[Use of variable number of tandem repeat polymorphism in assessing correct sampling in prenatal diagnosis of monogenic disorders].
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Amniocentesis↗
Biomedical subjects
F Simko
Publications and source records attributed to F Simko.
[Diagnosis of Duchenne and Becker muscular dystrophy in Slovak patients using multiplex polymerase chain reaction].
The authors of the paper describe the diagnostic method of deletion in the dystrophin gene by means of an improved variant of the polymerase chain reaction--so called multiplex PCR. The authors analyzed a group of 66 patients with developed clinical symptoms of the disease. The deletion screening included 22 exones of the dystrophine gene and it was performed in 5 multiplex PCR reactions. 20 patients yielded a verified deletion which was pre-assessed by Southern's hybridization. The relative simplicity of multiplex PCR which does not require the use of radioisotopes, its low time and financial needs, make this method to represents an appropriate alternative of Southern's hybridization in the assessment of deletion of the dystrophine gene. (Fig. 1, Ref. 19.)
Dystrophin↗
Captopril attenuates proteosynthesis in the aorta and decreases endothelaemia in rabbits with aortic insufficiency.
The effect of the angiotensin converting enzyme (ACE) inhibitor, captopril, on proteosynthesis in the aorta, acetylcholine-stimulated aortic relaxation and endothelaemia (circulating endothelial cells) was investigated in rabbits with aortic insufficiency. The animals were studied 28 days after experimental intervention. Cardiac volume overload stimulated proteosynthesis in the aorta as reflected by increased ribonucleic acid (RNA) concentration and [14C] leucine incorporation into proteins of the aorta. Moreover, the number of endothelial cells in the blood was increased. The administration of captopril starting from the second day of the haemodynamic overload, partially prevented the increase both in aortic proteosynthesis and in endothelaemia. Despite these alterations, the relaxing ability of the aorta to acetylcholine was not changed either by the haemodynamic overload or by captopril. We conclude that the increase of proteosynthesis in the aorta and of endothelaemia in the early period of chronic cardiac volume overload in rabbits were partially prevented by chronic captopril treatment. Neither aortic insufficiency nor captopril changed the acetylcholine-induced relaxation of the aorta.
Acetylcholine↗
Protein remodelling of the heart in NO-deficient hypertension: the effect of captopril.
Long-term administration of NG-nitro-L-arginine methyl ester (L-NAME) induces development of NO-deficient hypertension. The aim of the present study was to determine whether treatment with the angiotensin-converting enzyme (ACE) inhibitor captopril can prevent hypertension, left ventricular (LV) hypertrophy, changes in nucleic acid concentration, protein synthesis and protein profile of the left ventricle. Four groups of rats were investigated: control, L-NAME 40 mg/kg/day, captopril 100 mg/kg/day, L-NAME 40 mg/kg/day along with captopril 100 mg/kg/day. NO-synthase activity in the left ventricle was found to be decreased by 69% in the L-NAME group. Captopril did not influence this inhibition of NO-synthase activity. However, it completely prevented hypertension and left ventricular hypertrophy development. The increase in left ventricular RNA and DNA concentration and -14C-leucine incorporation observed in the L-NAME group was completely prevented by simultaneous captopril treatment. The protein profile of the left ventricle in the L-NAME group was characterized by higher concentration of metabolic proteins (MP), soluble collagenous proteins (SCP) and of hydroxyproline in insoluble collagenous proteins (ICP). The concentration of hydroxyproline in ICP was significantly decreased by simultaneous captopril treatment. We conclude that captopril prevented the development of hypertension, left ventricular hypertrophy, increase in nucleic acid concentration and diminished collagen concentration by mechanisms different from affecting NO-synthase activity.
Angiotensin-Converting Enzyme Inhibitors↗
[Y-chromosome mosaicism as markers of increased risk for development of gonadoblastoma in patients with Turner's syndrome].
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Female↗
Effect of captopril on the development of left ventricular hypertrophy in rabbits with aortic insufficiency.
We investigated the effect of captopril on the growth of the left ventricle in an experimental model of aortic insufficiency. Four groups of rabbits were studied 28 days after experimental intervention: 1. control, 2. control with captopril (10 mg/kg/day), 3. aortic insufficiency, 4. aortic insufficiency with captopril (10 mg/kg/day). Aortic insufficiency induced hypertrophic growth of the left ventricle demonstrated by increased weight and ribonucleic acid (RNA) concentration. Administration of captopril only slightly attenuated the weight increase of the left ventricle and the increase in concentration of left ventricular RNA. However, captopril reduced the concentration of left ventricular deoxyribonucleic acid (DNA) both in the control and even more in the group with aortic insufficiency. The chronic haemodynamic overload enhanced mitochondrial respiration in the left ventricle which was not influenced by captopril. We conclude that captopril in the dose 10 mg/kg/day did not prevent hypertrophy of the left ventricle but reduced left ventricular DNA concentration.
Angiotensin-Converting Enzyme Inhibitors↗
Medical researchers in the Slovak Republic seek cooperation with Canadians.
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Canada↗
Left ventricular hypertrophy regression as a process with variable biological implications.
OBJECTIVE: To determine whether myocardial hypertrophy regression, similarly to hypertrophy itself, is a process of variable nature with different biological implications. DATA SOURCES: Current Contents and MEDLINE searches under myocardial hypertrophy and regression of hypertrophy-related headings were conducted. DATA EXTRACTION: The search covered the period from 1969 to 1994, and 89 articles dealing with both human and animal studies were used. DATA SYNTHESIS: The positive adaptive effect of left ventricular myocardial hypertrophy may be counterbalanced by increased incidence of heart failure, myocardial infarction or sudden death. The risk of undesirable cardiovascular events varies according to the character of hypertrophic growth. Reduction of cardiac mass to that of a normal heart need not always mean that the ventricle is normal in all aspects. Several forms of left ventricular hypertrophy regression may be distinguished. The hypertrophy regression of the athletic heart is of a physiological nature. The spontaneous regression of left ventricular hypertrophy as seen in the rabbit model of aortic insufficiency has a pathological aspect resulting in heart failure. The nature of therapeutically induced regression of hypertrophy may vary according to fibrotic tissue concentration, energetical state and the function of the regressed heart. CONCLUSION: The biological implication of hypertrophy regression varies especially with respect to the nature of hypertrophy and the mode of achievement of hypertrophied mass reversal. Only long term prospective studies can clarify the question as to which types of hypertrophy regression result in decreased cardiovascular risk.
Animals↗
[ACE-inhibitors in the treatment of chronic heart failure: pathophysiologic principles of protective effects].
The aim of modern therapy of heart failure is not a pure removal of symptoms but an improvement of survival. The angiotensin-converting enzyme (ACE)-inhibitors reduced morbidity and mortality in several large clinical trials in patients with dysfunctional left ventricle or manifestant heart failure. Thus, ACE inhibitors are recommended for heart failure treatment as a drug of primary option, unless contraindications are present, and if tolerated by patient. The mechanism of action of ACE inhibitors in heart failure is hypothetical. Participation of three factors is supposed: improvement in the pumping function of the failing heart, reduction on the risk of sudden death and reduction in myocardial infarction incidence. Reduction of hemodynamic load, antiischemic action and reduction of fibrotic tissue proliferation in failing myocardium are responsible for heart function improvement. These mechanisms together with potential antiatherosclerotic, antiaggregative, fibrinolytic and protective effect on endothelial function are supposed to participate in reduction of acute myocardial infarction and sudden death origin. The mentioned effects are determined by interaction with both circulating and local renin-angiotensin systems. The negative hemodynamic effects and undesirable restructuralisation of the affected ventricle are thus influenced on systematic and local-tissue level. Similarly as any other therapy also the treatment of heart failure with ACE inhibitors needs experience and a rational well tailored individual approach. (Fig.1, Ref. 32.).
Angiotensin-Converting Enzyme Inhibitors↗
Captopril prevents NO-deficient hypertension and left ventricular hypertrophy without affecting nitric oxide synthase activity in rats.
The aim of the study was to assess whether angiotensin converting enzyme (ACE) inhibition with captopril prevents the development of hypertension and myocardial hypertrophy and affects nitric oxide synthase (NOS) activity in rats. Animals were divided into five groups: control, two groups receiving NG-nitro-L-arginine methyl ester (L-NAME) 20 or 40 mg/kg/day, a group receiving captopril 100 mg/kg/day and a group concomitantly treated with 40 mg/kg/day L-NAME plus 100 mg/kg/day captopril. After four weeks, systolic blood pressure (SBP) significantly increased in both L-NAME groups by 30% and 34%, respectively. In the captopril group, SBP significantly decreased by 30% and in the captopril plus L-NAME group SBP was not changed as compared to the control. Although left ventricular weight/body weight (LVW/BW) ratio in both L-NAME groups was significantly elevated by 19% and 29%, respectively, no alterations in LVW/BW ratio were found in the captopril group and captopril plus L-NAME group. In both groups receiving L-NAME, NOS activity significantly decreased by 17% and 69% in the heart, by 14% and 26% in the aorta, by 60% and 73% in the brain and by 13% and 30% in the kidney, respectively. Captopril did not influence NO synthase activity in any of the studied tissues. We conclude that captopril prevents the development of hypertension and LV hypertrophy without affecting NO formation.
Administration, Oral↗
Heart failure--the reason for or a consequence of failure of the periphery?
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Heart Failure↗
Spontaneous regression of left ventricular hypertrophy in a rabbit model of aortic insufficiency: possible clinical implications.
The right timing of surgical intervention in patients with aortic insufficiency is the crucial precondition for optimal postoperative course. To meet this demand, it is essential to have precise knowledge of the pathogenesis of this disease. Within the rabbit model of aortic insufficiency, four periods of adaptational changes to chronic haemodynamic overload were distinguished: developing hypertrophy, developed hypertrophy, regression of hypertrophy, and heart failure. The period of spontaneously developing regression of hypertrophy is linked with deterioration of function, metabolism, and structure of the left ventricle and represents an indication preceding heart failure. This paper presents the hypothesis that, in patients with severe aortic insufficiency, the left ventricle may undergo spontaneous regression of hypertrophy. Detection of this period may contribute to the insight into the pathogenesis of this disease and help to identify the patients who are candidates for surgery. Moreover, the onset of left ventricular diminution might represent the optimal phase for this intervention.
Animals↗
Pathophysiological aspects of the protective effect of magnesium in myocardial infarction (review).
Intravenous administration of magnesium has proved to have beneficial effect in acute myocardial infarction. Magnesium seems to act at different levels of the cardiovascular system. Of the greatest importance is the direct influence of Mg2+ on the cardiomyocyte which includes: reduction of cytoplasmatic calcium overload, protection of mitochondria against calcium influx, and diminution of cellular potassium, magnesium and ATP depletion. By means of these effects, or by its direct action on myocardium, Mg2+ inhibits the origin of postinfarctional dysrhythmias. Furthermore, magnesium reduces afterload by decrease in vascular resistance, and improves coronary flow. The mechanism underlying the protective effect of magnesium remains complex and poorly understood. Nevertheless, Mg2+ therapy is effective, undemanding, and easy to procure. Expectably, intravenous administration of Mg2+ may become a routine part of myocardial protection in acute myocardial infarction.
Coronary Circulation↗
Pathophysiological principles of the relation between myocardial hypertrophy of the left ventricle and its regression.
Hypertrophy of the left heart ventricle as a consequence of a haemodynamic overload is a process of ambiguous biological value. Although hypertrophy allows to increase the performance of the ventricle without substantial elevation in wall tension, it represents a risk factor of cardiac morbidity and mortality. The regression of hypertrophy seems to be a rational outcome of this ambivalent situation. Not every reversal of hypertrophied muscle mass, however, can be unambiguously considered therapeutic success. The biological value of hypertrophy regression depends on the type of hypertrophy, on the level of deterioration of the heart by a long-lasting haemodynamic overload, as well as on the way in which the reversal of hypertrophy is achieved. Even in the case when functional characteristics are preserved or even improved compared to the hypertrophied heart, hypertrophy regression need not automatically mean a decrease of the cardiovascular risk induced by ventricular hypertrophy. Regression of hypertrophy may be even disadvantageous in those situations when reduction of hypertrophy and reduction of the haemodynamic overload proceed in a disproportional manner. Spontaneously developing regression of the hypertrophied left ventricle as demonstrated on the model of aortal insufficiency, is an explicitly pathological state, resulting in heart failure. Regression of myocardial hypertrophy should not be considered the primary therapeutic aim but rather a part of the management of haemodynamic overload of the heart. The main aim is to achieve optimal perfusion of the periphery, yet at the same time to provide such conditions which would prevent the working load of the heart to become a limiting factor of survival.
Animals↗
Some actual aspects of ischemic heart disease.
The 59th annual conference of the German Society for Heart and Vessel Research was held from 15th to 17th April 1993 in Mannheim. More than six hundred lectures and posters were presented (including those invited from abroad) introducing the topics of current experimental and clinical cardiology. The primary lectures dealt with problems of etiology and pathogenesis of atherosclerosis and its complications. Also the principles of treatment of ischemic heart disease were discussed. Moreover, insights into confusing problems of reperfusion injury, hibernating myocardium and stunned myocardium were introduced. The presented data have shown that myocardial ischemia, its etiology, pathogenesis, manifestations and treatment form a bulk of challenging problems of present cardiology. Many such phenomena were described, which provoke more questions than give answers. Only close interdisciplined cooperation can help to solve some of them in the near future. (Ref. 35.)
Humans↗
[The effect of long-term administration of metipranolol on passive diastolic properties of the hypertrophic ventricle].
In the course of adaptation of the rabbit heart to volume load passive diastolic properties of the hypertrophic ventricle and myocardium were changing significantly. On day 30 following perforation of the aortic valve stiffness of the ventricle was reduced, yet normalized ventricular stiffness and myocardial stiffness were increased. These changes were prevented by beta adrenergic blockade during development of adaptation of the heart to volume load. Although ventricular stiffness was reduced, normalized ventricular stiffness and myocardial stiffness remained at the level of control values. The demonstrated effect of beta adrenergic blockade on passive diastolic properties of the ventricle and myocardium may be of value in preventing heart failure due to chronic hemodynamic load. (Tab.3,Ref.15.).
Animals↗
[Modification of the composition of the hypertrophic myocardium by beta adrenergic blockade].
Adaptation of the rabbit heart to volume load of the left ventricle is characterized by hypertrophic growth. This process involves an increase in the mass and changes in the composition of the myocardium. In the fifth week after perforation of the aortic valve an increase in phospholipid content and in mitochondria and a decrease in protein content was observed in the myocardium. These changes precondition a transient hyperfunction of the cardiomyocytes, but they presumably lead also to the eventual loss of contractile capacity. When the hypertrophic process occurs under conditions of nonspecific beta-adrenergic blockade, the required increase in left ventricular mass is achieved yet the content of phospholipids, proteins and mitochondria remains unchanged. Long-term blockade of beta-adrenergic receptors may be one of the modes of affecting the expression of cardiac genes in such a way that the hypertrophic myocardium does not develop conditions resulting in heart failure.
Animals↗
[Strategies in the use of isolated cardiomyocytes in relation to other models in experimental cardiology].
Selection of the optimal model for a specific experiment considerably determines the results and their correct interpretation. The model of the isolated cardiomyocyte is increasingly being used in experimental cardiology as it provides several advantages in comparison to models in which the heart tissue remains relatively complete. Similarly as in other models, the factors limiting its use have to be known also in the case of the isolated cardiomyocyte. To minimalize misinterpretation of results the given problem is to be handled at all available levels.
Heart↗