Репозиторий Университета

© 2018 by the authors; licensee Modestum Ltd., UK. Objective: Prolongation of the QT interval in patients with coronary heart disease (CAD) is a risk factor of polymorphic ventricular tachycardia (PVT) and as consequence, the sudden death. Drug-drug interactions (DDI) on metabolic rate involving cytochrome P-450 (CYP) is the one of the major cause of Long QT Syndrome (LQTS). The aim of the present study was to improve the safety of combined pharmacotherapy when using drugs that affect the QT interval. Method and Results: Medication occurrence of potential dangerous combination of medicines that are affected on QT interval duration in patients with CAD are researched (outpatient medical records (patient history) analysis). Clinical relevance of DDI, which are associated with changes in CYP enzyme activity, categorized by drugs.com Medication Guide. Finding potential dangerous combination of medicines that are affected on QT interval duration were administered to patients with CAD in 3.6% cases in outpatient clinical practice. The most often prescribed combination of drugs is amiodarone and torasemide (13.3% evidence of all concomitant administration that are leading to QT prolongation). The potential mechanism of Amiodarone and Torasemide interaction on metabolic rate that are leading to QT prolongation are competitive substrates CYP 2C8 and a result of inhibited CYP 2C9 by amiodarone. Conclusion: Ability to predict the prolongation of the QT interval caused by DDI on metabolic rate make possible to improve the safety concomitant administration to patients with CAD.

© 2018, Silicea-Poligraf. All rights reserved. Aim. To evaluate the exact efficacy of the implantable cardioverter-defibrillators (ICD) and combination devices (CRT-D), and to evaluate their influence on the rate of sudden death and overall mortality in patients with the dilation cardiomyopathy syndrome (DCMP), and to clarify the selection criteria for implantation. Material and methods. Totally, 220 DCMP patients investigated: 66 (30%) of them (mean age 48,5±12,8 y. o., 47 males) underwent implantation of ICD (n=37) and CRT-D (n=29), 154 (70%) patients were in comparison group (mean age 47,1±12,4 y. o., 104 males). In 60 patients (93,9%) the devices were implanted for primary prevention of sudden cardiac death (SCD). Follow-up lasted for 16 [6; 37] months. As primary endpoints, the following parameters were used: “death+transplantation”, mortality, SCD, “SCD+shock” and “death+transplantation+proper shocks of the defibrillators”. Results. Mortality in all DCMP patients was 19,1%, “death+transplantation” — 21,4%, SCD — 2,7%. There were no significant differences by these values in patients with both devices (19,7%; 22,7% and 1,5%), ICD (21,6%; 24,3% and 2,7%), CRT-D (17,2%; 20,7; and 0) and patients with no devices (18,8%; 20,8% and 3,2%). Significantly higher rates by “SCD+shocks” (18,2% v 3,2%, p<0,001) and “death+transplantation+shocks” (36,4% vs 20,8%, p<0,05) in patients with the implanted devices witness for real impact of the defibrillators in equality of overall mortality and SCD parameters. Among the patients with implanted devices, the genetic and mixed (genetic and inflammatory) nature of DCMP predominated (62,1 v 35,7%, p<0,001), there was significantly lower EF (26,3±9,2 v 30,7±10,3%, p<0,01), its end value (31,1±11,0 v 39,2±13,5%, p<0,01), significantly higher end diastolic size of the left ventricle (EDS, LV, 6,8±0,8 v 6,5±0,8 cm, p<0,05) and the grade of mitral regurgitation. In patients with the devices, rate of proper shocks was 18,2%. In isolated myocarditis there were no shocks (35,3±9,1% v 26,8±9,3%, p<0,05), EDS significantly lower (6,2±0,6 cm v 6,9±0,9 cm, p<0,01), ECG signs of LV hypertrophy were more rare (16,7% v 56,3%, p<0,05), but more commonly — the low voltage of QRS (33,3% v 10,6%, p=0,53); there were no differences in the rates of cardiotropic drugs prescription. Main predictors of the shocks were genetic origin of DCMP (isolated or with myocarditis, 25/75%, comparing with 20/33% in patients with no shocks, p<0,01, HR 1,58, OR 10,93, sensitivity 94,1%, negative predictive value 99,2%), and sustained (HR 18,0, sensitivity 98,1%) and non-sustained ventricular tachycardia (HR 1,43, sensitivity and negative predictive value 100%), decrease of QRS voltage and absence of the signs of LV hypertrophy on ECG (negative predictive value 92,8% and 95,6%). Conclusion. In DCMP patients, implanting of ICD/CRT-D was performed with acknowledged additional criteria (genetic or mixed DCMP etiology, lower EF and worse response to treatment); due to more effective ICD therapy, the values of mortality, “death+transplantation” and SCD were not higher than in less severe patients with no such devices. Proper shocks developed in patients with significantly higher EF. As an independent SCD risk factor and a criteria for patients selection to defibrillator implantation, genetic origin of DCMP should be used, especially if comorbid with myocarditis. As the predictors for benign outcome — absence of non-sustained ventricular tachycardia, lower QRS voltage, signs of LV hypertrophy on ECG. An algorithm proposed of DCMP patients selection for ICD treatment.

© 2018 Media Sphera Publishing Group. All rights reserved. The detection of grade II-III central obesity on a corpse in conjunction with the identification of two additional criteria (such as arterial hypertension and impaired glucose tolerance) provides, if combined with the autopsy data (including the visual reduction of muscular mass, the increased total amount of the adipose tissue, gynecomastia in men together with hypertrophied abdominal adipose tissue accumulation, decreased face and body pilosis), a basis for diagnostics of metabolic syndrome (MS). The objective parameters for this purpose are waist circumference measurements, corpse weight and height, the degree of visceral obesity, narrowing of the renal arteries as a result of their compression by the surrounding adipose tissue, and accumulation of epicardial fat confirmed by the results of the biochemical analysis. The signs of plasmorrhagia combined with fibrinoid degeneration of the vascular walls in the microcirculatory bed make it possible to suspect, with a high degree of probability, the development of hypertensive crisis that may result in a sudden death of the patients presenting with metabolic syndrome.

© 2018 Media Sphera Publishing Group. All rights reserved. This article presents an overview of the literature publications concerning pathological changes in the cerebral blood vessels and the factors underlying the development of hemorrhagic complications leading to sudden death of young people. The special emphasis is placed on the most important causes behind the changes in the vascular wall (including the congenital ones) responsible for the high risk of rupture of the intracerebral vessels associated with the development of hemorrhagic complications.