Relations between particle size of HDL and LDL lipoproteins and cholesterol esterification rate.

Particle size of low density (LDL) and high density (HDL) lipoproteins and cholesterol esterification rate in HDL plasma (FER(HDL)) are important independent predictors of coronary artery diseases (CAD). In this study we assessed the interrelations between these indicators and routinely examined plasma lipid parameters and plasma glucose concentrations. In 141 men, healthy volunteers, we examined plasma total cholesterol (TC), triglycerides (TG), HDL and LDL cholesterol (HDL-C, LDL-C) and HDL unesterified cholesterol (HDL-UC). Particle size distribution in HDL and LDL was assessed by gradient gel electrophoresis and FER(HDL) was estimated by radioassay. An effect of particle size and FER(HDL) on atherogenic indexes as the Log(TG/HDL-C) and TC/HDL-C was evaluated. Subjects in the study had plasma concentrations (mean +/- S.D.) of TC 5.2+/-0.9 mmol/l, HDL-C 1.2+/-0.3 mmol/l, TG 2.1+/-1.7 mmol/l, glucose 5+/-0.8 mmol/l. Relative concentration of HDL(2b) was 17.6+/-11.5 % and 14.6+/-11.8 % of HDL(3b,c). The mean diameter of LDL particles was 25.8+/-1.5 nm. The increase in FER(HDL) significantly correlated with the decrease in HDL(2b) and LDL particle size (r = -0.537 and -0.583, respectively, P<0.01) and the increase in HDL(3b,c) (0.473, P<0.01). Strong interrelations among TG and HDL-C or HDL-UC and FER(HDL) and particle size were found, but TC or LDL-C did not have such an effect. Atherogenic indexes Log(TG/HDL-C) and TC/HDL-C correlated with FER(HDL) (0.827 and 0.750, respectively, P<0.0001) and with HDL and LDL particle size.

Correction of aortico-left ventricular tunnel during the first day of life.

Two critically ill newborns with aortico-left ventricular tunnel and severe heart failure were operated on at six and 14 hours after birth. The diagnosis was established clinically by the auscultatory finding of systolic and diastolic murmurs and by two-dimensional and Doppler echocardiography. In the first newborn, the left aortic sinus was connected with the left ventricle below the aortic valve by an aneurysmatically dilated tunnel. In the second patient, the tunnel connected the right aortic sinus and the left ventricle. The repair was performed under deep hypothermia, total hemodilution, and cardiopulmonary bypass. The tunnel was closed with two patches of Gore-Tex on the aortic and ventricular orifices. Both children are free from symptoms and are developing normally 10 and 8 months after repair.

Long-term ventricular performance after intra-atrial correction of transposition: left ventricular filling is the major limitation.

OBJECTIVE: To establish the incidence of systolic and diastolic dysfunction of the right and left ventricle in a large cohort of patients after Mustard or Senning operations and to assess changes in the incidence on long term follow up. DESIGN: Postoperative case-control study using radionuclide ventriculography. Ejection fractions, peak filling rates, rapid filling periods and fractions, slow filling periods and fractions, and atrial contraction periods and fractions were studied. SETTING: Tertiary care centre, ambulatory and hospital inpatient care. PATIENTS: A convenience sample of 153 patients studied at median age of 6.9 years (median 4.4 years after surgery). In 99 cases another study was available at a median age of 15.3 years (median 13 years after surgery and 8.8 years after the first study). RESULTS: Respective incidences of dysfunction in the first and the second study were as follows: ejection fraction-right ventricle 7.8% and 8.1%, left ventricle 7.2% and 10.1%: peak filling rate-right ventricle 0% and 4.2%, left ventricle 14.3% and 29.5% (p < 0.05); rapid filling period-right ventricle 18.3% and 11.6%, left ventricle 30.2% and 30.5%; slow filling period-right ventricle 4.8% and 3.2%; left ventricle 11.9% and 23.2%; atrial contraction period-right ventricle 0.8% and 4.2%, left ventricle 15.1% and 26.3%; rapid filling fraction-right ventricle both 0%, left ventricle 82.5% and 79.0%; slow filling fraction-right ventricle 0.8% and 4.2%, left ventricle 37.3% and 30.5%; atrial contraction fraction-right ventricle both 0%, left ventricle 79.4% and 71.6%. CONCLUSIONS: The incidence of systolic ventricular dysfunction is 8% (right ventricle) and 10% (left ventricle) 13 years after surgery, without a significant increase over the eight year follow up. Diastolic filling is abnormal in up to 80% of patients and left ventricular peak filling rate deteriorates with time.

Pulmonary function in children with atrial septal defect before and after heart surgery.

OBJECTIVE: To test the effect of heart disease and heart surgery on lung function. DESIGN: A pulmonary function study of children undergoing surgery for atrial septal defect (ASD). SETTINGS: University hospital. PATIENTS: 26 children tested before surgery (at mean (SD) age 11.8 (3.8) years) and 24 patients tested 1.8 (0.2) years after surgical correction. METHODS: Lung volumes, lung elasticity, and airway patency indices were measured using standard techniques. RESULTS: Before surgery: pulmonary function test abnormalities were found in 18 of the 26 patients. Stiff lung was found in 12, lung hyperinflation in five, and indices of decreased airway patency in four. Total lung capacity decreased in only two patients. After surgery: pulmonary function test abnormalities were found in 12 of the 24 patients (informed consent not given for two patients). Stiff lung was detected in nine and indices of peripheral airway obstruction in four. Mean values of specific airway conductance and peak expiratory flow were all normal. Lung hyperinflation was found only in one of 24 patients. No correlation between perioperative events and pulmonary function test data was found. CONCLUSIONS: Pulmonary function test abnormalities persist in half the patients almost two years after surgery for ASD. A decrease in the total frequency of pulmonary function test abnormalities (in 19% of the patients), with a decrease in stiff lung in 8% and lung hyperinflation in 15%, was not significant. Impairment of lung function related to ASD is associated with the disease itself rather than the surgical procedure.

Lung function in children and adolescents with tetralogy of Fallot after intracardiac repair.

We studied lung function in 41 patients, aged 6-27 years, 1-5 years after intracardiac surgical repair (ICR) of tetralogy of Fallot (TOF) and about 5 years after the establishment of the Pediatric Cardiac Center in Prague. The measurements included vital capacity (VC), total lung capacity (TLC), functional residual capacity (FRC), residual volume (RV), forced expiratory flows (FEF), specific airway conductance (SGaw), lung recoil pressure (Pst), and specific static lung compliance (SC1st). Single or multiple abnormal lung function parameters were found in 83% of patients. Lung function was not related to shunting operations prior to ICR, hemoglobin concentration, and hematocrit, and had no specific pattern. Pst at 100% TLC and 90% TLC declined with increasing age at ICR and at lung function testing, while SC1st rose, as did the ratio FRC/TLC. Fifteen patients were studied before and after surgery. Single or multiple lung function tests were abnormal in 93% before and in 84% after ICR. After ICR the ratios FRC/TLC and also RV/TLC, FEF at 25% VC, and FEF at 60% TLC were less frequently abnormal, while Pst at 100% TLC and at 90% TLC, as well as SGaw and TLC, were more frequently abnormal after ICR. The results indicated a regression of smaller airway obstruction and lung hyperinflation after ICR. The evolution of abnormally compliant (emphysematous) lungs with growth of the patients might be a sign of permanent sequelae of early lung damage from abnormal pulmonary hemodynamics.

Lung function in children and adolescents with idiopathic interstitial pulmonary fibrosis.

Lung function of 65 patients who had idiopathic interstitial pulmonary fibrosis (IIPF) that had been treated with prednisone was evaluated by tests of ventilatory function, lung mechanics, and gas exchange at rest and during exercise. Ages on initial investigation ranged from 5 to 20 years. In 35 of 65 patients the studies were repeated an average of four times over a period of 1 to 9 years. Results of the first testing were as follows: vital capacity (VC)-significantly reduced in all patients; inspiratory capacity (IC)-significantly reduced in all patients; total lung capacity (TLC)-reduced in 91%; functional residual capacity (FRC)-reduced in 31%; residual volume (RV)-reduced in 6%; elastic recoil of the lungs (Pstl)-significantly increased in 97% at 100% TLC, significantly increased in 52% at 90% TLC, reduced in 68% at 60% TLC; 7) static compliance (Cst)-reduced in 83%; 8) dynamic compliance (Cdyn)-reduced in 88%; 9) specific airway conductance at FRC level (Gaw/TGVex)-significantly increased in 50%; 10) maximum expiratory flow rates at 60% TLC (Vmax 60% TLC, in TLC/s)-significantly reduced in 33%; 11) upstream airway conductance (Gus 60% TLC, in TLC/s/cm H2O)-reduced in 32%; 12) diffusing capacity of the lungs for carbon monoxide (DLco) related to body-surface area-abnormal in 58% (when corrected for lung size, i.e., DLco/TLC, abnormal in only 8%); 13) PaO2 at rest and after 6 minutes submaximal exercise-reduced in 25% and 63%, respectively. Changes in lung function that occurred with growth were assessed in terms of percentages of predicted values. Results showed that the VC and IC remained significantly reduced. An actual reduction of TLC, FRC, RV, breathing frequency, DLCO, and Pstl at 100% and 90% TLC was observed. Increases were seen in Pstl at 60% TLC, Gaw/TGVex, Vmax, and Cst. Indices of lung elasticity suggested that regions of fibrosis and emphysema had become present. Smaller patients were also noted to have stiffer lungs.

Infants with critical heart disease in a territory with centralized care.

All children with a critical heart disease in a 6.3 million inhabitants territory were referred and all infants who died were autopsied and the protocols sent to the only Center of Pediatric Cardiology and Cardiovascular Surgery. In the first 5 years of the centralized care, 1,122 infants, i.e. 2.36/1,000 live births suffered from a critical heart disease. 639 (57%) were admitted to the Center and the rest died in provincial hospitals with but not always from a heart disease found at autopsy. An additional 43 (6.2%) patients had nonstructural heart disease and 12 (1.7%) had heart diseases not considered to be critical. The total incidence of critical heart disease fluctuated from 2.15 to 2.51/1,000 live births without any well-defined trend. A decrease in the relative frequency throughout the 5-year period was found for common arterial trunk, pulmonary stenosis and atresia while an increase was observed in patency of the arterial duct. The most frequent critical heart diseases in infancy were: ventricular septal defect (18.2%) - mostly in isolation; complete transposition (14.6%); aortic coarctation (10.0%); hypoplastic left heart syndrome (9.1%) and pulmonary atresia (6.3%). The majority (51.4%) of patients became critically ill or died in the neonatal period. The most common conditions seen in neonates were complete transposition (22.5%), hypoplastic left heart syndrome (16.1%) and coarctation of the aorta (9.5%). The highest share of critically ill patients was encountered in complete transposition (100%), pulmonary atresia (98.7%), common arterial trunk (97.4%) and double outlet right ventricle (92.1%). The least dangerous were atrial septal defect (6.6%), pulmonary stenosis (7.0%), aortic stenosis (12.2%) and ventricular septal defect (21.0%). The mean age was 76 (+/- 56) days at admission and 59 (+/- 73) days at death. Urgent cardiovascular surgery was performed in 235 (36.8%) of the 639 patients admitted in infancy, that is 0.5 per 1,000 live born children.

Distribution of congenital heart malformations in an autopsied child population.

All stillborn and all deceased children were autopsied during a 27-year period in a given territory with some 1,220,000 inhabitants. Of the 3969 stillborn children, 81 (2.1%) had a congenital heart malformation. Out of the 470,188 liveborn children, 13,629 died before the age of 15 years. Autopsy demonstrated a heart malformation in 1008 (0.21%) of these liveborn children. Thus, with 1089 cases found in the combined stillborn and liveborn and later deceased children, congenital heart malformation was found in 6.2% of all autopsied children. This represented 7.4% of the total mortality of liveborn children and 41.4% of all congenital malformation discovered in the deceased children. In total, 2257 congenital heart lesions were identified with a mean of 2.1 lesions per child. The lesions were classified in 37 categories of heart malformation. The most common malformation was ventricular septal defect, followed by hypoplastic left ventricle and complete transposition. The most frequent heart lesion was also ventricular septal defect followed by patency of the arterial duct. The frequency of the different heart malformations in stillborns differed from that in the liveborn children. The ratio of boys and girls in the overall series was 1.28:1, with pronounced differences in sex distribution being observed in some malformations.

Causes of death in neonates born with a heart malformation.

All deceased infants were autopsied in a territory with a population of 1 220 000 inhabitants and a mean of 17 410 live births a year. During a period of 25 years (which preceded the introduction of advanced neonatal cardiac surgery), 393 neonates (6% of all deceased neonates) had died in whom a congenital heart malformation was found at autopsy. 118 (30%) of deaths were due to noncardiac causes. Lethal congenital noncardiac malformations caused death in 38 (10%) neonates. A perinatal disease (including birth trauma) was the cause in 65 (16%) neonates. An association of a noncardiac congenital malformation with a perinatal disease was involved in 6 (2%) neonates and a birth weight lower than 1000 g (together with a lethal perinatal disease or alone) was considered responsible in 9 (2%) neonates. Noncardiac but not unambiguously lethal malformations (mostly multiple) could at least have contributed to the fatal outcome in a further 86 (22%) neonates. A low birth weight could have contributed to death in 102 (26%) neonates, particularly in 42 (11%) neonates with a low birth weight associated with multiple noncardiac nonlethal malformations. A most probable or possible noncardiac cause of death was found in all cases of atrial septal defect, in 93% of tetralogies of Fallot, in 84% of ventricular septal defects, in 72% of hearts with double outlet right ventricle and in 57% of those with aortic coarctation. A congenital heart malformation was considered responsible for a fatal outcome in 82% of cases with discordant ventriculoarterial connexions ("transposition of the great arteries"), 79% of hypoplastic left hearts, 68% of pulmonary atresias and 53% of tricuspid atresias. The high proportion of noncardiac death noted to occur in the first postnatal day was found rapidly to decrease in the following days.

Lung function in atrial septal defect after heart surgery.

Lung volume, indices of lung elasticity and airway patency were measured in 74 patients, 9-21 yr old (15.0 +/- 2.5 yr) with atrial septal defect (secundum type) from 2-11 (5.1 +/- 2.5) yr after successful surgical correction. Clinical condition in all patients was classified as excellent. Heart surgery was performed at the age of 4-14.8 (9.9 +/- 3.0) yr. Lung function abnormalities were found in 35 (47.3%) patients. Lung recoil pressure was significantly increased in 24 (32.4%) patients. The mean value of lung recoil pressure at 100% of total lung capacity reached 123 +/- 31% of the predicted value (P < 0.0001). Specific static compliance was within normal limits. Specific airway conductance was significantly reduced in 13 (17.6%) patients. Maximum expiratory flow at 25% of vital capacity was significantly reduced in 4 (5.4%) patients. Static lung volumes did not differ from reference values. Since various abnormalities of lung function tests (most frequently the tests suggested increased lung stiffness and obstruction of larger airways) were revealed in almost half of the studied children and adolescents after successful surgery for atrial septal defect, we propose to carry out lung function tests routinely as another criterion of health conditions in these patients.

Lung function in simple complete transposition after intracardiac repair.

Pulmonary function was measured in 35 patients (mean age 11.6 years) with simple complete transposition 4.4 years after intracardiac repair. A disturbance in the lung function (greater than 2 SD from the normal value) was found in 88% of the patients. A marked increase in static recoil pressure (P less than 0.001) was most frequent (in 66%). Static lung compliance was only 75.1% of the predicted values. Values of mean vital and total lung capacity were decreased (P less than 0.01 and 0.001). Residual volume, the ratios of functional residual versus total lung capacity and residual volume versus total capacity were all increased. The signs of decreased patency of the airways were found in only 4 patients. A negative correlation was detected between the indices of lung stiffness and the age of assessment of lung function. A positive correlation was found between the ratios between functional residual and total capacity and pulmonary blood flow. No other correlation between lung function data and pulmonary arterial pressure or flow was proved. Increased lung stiffness, restriction of lung volume and hyperinflation could influence unfavorably the long-term results in successfully treated patients with simple complete transposition.

Effect of hypoxaemia on enzymes supplying myocardial energy in children with congenital heart disease.

The differences in energy metabolism of the myocardium in children with congenital cardiac malformations producing hypoxaemia (arterial oxygen saturation 77 +/- 2%) or normoxaemia (arterial oxygen saturation 94 +/- 2%) were analysed by measuring the activity of the representative energy-supplying enzymes. Right atrial and ventricular tissue samples were obtained during surgical interventions. We demonstrated that myocardial metabolism was significantly influenced by hypoxaemia: the aerobic capacity of the energetic metabolism was reduced both in the atriums and ventricles. Atrial myocardium was more affected: in addition to citrate synthase, the activity of enzymes connected with lactate uptake and carbohydrate catabolism was also significantly decreased. These results demonstrate that the human heart is able to adapt to hypoxaemia by changing its energetic metabolism.

The physiological closure of ductus arteriosus in the rat. An ultrastructural study.

The evolution of morphological changes in the wall of the ductus arteriosus during its physiological closure in newborn rats was examined by electron microscopy. The contraction of smooth muscle cells in the tunica media seems to be the primary mechanism which leads to the physiological closure of the ductus arteriosus. For this reason our attention was centred mainly on the morphology of the tunica media. No important changes in the ultrastructure of smooth muscle cells can be observed in the early phases of the closure. Most of them exhibit ultrastructural features of cells with enhanced synthetic activity during all phases of the closure. The permanent contraction of smooth muscle cells results in their morphological changes. The most striking is the herniation of smooth muscle cell cytoplasm into the endothelial and later into adjoining muscle cells. These changes together with signs of degeneration of the smooth muscle cells are already clearly discernible 120 min after birth. The elastic component of the tunica media exhibits surprisingly fast changes. As soon as 60 min after birth, the fragmentation of elastic membranes and their structural changes provided evidence about the degradation of elastic material. The matrix vesicles, probably derived from the lysosomal apparatus of the muscle cells, may play an essential role in this process.

Good exercise tolerance and impaired lung function after atrial repair of transposition.

OBJECTIVE: Evaluation of long-term results of atrial correction of transposition of the great arteries (TGA), focusing on the relationship between pulmonary function and exercise tolerance. METHODS: A prospective population-based study-56 out of 60 survivors of Mustard/Senning repair, born in Bohemia in 1980-1984 (median age at surgery 0.85 years) were followed up over 13.4 +/- 1.2 years and studied by complete lung function and bicycle exercise testing. RESULTS: Maximum heart rate on exercise reached 181 +/- 14 bpm (Z-score: -1.06 +/- 1.66, range -6.7 to +1.6); VO2max: 40.6 +/- 6.7 ml/kg per min (Z-score: -0.97 +/- 1.4, range -5 to +1.8). A total of 73.6% had abnormal lung function, most frequently features of stiff lung (39.6%) and lung restriction (32.1%). Static recoil pressure of the lungs measured at 100, 90 and 60% of total lung capacity reached 137, 126 and 130%, respectively (Z-score: 1.93 +/- 2.33, 1.64 +/- 1.96, and 1.14 +/- 1.95, respectively). There was an inverse relationship between static recoil pressure of the lungs and VO2max (r = -0.306, P = 0.043), indicating the impact of lung function abnormalities on exercise tolerance. Comparison with lung function study of the group of 'pioneer' Mustard patients operated at the mean age of 4.4 years revealed a similar pattern and frequency (73.6% in current series vs. 88%, NS). CONCLUSIONS: Long-term follow-up has shown good exercise tolerance in the majority of patients after atrial correction of TGA performed in infancy. Many of them, however, have impaired lung function, especially stiff lung, although less frequently than original patients operated at a later age. The stiff lung can impair the exercise tolerance.

Differences between atrial and ventricular energy-supplying enzymes in five mammalian species.

The purpose of this study was to compare a pattern of 7 enzymes of energy-supplying metabolism in atrial and ventricular myocardium in some mammalian species. Tissue samples of right and left atria and ventricles were obtained from adult male rats, guinea-pigs, rabbits, dogs and pigs. The results clearly demonstrate significant differences in enzyme activities between the atria and ventricles in all these species. In the atria the activity of enzymes connected with aerobic and lactate metabolism (hydroxyacyl-CoA-dehydrogenase, citrate synthase, malate dehydrogenase and lactate dehydrogenase) was markedly lower than in ventricles. On the other hand, in rats, dogs and pigs glucose phosphorylation capacity (hexokinase) was approximately the same in atrial tissue as in ventricles. Right-to-left metabolic differences were much less expressed; conspicuous was only the higher activity of hydroxyacyl-CoA-dehydrogenase in the left atria and ventricles of guinea-pigs and rabbits indicating higher fatty acid utilization capacity in the left heart.

Effect of prostaglandin E2 on the ductus arteriosus in the newborn rat. An ultrastructural study.

A patent ductus arteriosus (DA) was maintained in newborn rats (Wistar strain) by administering prostaglandin E2 (PG E2) in doses of 15 micrograms.kg-1 at 30 min intervals up to 300 min after birth. In the control animals, the DA was functionally closed 300 min after birth. The lumen was blocked by clustered endothelial cells at various stages of degeneration. Elastic membranes of the media had disintegrated into irregular fragments and the smooth muscle cells were contracted. Cytoplasm excrescences formed on their surface as a result of contraction protruded as hernias into adjacent muscle cells and into endothelial cells. The smooth muscle cells degenerated. The administration of PG E2 inhibited contraction of the smooth muscle cells and so also the development of degenerative changes; 300 min after birth the DA was fully patent, the elastic membranes were structurally intact, regularly organized and continuous. The smooth muscle cells had the character of synthesizing cells with richly developed granular endoplasmic reticulum. The intima and its endothelial lining were likewise free from structural changes. The ultrastructural image of the wall of the DA correspondent to the state 10 min after birth, when the DA was fully patent. The administration of PG E2 did not induce any ultrastructural changes indicative of injury to the wall of the DA.

Protein profiling of human atrial and ventricular musculature: the effect of normoxaemia and hypoxaemia in congenital heart diseases.

Samples of myocardial tissue were obtained during surgical intervention from children operated for different types of congenital heart disease (tetralogy of Fallot, ventricular and atrial septal defect). Sarcoplasmic, contractile and collagenous proteins were isolated by stepwise extraction from the both right ventricular and atrial musculature. It has been found that: a) the concentration of contractile proteins is significantly higher in the ventricles, b) the concentration of collagenous proteins is significantly higher in the atrium, c) the concentration of sarcoplasmic proteins was not different, d) in children with chronic hypoxia the above atrio-ventricular differences persisted. Moreover, the proportion of the soluble collagenous fraction in the atria was significantly increased.

Ontogenetic development of energy-supplying enzymes in rat and guinea-pig heart.

The purpose of the present study was to compare the ontogenetic development of the activity of myocardial energy-supplying enzymes in two mammalian species, differing significantly in their level of maturation at birth. The animals were investigated during the late prenatal period and 2, 7, 14, 21, 25, 30, 63, 120 and 730 days after birth in the rat and 2, 21, 84 and 175 days in the guinea-pig. The following enzymes were assayed in the right and left ventricular myocardium: lactate dehydrogenase (LDH, lactate uptake and/or formation), triose phosphate dehydrogenase (TPDH, carbohydrate metabolism), glycerol phosphate dehydrogenase (GPDH, glycerol-P shuttle)), hexokinase (HK, glucose phosphorylation), malate dehydrogenase (MDH, tricarboxylic cycle), citrate synthase (CS, tricarboxylic cycle) and hydroxyacyl-CoA dehydrogenase (HOADH, fatty acid breakdown). The rat heart, highly immature at birth, exhibits three different developmental patterns of energy-supplying enzymes, identical in both ventricles: (i) two mitochondrial enzymes of aerobic metabolism (CS, HOADH) and GPDH have a relatively low activity at the end of prenatal life; thereafter their activity steadily increases, approaching the adult levels between the 3rd and 4th postnatal weeks. A significant decrease was observed between the 4th and 24th months. (ii) MDH and LDH: prenatal values were significantly higher as compared with the 2nd postnatal day; after this period the activities increased up to adulthood (4 months) and decreased during senescence. (iii) The activities of HK and TPDH are characterized by only moderate changes during development. HK differs from all other enzymes by the highest prenatal values, which exceed even adult values. In contradiction to the rat heart, the developmental differences in more mature guinea-pig heart were significantly less pronounced. The only ontogenetic differences observed were the lower activities of enzymes connected with aerobic metabolism at the end of the prenatal period. Our results point to possible differences in the development of adaptive metabolic pathways in animals with different levels of maturation at birth.

[Energy-supplying metabolism of the volume overloaded and hypoxia stressed heart in children]. / Energieliefernder Stoffwechsel des volumen- und hypoxiebelasteten Herzens bei Kindern.

This study summarizes results obtained with regard to atrial and ventricular enzymes of energy supplying metabolism in children with different types of congenital heart disease. In all groups of patients - normoxemic as well as hypoxemic - significant atrio - ventricular differences were observed: the right ventricle is amply equipped for utilization and oxidation of all major nutrients, while the right atrium utilizes glucose predominantly. Myocardial metabolism in children with congenital heart disease was significantly influenced by hypoxemia: the capacity of aerobic enzymes in cyanotic patients was significantly lower, both in atrial and ventricular tissue, whereby the atrial changes were even more striking. No marked differences were found between atrial and ventricular septal defects in normoxemic patients; the only difference was a lower capacity of fatty acid catabolism in children with atrial septal defect.

[Does moderate alcohol drinking decrease the incidence and mortality rate in ischemic heart disease?]. / Snizuje mírné pití alkoholu výskyt i úmrtnost na ischemickou chorobu srdecní?

Moderate drinking of alcohol decreases the progress of atherosclerosis, cardiovascular morbidity and mortality rate and total mortality. The mechanisms of action have not been clarified yet, but changes of lipid metabolism, antioxidative effect and changes in hemostasis are accused to play the major role. Moderate drinking leads to the increase of HDL cholesterol and decrease of LDL cholesterol. Antioxidants are distributed throughout the skin of grapes and therefore are present in higher concentration in red wine. Alcohol decreases the fibrinogen level and increases tPA, inhibits platelet aggregation and reduces factor VIIc. It positively influences stress, fear, anxiety and depression. Optimal daily consumption should be 20 to 40 g in men and half of it in women. Everyday drinking is important. There is no big difference between drinking beer, wine or drinks. The most crucial is to keep the moderate level of consumption.