[Sustained ventricular tachycardia in a patient with a single ventricle of the heart and a pheochromocytoma].

A pheochromocytoma is a rare tumor that develops from adrenomedullary chromaffin cells and produce ones or more catecholamines, including adrenaline, norepinephrine, and dopamine. On rare occasions a pheochromocytoma is hormonally inactive. Cyanotic heart disease is also a relatively rare pathology. One of its least frequently occurring variants is the single ventricle of the heart. Presumably, in patients with cyanotic heart defects, the occurrence of pheochromocytes and paragangliomas will be higher due to the presence of certain germinative and somatic mutations. In cyanotic heart defects, the development of malignant arrythmias is one of the frequent causes of death. A combination of a pheochromocytoma with a single ventricle of the heart is extremely rare: only eight such cases have been described in the literature. This article describes a young patient with a unique case of a single ventricle of the heart, pheochromocytoma and sustained ventricular tachycardia. The cause of the ventricular tachycardia, in all likelihood, was inappropriate medical care - in this case, a prescription for verapamil. The surgical excision of the pheochromocytoma and the referral of the patient for cardiac surgery became possible only after correcting the antihypertensive and antiarrhythmic therapy. Verapamil was replaced with a combination of doxazosin and amiodarone, resulting in relatively satisfactory blood pressure readings and sinus rhythm.

[Risk factors and glycation end products in patients with different forms of coronary heart disease and type 2 diabetes mellitus]. / Faktory rosta i konechnye produkty glikirovaniya u bol'nykh s razlichnymi formami ishemicheskoi bolezni serdtsa i sakharnym diabetom 2-go tipa.

AIM: To determine the levels of growth factors and glycation end products in patients with different forms of coronary heart disease (CHD) and type 2 diabetes mellitus (T2DM). MATERIAL AND METHODS: A total of 134 patients with CHD and T2DM, including 38 patients with non-ST-elevation acute coronary syndrome (ACS), were examined. The arterial and venous serum levels of basic fibroblast growth factor-ß (FGF-ß), transforming growth factor-ß (TGF-ß), placental growth factor (PlGF), advanced glycation end products (AGEs) and their receptors (RAGE) were estimated in all the patients. RESULTS: A direct correlation was found between the degree of arterial stenosis and the level of growth factors and AGEs in the patients with T2DM; there was also a direct correlation of the examined factors with lipid metabolic parameters. There was a significant two-fold increase in FGF-ß, PlGF, and RAGE levels in the patients with ACS. CONCLUSION: Hyperglycemia was found to negatively affect the progression of atherosclerotic changes in the vessel wall and on that of fibrotic processes.

Cardiotropic effect of extracardiac transplantation of embryonic human myoblasts to mice with bradycardia: various effects of cell material.

Animals with bradycardia were detected in reproductive colony of mdx mice. Low pulse rate was associated with poor survival and predisposition to sudden death, but did not directly depend on the presence of dystrophin mutant gene or animal age. Heart rate increased in old mice with bradycardia after extracardial, intramuscular, and intravenous injection of human embryonic myoblasts. Stable normalization of the pulse was observed 2 weeks after transplantation, but early peak of heart rate was observed as early as 24 h after cell transplantation. Cell suspensions, which could contain stem cells (blood mononuclears and CD34+ lymphocytes), also corrected heart rhythm. Unlike the effect of myoblasts, cardiotropic effect of mononuclears was preceded by a period of tachycardia, while the effect of CD34+ lymphocytes was very unstable. The cardiotropic effect of myoblasts was combined with life span prolongation and certain rejuvenation in some animals. Erythrocytes and supernatant obtained during blood cell fractionation did not modify the heart rhythm in mice with bradycardia. After injection of myoblasts to mice with rare and normal pulses serum creatine kinase activity decreased with different rates. These data attest to a variety of biological effects of stem cells and/or their derivatives and to ambiguous mechanisms of these effects.

Hereditary muscular dystrophy in MDX mice as a homologous model for introduction of cell technologies in the treatment of progressive muscular dystrophies in humans.

Life-time monitoring of the main clinical and laboratory manifestations of hereditary muscular dystrophy in mdx mice confirmed the presence of mutation in exon 23 of dystrophin gene and the absence of this protein in skeletal muscles of mutant animals. Muscular dystrophy in mice was similar to human progressive muscle disorder, which allows the use of this model for the development of cell technologies for the treatment of hereditary muscular diseases in humans.

Xenotransplantation of embryonic precursors of human myogenesis for the correction of dystrophinopathy in mice with hereditary muscular dystrophy.

Human embryonic myogenic precursors were transplanted into muscles of mdx mice with hereditary dystrophin-deficient muscular dystrophy. Transplantation induced the synthesis of human dystrophin. The number of dystrophin-positive fibers progressively decreased, however, some of them were preserved even 5 months after transplantation. Our results indicate that xenogeneic transplantation of embryonic myogenic precursors compensates the genetic defect in dystrophin-deficient mice.

[Effect of the contractile function of the myocardium on the nature of hemodynamic reactions in patients with ischemic heart disease during Valsalva's test]. / Vliianie sostoianiia sokratitel'noi funktsii miokarda na kharakter gemodinamicheskikh reaktsii u bol'nykh ishemicheskoi bolezn'iu serdtsa pri provedenii testa Val'sal'vy.

Application of contrast cineventriculography and probe of the left ventricle indicated that there was a relationship between the status of myocardial contractility, its function, some hemodynamic parameters, the severity of regional left ventricular wall contractility impairments and the nature of a hemodynamic response to Valsalva's test. Normal left ventricular contractility determined sinusoidal responses. Decompensated impairments of myocardial contractility gave rise to a square wave. A response represented as a nil ++super-elevation was caused by a moderate impairment of left ventricular contractility and, probably, by the absence of adequate vasoconstriction in the fourth phase of Valsalva's test.

[The possible mechanisms for the development of myocardial ischemia during the performance of Valsalva's test by patients with ischemic heart disease]. / Vozmozhnye mekhanizmy razvitiia ishemii miokarda pri vypolnenii testa Val'sal'vy bol'nymi ishemicheskoi bolezn'iu serdtsa.

Changes in hemodynamics associated with Valsalva's test are responsible for a reduction in myocardial oxygen consumption and a decrease in diastolic coronary perfusion pressure in ischemic patients and subjects free of coronary heart disease. Due to stenosis and occlusion of coronary arteries lowering of perfusion coronary pressure in relevant patients becomes more profound and may induce ischemia in spite of diminished oxygen consumption. The main cause underlying onset of myocardial ischemia in patients with marked lesions of coronary arteries is initially low perfusion pressure and limited coronary reserve.