украинская медицинская стоматологическая академия" (Полтава) Higher state educational institution of Ukraine "Ukrainian Medical Stomatological Academy" (Poltava) shkapovl@gmail.com Infectious endocarditis (IE) is a septic process, mainly affecting heart valves. In the recent years, the number of IE cases has increased in three or even four times due to the reduced immunoreactivity. There are also cases of atypical course of IE, caused by the bacterium, which is not pathognomonic agent of IE. One of its atypical causative agents it is the Klebsiella pneumoniae, which is an opportunistic anaerobic microorganism that is long persisting in human organism but becomes virulent under conditions of immune deficiency. According to its description in literature, IE, caused by anaerobes, quite often declares itself with thromboembolism – obstruction of blood vessels of heart, lungs, and brain. The death rate from IE of the Klebsiella pneumoniae aetiology reaches 49 percents. The aim of the work is to undertake clinicopathologic analysis of IE, caused by the Klebsiella pneumoniae. Materials and methods: patient’s clinicopathologic data, which is analysed in compare with the other IE cases, described in literature. The achieved results: Patient S., 46 y. o., in April 2012, admitted to hospital on emergency basis. The patient was complaining of angina pain, which lasted more than 30 min. It was arterial hypertension in past history. On ECG there was sinus rhythm, persistent ST segment elevation in leads V2-V5. Troponin I test was positive. Echocardiogram displayed hypertrophy of aortic ventricle, mitral valve regurgitation. It was given a diagnosis of anteroseptal myocardial infarction (STEMI). Persistent subfebrility and inflammatory markers remained in course of treatment. Diagnostic investigation showed a frontal lobe tumour, and a pancreatic cyst. Surgical treatment was not recommended. In August 2012, the patient admitted to hospital again on emergency basis, complaining of heart pain, short-wind, and asthenia. Clinical testing showed recurrent anteroseptal myocardial infarction (NSTEMI). During the treatment the subfebrile rise in temperature and inflammatory markers persisted. After a while as he had been discharged, the patient had symptoms of heart failure. In October 2012 the patient’s condition worsened gravely: shot-wind, asthenia, tachycardia increased, cutaneous edema of legs appeared. He was rehospitalised. Subfebrility and inflammatory markers persisted. During auscultation, a rough systolic murmur was heard at the cardiac apex. Echocardiogram displayed hypertrophy of all the heart cavities, rupture of tendinous chords, mitral and aortal regurgitation. The patient’s condition was diagnosed as a destabilisation of cardiac insufficiency after myocardial infarction. Conservative therapy was prescribed. He was recommended undergoing surgical treatment – reconstructive operation. On the third day, suddenly, patient fainted. Reanimation was unsuccessful. During the pathologicoanatomic investigation detected hypertrophy of all the heart cavities, cicatrical changes in anterior myocardium of the aortic ventricle. Some signs of myocardium necrosis 2-3 weeks ago, as well as degeneration of the both mytral and aortal septal cusps with infiltrative increase of К. pneumoniae colonies in the valve cusps. Consideration of the results: we think that the atypical clinical course of the IE, having been brought on with К. pneumoniae, consisted in development of infarct-like clinical symptomatic, which is the same as clinical course of coronary myocardial infarction for patients with coronary heart disease (CHD). According to literature, cardiac infarction is cause of death for 6 percent patients with IE. Histological investigation detects the infarction foci, miomalation on background of coronary embolism with vegetations. Persistence of the IE brings on damage of blood vessels with development of tromboendovasculitis. Lack of vegetation on the cusps, endophyte spread of К. pneumoniae complicates the task of diagnostic investigation. Література
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