Cardiac amyloidosis (amyloid cardiomyopathy) is a disease damage to the heart caused by extracellular amyloid deposition. In some cases, there may be local damage to the structures of the heart, for example, the atria; more often, heart damage is part of a systemic (generalized) pathology. Depending on the amyloid precursor protein, 36 types of amyloidosis are described, among which hereditary and acquired forms are distinguished. Cardiac amyloidosis is diagnosed 1) in the case of the amyloid infiltration in the myocardial bioptates or 2) in the case of non-cardiac amyloid deposition and the left ventricular wall thickening >12 mm without arterial hypertension and other reasons. The heart is most often affected in AL-, ATTR-, AA-, AANF-types of amyloidosis. Cardiac amyloidosis should be considered in patients with a heart failure with an unclear etiology, especially with preserved left ventricular ejection fraction, refractory to treatment, with proteinuria and CKD 4-5, in patients with idiopathic atrial fibrillation and conduction disturbances, in patients with left ventricular wall thickening of unclear etiology, low ECG voltage, unexplained arterial hypotension and pulmonary hypertension. Screening for cardiac amyloidosis should include non-invasive methods such as electrophoresis and immunofixation of blood and urine proteins, the free light lambda and kappa chains of immunoglobulins, 99Tc-DPD scintigraphy, genetic testing (if hereditary variants of amyloidosis are suspected), as well as a histological examination of biopsy samples stained with Congo red and polarizing microscopy.

Infiltrative cardiomyopathies are a group of diseases characterized by the deposition of abnormal substances in heart tissues, which leads to thickening of the walls or dilation of chambers with a secondary decrease in wall thickness and the development of diastolic, less often systolic, ventricular dysfunction. Most often, these are progressive diseases that, in the absence of adequate therapy, have an unfavorable prognosis. Clinical manifestations of infiltrative cardiac diseases are variable, which often leads to diagnostic difficulties and errors. In most cases, specific laboratory and morphological tests are required to confirm or clarify the diagnosis. Early diagnosis is critical to initiating therapy and improving patient prognosis. This article provides characteristic signs and symptoms, the so-called "red flags", making it possible to suspect infiltrative cardiomyopathies, diagnose them at an early stage and start life-saving therapy.

Introduction Processing of emotional stimuli is altered in patients with depression. The present feasibility study investigated the features of emotional information recognition in people with depressive disorders and how these differ from individuals without depression to determine whether response times could potentially be used as a diagnostic marker to identify individuals at high risk of depression and as an indicator of antidepressant medication response. Methods The study recruited 32 individuals, 16 with single or recurrent depressive episodes and 16 control subjects without depression. Patients with depression received 8 weeks of antidepressant therapy. The severity of depressive symptoms at baseline and their changes on prescribed therapy were assessed using the Montgomery-Åsberg Depression Rating Scale (MADRS). The processing of emotional information was assessed using the computerized Penn Emotion Recognition Task (ER-40). Results The two groups were well matched in terms of age and gender. There was no difference between the groups in their ability to correctly recognize happy or sad emotional facial expressions, but the average time patients with depression took to recognize a happy face was significantly longer than controls. In addition, they were more likely to misinterpret facial expressions as non-emotional. In patients with depression, the mean MADRS total score decreased from 26.3 ± 4.4 at baseline to 11.1 ± 8.9 at 8 weeks, a reduction of 57.8%. The proportion of responders with greater than 50% reduction in their baseline MADRS total score was 64.3%. Antidepressive treatment was associated with a reduction in the mean time required for recognition of a happy face (P < 0.05). Conclusions Patients with depression are slower to identify positive emotions but have a similar time to recognition of negative emotions as patients without depression. The greater time required for recognition of happiness distinguished the patients with depression from control subjects, and was also the only parameter that showed an improvement with antidepressant therapy, suggesting a specific relationship of this parameter with the depressive state.

Background: The present study evaluated the cortical activation during emotional information recognition. Methods: The study group included 16 patients with depression, and 16 healthy subjects were enrolled as a control group. Patients received eight weeks of antidepressant therapy. Functional MRI evaluated the cortical activation twice in the patient group and once in the control group. The fMRI task processed the emotional information with face demonstration from the PennCNP test battery. Results: During the processing of emotional information, patients showed activation in the middle and the inferior frontal gyri, the fusiform gyrus, and the occipital cortex. After treatment, patients showed a significant decrease in the frontal cortex activation for negative face demonstration and no frontal activation for positive emotion recognition. The left superior temporal gyrus activation zone appeared in patients after treatment and in the control group. Healthy subjects showed more intense frontal cortex activation when processing neutral emotions and less when showing happy and sad faces. Activation zones in the amygdala and the insula and deactivation zones in the posterior cingulate cortex were revealed in the controls. Conclusion: This study confirms the hypothesis that anomalies in the processing of emotional stimuli can be a sign of a depressive disorder.