Infective Endocarditis: Morphological Changes of the Myocardium in Patients Operated under Conditions of Angiogenic Sepsis and Heart Failure

Introduction. Infective endocarditis (IE) is frequently accompanied by heart failure, which is associated with angiogenic sepsis. The exact mechanism underlying the development of so-called sepsis-induced cardiomyopathy (SIC) has not yet been fully elucidated. Aim. To study the morphological features of the myocardium in patients with infective endocarditis complicated by SIC. Materials and Methods. The study was based on autopsy material; histopathological methods were used. The main group (Group I) included 12 cases of IE affecting the left ventricular (LV) valves. The comparison group (Group II) consisted of 10 cases of valvular defects of non-inflammatory origin. Twenty patients underwent surgical treatment, while two patients from Group I died before surgery. Results. In myocardial specimens from patients of the comparison group and in 6 patients with secondary IE, changes associated with myocardial remodeling in response to LV pressure or volume overload were observed. In all cases of IE, marked damage to the microvasculature was noted, accompanied by extravasation of vascular contents into the interstitium along with bacterial toxins. In cardiomyocytes, destruction of the sarcolemma and intermyocytic junctions occurred, aggravated by lymphoid cell infiltration. In 4 cases from Group I, abscesses spreading from the valves to the myocardium were detected, while in two cases the process extended to the aorta. In tissues adjacent to the abscesses, the manifestations of SIC were most pronounced; as a result, the myocardium, deprived of the majority of cardiomyocytes, exhibited a very loose structure. Conclusions. Three factors initiating the complex pathogenesis of heart failure in IE were identified: 1.Toxic-immune diffuse myocardial injury in the setting of angiogenic sepsis with the development of SIC. 2. Increased functional load on the myocardium due to infectious destruction of the LV valve leaflets, leading to LV volume overload. 3. Local infectious myocardial involvement by microorganisms with abscess formation, the surgical management of which requires special technical approaches due to reduced mechanical strength of the myocardium.